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  • 1. European Manual of Medicine Vascular Surgery C. D. Liapis Chief Editor K. Balzer, F. Benedetti-Valentini, J. Fernandes e Fernandes Editors
  • 2. Editors C. D. Liapis, K. Balzer, F. Benedetti-Valentini, J. Fernandes e FernandesVascular SurgeryWith 385 Figures and 58 Tables123
  • 3. Series Editors Volume EditorsWolfgang Arnold, MD Christos D. Liapis, MD, FACS, FRCSHNO und Poliklinik Department of Vascular SurgeryKlinikum rechts der Isar Athens University Medical SchoolMünchen Attikon University HospitalGermany Athens GreeceUwe Ganzer, MDHNO und Poliklinik Klaus Balzer, MDHeinrich-Heine-Universität Division of Vascular SurgeryDüsseldorf Evangelisches KrankenhausGermany Mülheim Germany Fabrizio Benedetti-Valentini, MD Department of Vascular Surgery University of Rome „La Sapienza“ Rome Italy José Fernandes e Fernandes, MD, PhD Chief of Service Department of Vascular Surgery Hospital Santa Maria and Faculty of Medicine Director Instituto Cardiovascular de Lisboa Lisbon PortugalISBN-10 3-540-30955-1Springer Berlin Heidelberg NewYorkISBN-13 978-3-540-30955-0Springer Berlin Heidelberg NewYorkLibrary of Congress Control Number: 2006928312 The use of general descriptive names, registered names, trademarks,This work is subject to copyright. All rights are reserved, whether etc. in this publication does not imply, even in the absence of a spe-the whole or part of the material is concerned, specifically the rights cific statement, that such names are exempt from the relevant pro-of translation, reprinting, reuse of illustrations, recitation, broad- tective laws and regulations and therefore free for general use.casting, reproduction on microfilms or in any other way, and stor- Product liability: The publishers cannot guarantee the accuracy ofage in data banks. Duplication of this publication or parts thereof is any information about dosage and application contained in thispermitted only under the provisions of the German Copyright Law book. In every individual case the user must check such informationof September 9, 1965, in its current version, and permission for use by consulting the relevant literature.must always be obtained from Springer-Verlag. Violations are liablefor prosecution under the German Copyright Law. Editor: Gabriele M. Schröder, Heidelberg, Germany Desk Editor: Waltraud Leuchtenberger, Heidelberg, GermanySpringer is a part of Springer Science + Business Media Production: LE-TeX Jelonek, Schmidt & Vöckler GbR,springer.com Leipzig, Germany© Springer-Verlag Berlin Heidelberg 2007 Cover Design: Frido Steinen-Broo, eStudio Calamar, Spain Printed on acid-free paper 24/3100Wa 5 4 3 2 1 0
  • 4. VAcknowledgementsWhen the invitation came from Springer-Verlag to produce this first Europeanmanual of vascular surgery, it was accepted enthusiastically by the editors, al-beit with some trepidation concerning the demands of such a venture. Thisconcern was due to the diverse nature of the vascular system, which coversevery part of the human body; therefore, diseases of the vascular system affectall organs and all parts of the human anatomy and in order to provide a thor-ough perspective on the discipline of vascular surgery, the manual would haveto cover the full spectrum of vascular diseases. However, the pressing need to produce a long-overdue European manu-al on vascular surgery was the driving force that brought together several ofthe finest minds in Europe, who so generously accepted the task of impartingtheir expert knowledge by contributing chapters in their own specific areas.The diversity of the discipline, coupled with the differences in managementof vascular diseases by authors originating from different European countries,required the work to be carefully formatted to render it an effective referencebook, based on recommended European standards for professionals and train-ees with a common goal: optimum care of the vascular patient. The editors are deeply grateful to the distinguished authors and all theirassociates involved in this compilation. Apart from these tremendous contri-butions, this project would not have been possible without the enormous as-sistance of my associate Dr. Yannis Kakisis and the invaluable cooperation ofMs. Gabriele Schroeder and Ms. Waltraud Leuchtenberger of Springer-Verlag,Patrick Waltemate of LE-TeX and my administrative assistant Ms. VivienneRose. We hope the readership will benefit from this first European Manual ofMedicine: Vascular Surgery. The editors Christos D. Liapis Klaus Balzer Fabrizio Benedetti-Valentini José Fernandes e Fernandes
  • 5. VIIForewordGregory D. SkalkeasProfessor Emeritus, Academician,President of the Foundation of BiomedicalResearch of the Academy of AthensVascular surgery has acquired a well-established identity throughout the Euro-pean Union, where vascular diseases are still the leading cause (40%) of deathand disability. Proper management of vascular diseases is dependent on public awarenessand appropriate training of specialists. This stands true for every medical dis-cipline. For vascular surgery it has an additional aspect because, besides therequired above-average standard of technical dexterity, the vascular surgeonshould also be well versed in a variety of subjects such as molecular biology, inthe use of ultrasound and – with the introduction of endovascular techniques– a skilful operator of guidewires and laparoscopic instruments. All the accu-mulated know-how and skills required for proper management of the vascularpatient demand a rapid change in the training of vascular surgeons and an in-depth knowledge of the various manifestations of vascular diseases. The information necessary for the above is disseminated through books,journals and the internet. Most of the time, however, articles in journals reflectthe experience and enthusiasm of the authors on the subject but not the levelof knowledge of the medical community as a whole. Electronic information isfast and reliable but always gives the reader the impression of being short-lived.Books, on the other hand, allow a reflection of what has been written and a trueinteractive role for the reader. Multi-author books have the inherited handicap of not conveying a specificmessage by virtue of the diversity of thought; however, when the authors hap-pen to be experts in their field and to represent most of the countries within theEuropean Continent that is striving to prove its successful function as a union,then such a collaboration can indeed convey a message: the level of knowledgeand the modus vivendi of vascular surgery in Europe. The editor and authors of this compilation are to be congratulated for suchan endeavour, worthy of the European spirit of unity and collaboration.
  • 6. IXPrefaceSir Peter BellProfessor of Surgery, University of LeicesterEuropean Manual of Medicine: Vascular SurgeryVascular surgery has evolved and expanded in a spectacular fashion during thelast 50 years. During this time previously untreatable conditions have becometreatable and dealt with on a regular basis by vascular surgeons. Many of thepioneers of vascular surgery were from Europe, starting with Cid Dos Santoswho invented angiography and made the whole field of vascular surgery pos-sible. Jean Kunlin in 1949 was the first surgeon to use a reversed vein by-passgraft successfully. In the field of aortic surgery, Lerich and Matas were pio-neers in this area and Felix Eastcott started the long and successful treatmentof carotid artery stenosis by surgery. Successive generations of Europeans havecontinued to be involved in the evolution of vascular surgery, taking it to a newphase of activity. European surgeons continue to be at the forefront of changesin vascular practice and have made it possible for the new era of laparoscopicand endovascular surgery to progress and flourish. One might ask why we need yet another textbook of vascular surgery. Thisis a perfectly reasonably question and the answer is because no book exists thatoffers comprehensive knowledge, both theoretical and practical, to every levelof vascular surgeon. Buying books is expensive and it is therefore importantthat such books are of use to all of those who may wish to read them. The aimof this book is to be as useful to the vascular trainee as to the established vas-cular consultant. To this end the editors have enlisted and given a clear briefto leading practitioners in the field. All of the topics that one would normallyexpect to see in such a book are included and the text is sufficiently referencedto make it authoritative. Pictures and figures are also used but not extensivelyand are not a major selling point of this volume. The theoretical and practi-cal aspects of open surgery, endovascular procedures and laparoscopic surgeryare all covered in detail and venous disease and lymphatic problems are notignored. One question that might be asked is: why are all the contributing surgeonsfrom Europe and none from other countries or continents? This is intentionaland not xenophobic, but an attempt to show that the necessary expertise tocover all aspects of the practice of vascular surgery exists in the expanded Eu-ropean community. It is also to acknowledge the fact that vascular proceduresand practice are not necessarily the same the world over. The approach to someproblems is different in Europe than it is in other continents and these differ-ences are reflected in this book. I am sure that those who buy and read thisbook will not be disappointed in its content or style. It will be extremely usefulto all readers and be a signpost to the future of vascular surgery.
  • 7. XIIntroductionChristos D. Liapis, John D. KakisisVascular diseases are the most frequent cause of death and disability of Eu-ropeans. The aim of the present book, European Manual of Medicine: Vascu-lar Surgery, is to give an indication of European standards for the diagnosisand therapy of vascular diseases. It is designed with the same format as otherbooks in the series European Manuals of Medicine and focuses on the descrip-tion of each clinical entity (definition, epidemiology, aetiology, symptoms andcomplications) and on the recommended European standard diagnostic andtherapeutic steps. In contrast to other textbooks, most of the information ispresented in bulleted listings instead of lengthy paragraphs. This is done in thehope of enabling the reader to retrieve information easily and quickly. The first chapters of this book refer to the pathogenesis of vascular diseases,including the development of atherosclerosis and the effect of dyslipidaemia,clotting disorders and emerging biochemical risk factors. Subsequent chapterspresent the noninvasive and invasive means of diagnosis, including latest de-velopments such as computer-guided diagnosis of vascular diseases. The pre-operative evaluation and optimization as well as the peri-operative care of thevascular patient are also discussed. The book includes a review of the history ofvascular surgery in Europe and a chapter on the training of vascular surgeonsfor endovascular procedures in order to highlight the continuity and the prog-ress of vascular surgery over the past century and the future perspectives. Thechapters of the book cover the entire range of arterial, venous and lymphaticdisorders with an emphasis on all recent developments including endovascularand laparoscopic surgery. The text is comprehensive since the book is intendednot only for vascular specialists but also for students, residents in vascular sur-gery and other interested physicians. The chapters have been written mainly by national representatives on thenewly established Section of Vascular Surgery of the European Union of Medi-cal Specialists (UEMS), thus drawing upon the collective experience of vascu-lar surgeons/specialists from the various European countries. The authors areexperts in their field, providing the reader with a professional opinion reflect-ing what is generally considered to be the state-of-the-art in each area. We hope that the readers, especially the hard working trainees in vascularsurgery to whom this book is dedicated, will find it useful.
  • 8. XIII ContentsVascular Surgery and the Vascular Patient 1.2.2.2 Initiation of Atherosclerosis and Role of Endothelial1.1 The History of Vascular Surgery Dysfunction . . . . . . . . . . . . . . . . . . . . . . 23 in Europe . . . . . . . . . . . . . . . . . . . . . . . . . . 3 1.2.2.3 Evolution of the Atherosclerotic1.1.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . 3 Plaque . . . . . . . . . . . . . . . . . . . . . . . . . . . 261.1.2 The Origin and the Foundations 1.2.3 Contributive Factors of European Vascular Surgery . . . . . . . 3 to Endothelial Dysfunction1.1.3 Europe, Cradle of the World’s and Plaque Formation . . . . . . . . . . . . . 28 Vascular Surgery . . . . . . . . . . . . . . . . . . . 7 1.2.3.1 Miscellaneous Factor . . . . . . . . . . . . . . 281.1.3.1 The Nursery of Vascular Surgery 1.2.3.2 The Oxidized LDL Hypothesis . . . . . . 28 in Europe in the 1930s was 1.2.4 Plaque Instability the René Leriche School in and Complicated Plaques . . . . . . . . . . 30 Strasburg, France . . . . . . . . . . . . . . . . . . 8 1.2.5 Classification of Atherosclerotic1.1.3.2 Reference to European Surgeons Plaques . . . . . . . . . . . . . . . . . . . . . . . . . . . 30 who Through their Pioneering 1.2.6 Assessment and Evaluation Work Developed Vascular of the Risk of an Atherosclerotic Surgery in their Continent with Plaque . . . . . . . . . . . . . . . . . . . . . . . . . . . 31 International Influence . . . . . . . . . . . . 10 1.2.7 General Therapeutic Measures . . . . . 311.1.3.3 Medical and Interventional 1.2.8 Conclusion . . . . . . . . . . . . . . . . . . . . . . . 32 Vascular Contributions to References . . . . . . . . . . . . . . . . . . . . . . . . 32 the Development of Vascular Surgery in Europe and Worldwide . . 12 1.3 Lipids and Peripheral Arterial1.1.4 European Vascular Surgical Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . 35 and Angiological Societies and 1.3.1 Introduction . . . . . . . . . . . . . . . . . . . . . . 35 Congresses . . . . . . . . . . . . . . . . . . . . . . . 14 1.3.2 Effect of Lipid Lowering on PAD . . . 351.1.5 Epilogue . . . . . . . . . . . . . . . . . . . . . . . . . . 17 1.3.2.1 Prevention of PAD . . . . . . . . . . . . . . . . 35 Acknowledgements . . . . . . . . . . . . . . . 19 1.3.2.2 Improvement of Symptoms References . . . . . . . . . . . . . . . . . . . . . . . . 20 Associated with PAD . . . . . . . . . . . . . 35 1.3.2.3 Reduction of the Risk of1.2 Development of Atherosclerosis Vascular Events Associated with for the Vascular Surgeon . . . . . . . . . . . 23 PAD . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 361.2.1 Introduction . . . . . . . . . . . . . . . . . . . . . 23 1.3.3 Peripheral Vascular Surgery and1.2.2 Physiopathology of Statins . . . . . . . . . . . . . . . . . . . . . . . . . . . 36 Atherosclerosis . . . . . . . . . . . . . . . . . . . 23 1.3.4 Additional Potential Actions1.2.2.1 Normal Blood Vessel of Lipid-lowering Drugs Morphology . . . . . . . . . . . . . . . . . . . . . . 23 that may Benefit PAD Patients . . . . . 37 1.3.5 Are all Statins the Same? . . . . . . . . . . . 37
  • 9. XIV Contents 1.3.6 Concluding Comments . . . . . . . . . . . . 37 1.6 Invasive Diagnosis of Vascular References . . . . . . . . . . . . . . . . . . . . . . . . 38 Diseases . . . . . . . . . . . . . . . . . . . . . . . . . . 65 1.6.1 Introduction . . . . . . . . . . . . . . . . . . . . . . 65 1.4 Clotting Disorders: What Should 1.6.2 History . . . . . . . . . . . . . . . . . . . . . . . . . . . 65 the Vascular Surgeon Know 1.6.3 Arteriography . . . . . . . . . . . . . . . . . . . . . 68 About Hypercoagulation States 1.6.3.1 Techniques . . . . . . . . . . . . . . . . . . . . . . . 68 in Venous Diseases? . . . . . . . . . . . . . . . 41 1.6.3.2 Pre-procedure Evaluation 1.4.1 Introduction . . . . . . . . . . . . . . . . . . . . . . 41 and Preparation . . . . . . . . . . . . . . . . . . . 69 1.4.2 Venous Thrombosis . . . . . . . . . . . . . . . 41 1.6.3.3 Technique . . . . . . . . . . . . . . . . . . . . . . . . 69 1.4.2.1 Risk Factors . . . . . . . . . . . . . . . . . . . . . . 41 1.6.3.4 Post-procedure Care . . . . . . . . . . . . . . . 70 1.4.3 What Should a Surgeon do when 1.6.3.5 Complications . . . . . . . . . . . . . . . . . . . . 70 Faced with Hypercoagulation? . . . . . 45 1.6.3.6 Direct Toxicity . . . . . . . . . . . . . . . . . . . 71 1.4.3.1 Should a Search for 1.6.4 Phlebography . . . . . . . . . . . . . . . . . . . . . 72 Thrombophilia be Undertaken? . . . . 45 1.6.4.1 Indications . . . . . . . . . . . . . . . . . . . . . . . 72 1.4.3.2 How Should the Search 1.6.4.2 Techniques . . . . . . . . . . . . . . . . . . . . . . . 72 be Done? . . . . . . . . . . . . . . . . . . . . . . . . . 45 References . . . . . . . . . . . . . . . . . . . . . . . . 74 1.4.3.3 Diagnosing Thrombotic Disease in Patients with Thrombophilia . . . . . 46 1.7 Computer-Aided Diagnosis 1.4.3.4 Treating Thromboembolic of Vascular Disease . . . . . . . . . . . . . . . . 77 Disease in Patients 1.7.1 Introduction . . . . . . . . . . . . . . . . . . . . . 77 with Thrombophilia . . . . . . . . . . . . . . 46 1.7.2 Computer-Aided Diagnosis 1.4.3.5 Specific Considerations in Vascular Imaging . . . . . . . . . . . . . . . 77 in Treating Thromboembolic 1.7.2.1 Image Pre-processing . . . . . . . . . . . . . . 78 Disease Related to Thrombophilia . . 46 1.7.2.2 Definition of Regions of Interest 1.4.4 Summary . . . . . . . . . . . . . . . . . . . . . . . . . 47 – Automatic Segmentation . . . . . . . . . 78 References . . . . . . . . . . . . . . . . . . . . . . . 47 1.7.2.3 Extraction and Selection of Characteristic Features . . . . . . . . . 78 1.5 Noninvasive Diagnosis 1.7.2.4 Classification . . . . . . . . . . . . . . . . . . . . . 80 of Vascular Diseases . . . . . . . . . . . . . . . 51 1.7.2.5 ANALYSIS: a Modular Software 1.5.1 Peripheral Arterial Disease . . . . . . . . . 51 System to Support Diagnosis 1.5.1.1 Introduction . . . . . . . . . . . . . . . . . . . . . . 51 of Vascular Disease . . . . . . . . . . . . . . . . 81 1.5.1.2 Physical Examination . . . . . . . . . . . . . . 51 1.7.3 Conclusion . . . . . . . . . . . . . . . . . . . . . . . 82 1.5.1.3 Basic Haematological References . . . . . . . . . . . . . . . . . . . . . . . 82 and Biochemical Tests . . . . . . . . . . . . . 51 1.5.1.4 Special Investigations, Other 1.8 Preoperative Evaluation Than Imaging . . . . . . . . . . . . . . . . . . . . . 51 of a Vascular Patient . . . . . . . . . . . . . . . 85 1.5.1.5 Imaging Techniques . . . . . . . . . . . . . . . 54 1.8.1 Introduction . . . . . . . . . . . . . . . . . . . . . . 85 1.5.1.6 Conclusion . . . . . . . . . . . . . . . . . . . . . . . 55 1.8.2 Systemic Evaluation . . . . . . . . . . . . . . . 85 1.5.2 Disease of Arteries Supplying 1.8.2.1 Cardiovascular System . . . . . . . . . . . . . 85 the Brain . . . . . . . . . . . . . . . . . . . . . . . . . 56 1.8.2.2 Respiratory System . . . . . . . . . . . . . . . . 86 1.5.2.1 Introduction . . . . . . . . . . . . . . . . . . . . . . 56 1.8.2.3 Renal System . . . . . . . . . . . . . . . . . . . . . 88 1.5.2.2 Imaging Techniques . . . . . . . . . . . . . . . 56 1.8.3 Evaluation of Specific Vascular 1.5.2.3 Conclusion . . . . . . . . . . . . . . . . . . . . . . . 59 Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . 89 1.5.3 Diseases of the Venous 1.8.3.1 Aneurysmal Disease: Circulation . . . . . . . . . . . . . . . . . . . . . . . 59 Abdominal Aortic Aneurysm . . . . . . 89 1.5.3.1 Introduction . . . . . . . . . . . . . . . . . . . . . . 59 1.8.3.3 Peripheral Vascular Disease: 1.5.3.2 Chronic Venous Insufficiency . . . . . . 59 Chronic Lower Limb Ischaemia . . . . 89 1.5.3.3 Deep Vein Thrombosis . . . . . . . . . . . . 61 1.8.3.4 Peripheral Vascular Disease: 1.5.3.4 Conclusion . . . . . . . . . . . . . . . . . . . . . . . 61 Acute Limb Ischaemia . . . . . . . . . . . . . 90 References . . . . . . . . . . . . . . . . . . . . . . . . 62 1.8.3.5 Carotid Disease . . . . . . . . . . . . . . . . . . . 91
  • 10. Contents XV1.8.3.6 Venous Disease . . . . . . . . . . . . . . . . . . . 92 1.10 Training of the Vascular References . . . . . . . . . . . . . . . . . . . . . . . . 93 Surgeonfor Endovascular Procedures . . . . . . . . . . . . . . . . . . . . . 1071.9 Peri-operative Care References . . . . . . . . . . . . . . . . . . . . . . 110 of the Vascular Patient . . . . . . . . . . . . . 951.9.1 Introduction . . . . . . . . . . . . . . . . . . . . . . 95 1.11 Peripheral Arterial Disease and1.9.2 Preoperative Planning . . . . . . . . . . . . . 95 Emerging Biochemical Vascular1.9.3 Effects of Anaesthesia . . . . . . . . . . . . . . 95 Risk Factors . . . . . . . . . . . . . . . . . . . . 1111.9.4 Peri-operative Monitoring . . . . . . . . . 96 1.11.1 Introduction . . . . . . . . . . . . . . . . . . . . 1111.9.4.1 Monitoring for Cardiac 1.11.2 Homocysteine (Hcy) . . . . . . . . . . . . 111 Ischaemia . . . . . . . . . . . . . . . . . . . . . . . . 96 1.11.3 C-reactive Protein (CRP) . . . . . . . . 1111.9.4.2 Peri-operative Temperature 1.11.4 Lipoprotein (a) [Lp(a)] . . . . . . . . . . 112 Control . . . . . . . . . . . . . . . . . . . . . . . . . . 96 1.11.5 Fibrinogen . . . . . . . . . . . . . . . . . . . . . . 1121.9.4.3 Level of Hypnotic Depth . . . . . . . . . . . 97 1.11.6 Endothelium . . . . . . . . . . . . . . . . . . . . 1131.9.5 Prevention of Cardiac Ischaemia . . . 97 1.11.7 PAD and Other Potentially1.9.5.1 Preoperative Revascularization . . . . . 97 Relevant Emerging Risk Factors . . 1131.9.5.2 Good Peri-operative 1.11.7.1 Creatinine . . . . . . . . . . . . . . . . . . . . . . 113 Haemodynamic Control . . . . . . . . . . . 97 1.11.7.2 Urate . . . . . . . . . . . . . . . . . . . . . . . . . . 1131.9.5.3 Anaemia . . . . . . . . . . . . . . . . . . . . . . . . . 97 1.11.7.3 Microalbuminuria . . . . . . . . . . . . . . 1141.9.5.4 Adrenergic Tone . . . . . . . . . . . . . . . . . . 97 1.11.7.4 Insulin Resistance and Metabolic1.9.5.5 Postoperative Ischaemia Syndrome . . . . . . . . . . . . . . . . . . . . . . 114 Prevention . . . . . . . . . . . . . . . . . . . . . . . 98 1.11.7.5 Platelets, Fibrinolysis1.9.6 Aneurysm Surgery . . . . . . . . . . . . . . . . 98 and D-Dimers . . . . . . . . . . . . . . . . . . 1141.9.6.1 Effects of Clamping and 1.11.7.6 Other Markers of Inflammation . . 114 Declamping . . . . . . . . . . . . . . . . . . . . . . 98 1.11.8 Conclusions . . . . . . . . . . . . . . . . . . . . 1141.9.6.2 Prevention of Spinal Cord References . . . . . . . . . . . . . . . . . . . . . 115 Ischaemia in Thoracic Aortic Surgery . . . . . . . . . . . . . . . . . . . . . . . . . . 99 1.12 Quality Control in Vascular1.9.6.3 Autotransfusion During Surgery . . . . 99 Surgery . . . . . . . . . . . . . . . . . . . . . . . . 1171.9.7 Heparin . . . . . . . . . . . . . . . . . . . . . . . . . . 99 1.12.1 Introduction . . . . . . . . . . . . . . . . . . . . 1171.9.7.1 Peri-operative Heparin . . . . . . . . . . . . 99 1.12.1.1 Physical Examination . . . . . . . . . . . . 1171.9.7.2 Prophylaxis of Deep Leg Vein 1.12.1.2 Angiography . . . . . . . . . . . . . . . . . . . . 117 Thrombosis . . . . . . . . . . . . . . . . . . . . . 100 1.12.1.3 Continuous Wave (CW)1.9.8 Peri-operative Monitoring Doppler . . . . . . . . . . . . . . . . . . . . . . . . 117 after Arterial Reconstructions . . . . 100 1.12.1.4 Duplex and Colour Duplex Scan . . 1181.9.9 Prophylactic Antibiotic 1.12.1.5 Intravascular Ultrasonography Administration . . . . . . . . . . . . . . . . . 100 (IVUS) . . . . . . . . . . . . . . . . . . . . . . . . . 1181.9.10 Postoperative Pain Treatment . . . . 100 1.12.1.6 Angioscopy . . . . . . . . . . . . . . . . . . . . . 1181.9.11 Pulmonary Complications, 1.12.1.7 Flowmetry . . . . . . . . . . . . . . . . . . . . . . 119 Prophylaxis and Treatment . . . . . . . 100 1.12.2 Arteries of the Abdomen . . . . . . . . 1191.9.12 Peri-operative Care 1.12.2.1 Abdominal Aorta . . . . . . . . . . . . . . . 119 and Endovascular Surgery . . . . . . . 101 1.12.2.2 Visceral Arteries . . . . . . . . . . . . . . . . 1191.9.13 Intensive Care Ward is Needed 1.12.2.3 Renal Arteries . . . . . . . . . . . . . . . . . . 120 Only for Selected Patients . . . . . . . . 101 1.12.3 Lower Extremity By-pass . . . . . . . . 1201.9.14 Pre- and Postoperative Gut 1.12.3.1 Angiography . . . . . . . . . . . . . . . . . . . . 121 Function and Nutrition . . . . . . . . . . 101 1.12.3.2 Ultrasound (CW Doppler, PW1.9.15 Discharge Planning . . . . . . . . . . . . . . 102 Doppler, Duplex, Colour Duplex) 1221.9.16 Summary . . . . . . . . . . . . . . . . . . . . . . . 103 1.12.3.3 Angioscopy . . . . . . . . . . . . . . . . . . . . . 123 References . . . . . . . . . . . . . . . . . . . . . . 103 1.12.3.4 Flowmetry . . . . . . . . . . . . . . . . . . . . . . 124 1.12.3.5 Conclusions . . . . . . . . . . . . . . . . . . . . 124
  • 11. XVI Contents 1.12.4 Carotid Arteries . . . . . . . . . . . . . . . . . 124 2.2.5.3 Technique of Carotid References . . . . . . . . . . . . . . . . . . . . . . 127 Endarterectomy . . . . . . . . . . . . . . . . . 146 2.2.6 Endovascular Treatment . . . . . . . . . 149 2.2.6.1 What are the Established Cerebrovascular Arteries Indications for Endovascular Procedures in Extracranial 2.1 Haemodynamic Changes Carotid Disease? . . . . . . . . . . . . . . . . 149 and Other Risk Factors References . . . . . . . . . . . . . . . . . . . . . . 150 for Complications During Carotid Procedures . . . . . . . . . . . . . . 131 2.3 Eversion Carotid 2.1.1 Cerebral Blood Flow . . . . . . . . . . . . . 131 Endarterectomy Technique . . . . . . 155 2.1.2 General Complications . . . . . . . . . . 131 2.3.1 Introduction . . . . . . . . . . . . . . . . . . . . 155 2.1.3 Cerebral Monitoring 2.3.2 Technique . . . . . . . . . . . . . . . . . . . . . . 155 and Protection During CEA . . . . . . 132 2.3.3 Advantages . . . . . . . . . . . . . . . . . . . . . 159 2.1.4 Cerebral Embolization during 2.3.4 Disadvantages . . . . . . . . . . . . . . . . . . 159 CEA and CAS . . . . . . . . . . . . . . . . . . 133 2.3.5 Conclusion . . . . . . . . . . . . . . . . . . . . . 159 2.1.5 Adjuvant Medical Therapy . . . . . . . 133 References . . . . . . . . . . . . . . . . . . . . . . 159 2.1.6 Conclusion . . . . . . . . . . . . . . . . . . . . . 134 References . . . . . . . . . . . . . . . . . . . . . . 134 2.4 Fibromuscular Dysplasia . . . . . . . . . 161 2.4.1 Basics . . . . . . . . . . . . . . . . . . . . . . . . . . 161 2.2 Extracranial Carotid Artery 2.4.1.1 Anatomy . . . . . . . . . . . . . . . . . . . . . . . 161 Disease . . . . . . . . . . . . . . . . . . . . . . . . . 137 2.4.1.2 Physiology, Pathophysiology . . . . . 161 2.2.1 Introduction . . . . . . . . . . . . . . . . . . . . 137 2.4.1.3 Organ-related Questions . . . . . . . . . 165 2.2.2 Pathogenesis of Brain Ischaemia . . 138 2.4.1.4 Principles of Clinical 2.2.3 Clinical Manifestations . . . . . . . . . . 140 Examination . . . . . . . . . . . . . . . . . . . . 165 2.2.3.1 Amaurosis fugax . . . . . . . . . . . . . . . . 140 2.4.1.5 Technical Diagnostic Procedures . . 165 2.2.3.2 Transient/Reversible Cerebral 2.4.1.6 Organ-specific Radiology . . . . . . . . 166 Ischaemia . . . . . . . . . . . . . . . . . . . . . . 140 2.4.2 Organ-related Diseases . . . . . . . . . . 166 2.2.3.3 Established Stroke . . . . . . . . . . . . . . . 140 2.4.2.1 Synonyms . . . . . . . . . . . . . . . . . . . . . . 166 2.2.3.4 Stroke in Evolution (“Waving 2.4.2.2 Definition . . . . . . . . . . . . . . . . . . . . . . 166 and Waning”) . . . . . . . . . . . . . . . . . . . 140 2.4.2.3 Epidemiology/Aetiology . . . . . . . . . 166 2.2.3.5 Global Cerebral Ischaemia . . . . . . . 140 2.4.2.4 Symptoms . . . . . . . . . . . . . . . . . . . . . . 167 2.2.3.6 Asymptomatic Carotid Disease . . . 141 2.4.2.5 Complications . . . . . . . . . . . . . . . . . . 168 2.2.4 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . 141 2.4.2.6 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . 168 2.2.4.1 Arteriography . . . . . . . . . . . . . . . . . . . 141 2.4.2.7 Treatment . . . . . . . . . . . . . . . . . . . . . . 168 2.2.4.2 Colour Flow Duplex Scan . . . . . . . 141 2.4.2.8 Differential Diagnosis . . . . . . . . . . . 169 2.2.4.3 High-resolution 2.4.2.9 Prognosis . . . . . . . . . . . . . . . . . . . . . . . 169 Ultrasonography . . . . . . . . . . . . . . . . 143 2.4.2.10 Exemplary Surgical Procedures . . . 169 2.2.4.4 Measuring the Degree of Stenosis . 143 2.4.2.11 Special Remarks . . . . . . . . . . . . . . . . . 170 2.2.4.5 Transcranial Doppler References . . . . . . . . . . . . . . . . . . . . . . 170 Examination . . . . . . . . . . . . . . . . . . . 144 2.2.4.6 Other Flow-imaging Techniques . . 144 2.5 Aneurysms of the Extracranial 2.2.4.7 Indications for Arteriography . . . . 144 Carotid Arteries . . . . . . . . . . . . . . . . 173 2.2.4.8 Computerized Tomography 2.5.1 Definition and Historical and Magnetic Resonance Imaging 144 Background . . . . . . . . . . . . . . . . . . . . 173 2.2.4.9 Examination of the Retina . . . . . . . 144 2.5.2 Epidemiology/Aetiology . . . . . . . . . 173 2.2.5 Selection, Treatment and Results . . 145 2.5.2.1 Atherosclerosis Aneurysms . . . . . . 173 2.2.5.1 Medical Treatment . . . . . . . . . . . . . . 145 2.5.2.2 Previous Surgery/POS 2.2.5.2 Surgical Treatment . . . . . . . . . . . . . . 145 Endarterectomy . . . . . . . . . . . . . . . . . 174
  • 12. Contents XVII2.5.2.3 Trauma . . . . . . . . . . . . . . . . . . . . . . . . . 174 2.6.8.1 Technical Failure . . . . . . . . . . . . . . . . 1932.5.2.4 Infection . . . . . . . . . . . . . . . . . . . . . . . 174 2.6.8.2 Contrast Encephalopathy . . . . . . . . 1932.5.2.5 Dissections . . . . . . . . . . . . . . . . . . . . . 174 2.6.8.3 Access Site Complications . . . . . . . . 1932.5.2.6 Other Possible Causes . . . . . . . . . . . 174 2.6.8.4 Hyperperfusion Syndrome2.5.3 Symptoms . . . . . . . . . . . . . . . . . . . . . . 175 (Fig. 2.6.16) . . . . . . . . . . . . . . . . . . . . . 1932.5.4 Complications . . . . . . . . . . . . . . . . . . 175 2.6.8.5 Hypotension and Bradycardia . . . 1942.5.5 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . 175 2.6.8.6 Embolic Complication . . . . . . . . . . . 1942.5.5.1 Recommended European 2.6.8.7 Complications Involving Brain Standard Diagnostic Steps Protection Devices . . . . . . . . . . . . . . 195 of Investigation . . . . . . . . . . . . . . . . . 175 2.6.9 Follow-up . . . . . . . . . . . . . . . . . . . . . . 1952.5.6 Treatment . . . . . . . . . . . . . . . . . . . . . . 176 2.6.10 Carotid Angioplasty and2.5.6.1 Conservative Treatment . . . . . . . . . 176 Stenting (CAS): Present and Future 1962.5.6.2 Surgery . . . . . . . . . . . . . . . . . . . . . . . . . 177 References . . . . . . . . . . . . . . . . . . . . . . 197 References . . . . . . . . . . . . . . . . . . . . . . 179 2.7 Carotid body tumour . . . . . . . . . . . . 2012.6 Endovascular Treatment 2.7.1 Synonyms . . . . . . . . . . . . . . . . . . . . . . 201 of Carotid Stenosis . . . . . . . . . . . . . . 181 2.7.2 Definition of the Disease . . . . . . . . . 2012.6.1 Introduction . . . . . . . . . . . . . . . . . . . . 181 2.7.3 Epidemiology/Aetiology . . . . . . . . . 2012.6.2 Indications for Surgery 2.7.4 Symptoms . . . . . . . . . . . . . . . . . . . . . . 202 – Indications for Angioplasty . . . . . 181 2.7.5 Complications . . . . . . . . . . . . . . . . . . 2022.6.3 Types of Stents . . . . . . . . . . . . . . . . . . 183 2.7.6 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . 2032.6.4 Brain Protection Devices . . . . . . . . . 184 2.7.6.1 Recommended European2.6.4.1 Distal Occlusion Balloon Standard Diagnostic Steps (Theron’s System, PercuSurge of Investigation . . . . . . . . . . . . . . . . . 203 GuardWire® Medtronic) 2.7.6.2 Additional Useful Diagnostic (Fig. 2.6.5) . . . . . . . . . . . . . . . . . . . . . . 184 Procedures . . . . . . . . . . . . . . . . . . . . . 2052.6.4.2 Filters . . . . . . . . . . . . . . . . . . . . . . . . . . 184 2.7.7 Therapy . . . . . . . . . . . . . . . . . . . . . . . . 2062.6.4.3 Proximal Occlusion System . . . . . . 186 2.7.7.1 Conservative therapy . . . . . . . . . . . . 2062.6.5 Preoperative Evaluation . . . . . . . . . . 187 2.7.7.2 Surgery . . . . . . . . . . . . . . . . . . . . . . . . . 2062.6.5.1 Neurological Examination . . . . . . . 188 2.7.8 Differential Diagnosis . . . . . . . . . . . 2082.6.5.2 Special Imaging Examination . . . . 188 References . . . . . . . . . . . . . . . . . . . . . 2082.6.5.3 Duplex Ultrasound . . . . . . . . . . . . . . 1882.6.5.4 Digital Subtraction Angiography 2.8 Combined Treatment of (DSA) . . . . . . . . . . . . . . . . . . . . . . . . . . 188 Coronary Plus Other Arterial2.6.5.5 Magnetic Resonance Pathologies: the Magnitude of Angiography (MRA) (Fig. 2.6.10) . . 189 the Polyatherosclerotic Patient . . . 2092.6.5.6 Brain Computed Tomography 2.8.1 Introduction . . . . . . . . . . . . . . . . . . . . 209 (CT) . . . . . . . . . . . . . . . . . . . . . . . . . . . 189 2.8.2 The Magnitude of Multifocal2.6.6 Technique . . . . . . . . . . . . . . . . . . . . . . 190 Arterial Disease . . . . . . . . . . . . . . . . . 2092.6.6.1 Step 1: Approach to the 2.8.2.1 Material and Methods . . . . . . . . . . . 209 Common Carotid Artery Access 2.8.2.2 Results . . . . . . . . . . . . . . . . . . . . . . . . . 209 Site . . . . . . . . . . . . . . . . . . . . . . . . . . . . 190 2.8.3 Multifocal Occlusive2.6.6.2 Step 2: Cannulation of the and Aneurysmal Arterial Disease . 211 Common Carotid Artery 2.8.4 Multifocal Carotid and (Fig. 2.6.12) . . . . . . . . . . . . . . . . . . . . . 191 Coronary Occlusive Disease . . . . . 2122.6.6.3 Step 3: Angioplasty and Stenting . . 192 2.8.4.1 Material and Methods . . . . . . . . . . . 2132.6.6.4 Step 4: Control Angiography . . . . . 193 2.8.4.2 Results . . . . . . . . . . . . . . . . . . . . . . . . . 2142.6.7 Peri-operative Monitoring . . . . . . . 193 Acknowledgements . . . . . . . . . . . . . 2142.6.8 Complications . . . . . . . . . . . . . . . . . . 193 References . . . . . . . . . . . . . . . . . . . . . . 214
  • 13. XVIII Contents Upper Extremity Arteries 3.2.2.2 Epidemiology/Aetiology . . . . . . . . . 240 3.2.2.3 Symptoms . . . . . . . . . . . . . . . . . . . . . . 240 3.1 Upper Extremity Occlusive 3.2.2.4 Treatment . . . . . . . . . . . . . . . . . . . . . . 241 Disease . . . . . . . . . . . . . . . . . . . . . . . . . 219 3.2.3 Acrocyanosis . . . . . . . . . . . . . . . . . . . 242 3.1.1 Introduction . . . . . . . . . . . . . . . . . . . . 219 3.2.3.1 Definition . . . . . . . . . . . . . . . . . . . . . . 242 3.1.2 Types of Upper Extremity 3.2.3.2 Epidemiology/Aetiology . . . . . . . . . 242 Occlusive Disease . . . . . . . . . . . . . . . 219 3.2.3.3 Symptoms . . . . . . . . . . . . . . . . . . . . . . 242 3.1.2.1 Acute and Chronic Ischaemia . . . . 219 3.2.3.4 Therapy . . . . . . . . . . . . . . . . . . . . . . . . 243 3.1.2.2 Raynaud’s Phenomenon . . . . . . . . . 219 3.2.4 Livedo Reticularis . . . . . . . . . . . . . . . 243 3.1.2.3 Trophic Lesions . . . . . . . . . . . . . . . . . 220 3.2.4.1 Definition . . . . . . . . . . . . . . . . . . . . . . 243 3.1.2.4 Differential Diagnosis of Upper 3.2.4.2 Epidemiology/Aetiology . . . . . . . . . 243 Extremity Occlusive Disease . . . . . 220 3.2.4.3 Symptoms . . . . . . . . . . . . . . . . . . . . . . 243 3.1.3 Embolism . . . . . . . . . . . . . . . . . . . . . . 220 3.2.4.4 Therapy . . . . . . . . . . . . . . . . . . . . . . . . 243 3.1.3.1 Definition . . . . . . . . . . . . . . . . . . . . . . 220 3.2.5 Cold Hypersensitivity . . . . . . . . . . . 243 3.1.3.2 Epidemiology/Aetiology . . . . . . . . . 220 3.2.5.1 Definition . . . . . . . . . . . . . . . . . . . . . . 243 3.1.3.3 Symptoms . . . . . . . . . . . . . . . . . . . . . . 220 3.2.5.2 Symptoms . . . . . . . . . . . . . . . . . . . . . . 244 3.1.3.4 Diagnosis . . . . . . . . . . . . . . . . . . . . . . 221 3.2.5.3 Therapy . . . . . . . . . . . . . . . . . . . . . . . . 244 3.1.3.5 Therapy . . . . . . . . . . . . . . . . . . . . . . . . 221 3.2.6 Complex Regional Pain 3.1.4 Occlusive Arterial Disease . . . . . . . 222 Syndrome . . . . . . . . . . . . . . . . . . . . . . 245 3.1.4.1 Definition . . . . . . . . . . . . . . . . . . . . . . 222 3.2.6.1 Synonyms . . . . . . . . . . . . . . . . . . . . . . 245 3.1.4.2 Proximal Arterial Disease . . . . . . . . 222 3.2.6.2 Definition . . . . . . . . . . . . . . . . . . . . . . 245 3.1.4.3 Distal Arterial Disease . . . . . . . . . . . 226 3.2.6.3 Aetiology . . . . . . . . . . . . . . . . . . . . . . . 245 3.1.5 Aneurysms . . . . . . . . . . . . . . . . . . . . . 232 3.2.6.4 Symptoms . . . . . . . . . . . . . . . . . . . . . . 245 3.1.5.1 Epidemiology/Aetiology . . . . . . . . . 232 3.2.6.5 Therapy . . . . . . . . . . . . . . . . . . . . . . . . 245 3.1.5.2 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . 232 References . . . . . . . . . . . . . . . . . . . . . . 246 3.1.5.3 Therapy . . . . . . . . . . . . . . . . . . . . . . . . 232 3.1.6 Arteriovenous Fistulae . . . . . . . . . . . 232 3.3 Thoracic Outlet Syndrome . . . . . . . 247 3.1.6.1 Epidemiology/Aetiology . . . . . . . . . 232 3.3.1 Definition . . . . . . . . . . . . . . . . . . . . . . 247 3.1.6.2 Symptoms . . . . . . . . . . . . . . . . . . . . . . 233 3.3.2 Neurogenic Thoracic Outlet 3.1.6.3 Investigations . . . . . . . . . . . . . . . . . . . 233 Compression Syndrome (N-TOCS) 247 3.1.6.4 Therapy . . . . . . . . . . . . . . . . . . . . . . . . 233 3.3.2.1 Epidemiology/Aetiology . . . . . . . . . 247 3.1.7 Vascular Trauma . . . . . . . . . . . . . . . . 233 3.3.2.2 Symptoms . . . . . . . . . . . . . . . . . . . . . . 247 3.1.7.1 Epidemiology/Aetiology . . . . . . . . . 233 3.3.2.3 Clinical Examination . . . . . . . . . . . . 247 3.1.7.2 Symptoms . . . . . . . . . . . . . . . . . . . . . . 233 3.3.2.4 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . 248 3.1.7.3 Therapy . . . . . . . . . . . . . . . . . . . . . . . . 233 3.3.2.5 Treatment . . . . . . . . . . . . . . . . . . . . . . 248 3.1.8 Iatrogenic Aetiologies . . . . . . . . . . . 233 3.3.3 Arterial Thoracic Outlet 3.1.9 Conclusion . . . . . . . . . . . . . . . . . . . . . 234 Compression Syndrome References . . . . . . . . . . . . . . . . . . . . . . 234 (A-TOCS) . . . . . . . . . . . . . . . . . . . . . 251 3.3.3.1 Epidemiology/Aetiology . . . . . . . . . 251 3.2 Vasospastic Disorders 3.3.3.2 Symptoms . . . . . . . . . . . . . . . . . . . . . . 251 of the Upper Extremities . . . . . . . . . 237 3.3.3.3 Investigations/Examination . . . . . . 251 3.2.1 Raynaud’s Syndrome . . . . . . . . . . . . 237 3.3.3.4 Treatment . . . . . . . . . . . . . . . . . . . . . . 251 3.2.1.1 Definition . . . . . . . . . . . . . . . . . . . . . . 237 3.3.4 A Case Apart: Primary 3.2.1.2 Epidemiology/Aetiology . . . . . . . . . 237 Subclavian–Axillary Vein 3.2.1.3 Symptoms . . . . . . . . . . . . . . . . . . . . . . 237 Thrombosis . . . . . . . . . . . . . . . . . . . . . 254 3.2.1.4 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . 237 3.3.4.1 Epidemiology/Aetiology . . . . . . . . . 254 3.2.1.5 Therapy . . . . . . . . . . . . . . . . . . . . . . . . 239 3.3.4.2 Primary SVT . . . . . . . . . . . . . . . . . . . 254 3.2.2 Hyperhidrosis . . . . . . . . . . . . . . . . . . . 240 3.3.5 Summary . . . . . . . . . . . . . . . . . . . . . . . 256 3.2.2.1 Definition . . . . . . . . . . . . . . . . . . . . . . 240 References . . . . . . . . . . . . . . . . . . . . . . 256
  • 14. Contents XIX3.4 Traumatic Injury of Upper 4.2.3.5 Localization . . . . . . . . . . . . . . . . . . . . 278 Extremity Arteries . . . . . . . . . . . . . . 257 4.2.3.6 Classification . . . . . . . . . . . . . . . . . . . 2783.4.1 Epidemiology . . . . . . . . . . . . . . . . . . . 257 4.2.3.7 Factors Determining Extension3.4.2 Aetiology . . . . . . . . . . . . . . . . . . . . . . . 257 of Dissection . . . . . . . . . . . . . . . . . . . 2793.4.2.1 Penetrating Trauma . . . . . . . . . . . . . 257 4.2.4 Symptoms . . . . . . . . . . . . . . . . . . . . . . 2823.4.2.2 Blunt Trauma . . . . . . . . . . . . . . . . . . . 257 4.2.4.1 Stanford Type A . . . . . . . . . . . . . . . . 2823.4.3 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . 257 4.2.4.2 Stanford Type B . . . . . . . . . . . . . . . . 2823.4.3.1 Recommended European 4.2.5 Complications . . . . . . . . . . . . . . . . . . 283 Standard Diagnostic Steps 4.2.5.1 Type A . . . . . . . . . . . . . . . . . . . . . . . . . 283 of Investigation . . . . . . . . . . . . . . . . . 257 4.2.5.2 Type B . . . . . . . . . . . . . . . . . . . . . . . . . 2833.4.4 Therapy . . . . . . . . . . . . . . . . . . . . . . . . 258 4.2.6 Diagnosis/Investigation . . . . . . . . . . 2853.4.4.1 Conservative Therapy . . . . . . . . . . . 258 4.2.6.1 Recommended European3.4.4.2 Endovascular Therapy . . . . . . . . . . . 258 Standard Diagnostic Steps3.4.4.3 Surgery . . . . . . . . . . . . . . . . . . . . . . . . . 258 of Investigation . . . . . . . . . . . . . . . . . 2853.4.5 Prognosis . . . . . . . . . . . . . . . . . . . . . . . 259 4.2.6.2 Additional Useful Diagnostic References . . . . . . . . . . . . . . . . . . . . . . 260 Procedures . . . . . . . . . . . . . . . . . . . . . 285 4.2.6.3 Clinical Judgement . . . . . . . . . . . . . . 285 4.2.7 Prognosis of Acute or SubacuteThoracic Aorta Aortic Dissection Without Treatment . . . . . . . . . . . . . . . . . . . . . . 2894.1 Thoracoabdominal Aneurysms . . . 265 4.2.8 Therapy . . . . . . . . . . . . . . . . . . . . . . . . 2894.1.1 Definition . . . . . . . . . . . . . . . . . . . . . . 265 4.2.8.1 Treatment of Type A Aortic4.1.2 Epidemiology/Aetiology . . . . . . . . . 265 Dissection . . . . . . . . . . . . . . . . . . . . . . 2894.1.3 Investigations . . . . . . . . . . . . . . . . . . . 266 4.2.8.2 Treatment of Type B Aortic4.1.3.1 Imaging . . . . . . . . . . . . . . . . . . . . . . . . 266 Dissection . . . . . . . . . . . . . . . . . . . . . . 2904.1.3.2 Additional Investigations . . . . . . . . 266 References . . . . . . . . . . . . . . . . . . . . . . 2964.1.4 Treatment . . . . . . . . . . . . . . . . . . . . . . 2674.1.4.1 Operative Repair . . . . . . . . . . . . . . . . 267 4.3 Trauma of the Thoracic Aorta . . . . 2994.1.4.2 Open Surgery: Operative 4.3.1 Introduction . . . . . . . . . . . . . . . . . . . . 299 Technique . . . . . . . . . . . . . . . . . . . . . . 267 4.3.2 Epidemiology . . . . . . . . . . . . . . . . . . . 2994.1.4.3 Open Surgery: Adjuvant 4.3.2.1 Automobile-related Incidences . . . 299 Techniques . . . . . . . . . . . . . . . . . . . . . 267 4.3.2.2 Blunt Thoracic Trauma . . . . . . . . . . 2994.1.5 Endovascular Intervention . . . . . . . 269 4.3.2.3 Outcome . . . . . . . . . . . . . . . . . . . . . . . 3004.1.5.1 Visceral Hybrid Procedure . . . . . . . 269 4.3.3 Aetiology . . . . . . . . . . . . . . . . . . . . . . . 3004.1.6 Outcome . . . . . . . . . . . . . . . . . . . . . . . 271 4.3.3.1 Anatomy . . . . . . . . . . . . . . . . . . . . . . . 3004.1.7 Summary and Conclusions . . . . . . . 272 4.3.3.2 Mechanism of Pathology . . . . . . . . . 301 References . . . . . . . . . . . . . . . . . . . . . . 273 4.3.4 Symptoms . . . . . . . . . . . . . . . . . . . . . . 301 4.3.5 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . 3024.2 Aortic Dissection . . . . . . . . . . . . . . . . 277 4.3.5.1 Recommended European4.2.1 Definition . . . . . . . . . . . . . . . . . . . . . . 277 Standard Diagnostic Steps4.2.2 Epidemiology . . . . . . . . . . . . . . . . . . . 277 of Investigation . . . . . . . . . . . . . . . . . 3024.2.3 Aetiology . . . . . . . . . . . . . . . . . . . . . . . 277 4.3.6 Therapy . . . . . . . . . . . . . . . . . . . . . . . . 3064.2.3.1 Association with Atherosclerotic 4.3.6.1 Surgery . . . . . . . . . . . . . . . . . . . . . . . . . 306 Disease . . . . . . . . . . . . . . . . . . . . . . . . . 277 4.3.6.2 Endovascular Approach . . . . . . . . . 3094.2.3.2 Association with Genetic References . . . . . . . . . . . . . . . . . . . . . . 312 Disease/Congenital Malformations . . . . . . . . . . . . . . . . . . 2774.2.3.3 Association with Trauma . . . . . . . . 2774.2.3.4 Other Associations . . . . . . . . . . . . . . 277
  • 15. XX Contents Abdominal Aorta and Iliac Arteries 5.3.4.2 Infection . . . . . . . . . . . . . . . . . . . . . . . 333 5.3.4.3 Autoimmune Disease . . . . . . . . . . . . 333 5.1 Abdominal Aortic Aneurysm 5.3.5 Symptoms . . . . . . . . . . . . . . . . . . . . . . 333 (AAA) . . . . . . . . . . . . . . . . . . . . . . . . . 317 5.3.5.1 Literature . . . . . . . . . . . . . . . . . . . . . . . 334 5.1.1 Introduction . . . . . . . . . . . . . . . . . . . . 317 5.3.5.2 Rupture . . . . . . . . . . . . . . . . . . . . . . . . 334 5.1.2 Definition . . . . . . . . . . . . . . . . . . . . . . 317 5.3.6 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . 334 5.1.3 Epidemiology/Aetiology . . . . . . . . . 317 5.3.6.1 Recommended European 5.1.3.1 Risk Factors . . . . . . . . . . . . . . . . . . . . 318 Standard Diagnostic Steps 5.1.3.2 Prevalence . . . . . . . . . . . . . . . . . . . . . . 318 of Investigation . . . . . . . . . . . . . . . . . 335 5.1.3.3 Incidence of AAA Rupture . . . . . . . 319 5.3.7 Therapy . . . . . . . . . . . . . . . . . . . . . . . . 336 5.1.3.4 Disease Progression . . . . . . . . . . . . . 319 5.3.7.1 Surgery . . . . . . . . . . . . . . . . . . . . . . . . . 336 5.1.3.5 Treatment . . . . . . . . . . . . . . . . . . . . . . 320 5.3.7.2 Endovascular Treatment . . . . . . . . . 338 5.1.4 Symptoms . . . . . . . . . . . . . . . . . . . . . . 320 References . . . . . . . . . . . . . . . . . . . . . . 341 5.1.4.1 Expanding Aneurysm . . . . . . . . . . . 320 5.1.4.2 Inflammatory AAA . . . . . . . . . . . . . . 320 5.4 Technically Challenging Cases 5.1.4.3 Rupture . . . . . . . . . . . . . . . . . . . . . . . . 320 for Endovascular Repair 5.1.5 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . 321 of Aortic Aneurysms . . . . . . . . . . . . 343 5.1.5.1 Recommended European 5.4.1 Introduction . . . . . . . . . . . . . . . . . . . . 343 Standard Diagnostic Steps 5.4.2 Universally Challenging of Investigation . . . . . . . . . . . . . . . . . 321 Situations . . . . . . . . . . . . . . . . . . . . . . 343 5.1.5.2 Aspects on Screening . . . . . . . . . . . . 321 5.4.2.1 Vascular Access Morphology . . . . . 343 5.1.6 Therapy . . . . . . . . . . . . . . . . . . . . . . . . 322 5.4.2.2 Aortic Aneurysm Configuration . . 343 5.1.6.1 Open Surgery . . . . . . . . . . . . . . . . . . . 322 5.4.3 Special Challenging Situations . . . . 347 5.1.6.2 Endovascular Aortic Repair 5.4.3.1 The Case of Aortic Arch (EVAR) . . . . . . . . . . . . . . . . . . . . . . . . 322 Aneurysm . . . . . . . . . . . . . . . . . . . . . . 347 5.1.6.3 Rupture and Reconstruction . . . . . 322 5.4.3.2 The Case of Aortic Dissection . . . . 347 5.1.6.4 Outcome . . . . . . . . . . . . . . . . . . . . . . . 323 5.4.3.3 The Case of Aortic Bronchial 5.1.7 Possible Complications and Enteric Fistula . . . . . . . . . . . . . . 349 of Surgery . . . . . . . . . . . . . . . . . . . . . . 323 5.4.3.4 Other Challenging Cases 5.1.8 Practical Recommendations . . . . . . 323 for EVAR . . . . . . . . . . . . . . . . . . . . . . . 350 References . . . . . . . . . . . . . . . . . . . . . . 323 5.4.4 Conclusion . . . . . . . . . . . . . . . . . . . . . 350 References . . . . . . . . . . . . . . . . . . . . . . 351 5.2 Treatment Options for Abdominal Aortic Aneurysm 5.5 Aortoiliac Occlusive Disease . . . . . 355 (AAA) . . . . . . . . . . . . . . . . . . . . . . . . . 325 5.5.1 Basics . . . . . . . . . . . . . . . . . . . . . . . . . . 355 5.2.1 Introduction . . . . . . . . . . . . . . . . . . . . 325 5.5.2 Synonyms . . . . . . . . . . . . . . . . . . . . . . 355 5.2.2 Open Repair . . . . . . . . . . . . . . . . . . . . 325 5.5.3 Definition . . . . . . . . . . . . . . . . . . . . . . 355 5.2.2.1 Complications . . . . . . . . . . . . . . . . . . 327 5.5.3.1 Morphological Features 5.2.3 Endovascular Repair . . . . . . . . . . . . 327 in the Chronic Forms . . . . . . . . . . . . 356 5.2.3.1 Complications . . . . . . . . . . . . . . . . . . 328 5.5.4 Epidemiology . . . . . . . . . . . . . . . . . . . 357 References . . . . . . . . . . . . . . . . . . . . . . 329 5.5.5 Aetiology . . . . . . . . . . . . . . . . . . . . . . . 357 5.5.6 Symptoms . . . . . . . . . . . . . . . . . . . . . . 358 5.3 Inflammatory Aneurysms 5.5.6.1 Chronic AIOD . . . . . . . . . . . . . . . . . . 358 of the Abdominal Aorta . . . . . . . . . 331 5.5.6.2 Acute AIOD . . . . . . . . . . . . . . . . . . . . 359 5.3.1 Introduction . . . . . . . . . . . . . . . . . . . . 331 5.5.7 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . 359 5.3.2 Definition . . . . . . . . . . . . . . . . . . . . . . 331 5.5.7.1 Recommended European 5.3.3 Epidemiology . . . . . . . . . . . . . . . . . . . 332 Standard . . . . . . . . . . . . . . . . . . . . . . . 359 5.3.4 Aetiology . . . . . . . . . . . . . . . . . . . . . . . 333 5.5.7.2 Additional/Useful Diagnostic 5.3.4.1 Extension of Inflammation . . . . . . . 333 Procedures . . . . . . . . . . . . . . . . . . . . . 360
  • 16. Contents XXI5.5.8 Treatment . . . . . . . . . . . . . . . . . . . . . . 360 5.6.3 Totally Laparoscopic Operative5.5.8.1 Conservative Treatment . . . . . . . . . 360 Procedures . . . . . . . . . . . . . . . . . . . . . 3775.5.8.2 Endovascular and Surgical 5.6.3.1 Retrocolic or Prerenal Treatment . . . . . . . . . . . . . . . . . . . . . . 361 Transperitoneal Procedure as5.5.9 Differential Diagnosis . . . . . . . . . . . 363 Described by Coggia [8, 11] . . . . . . 3775.5.9.1 In the Case of Chronic AIOD . . . . 363 5.6.3.2 Combined Transperitoneal5.5.9.2 In the Case of Acute AIOD . . . . . . . 363 and Retroperitoneal Procedures . . 3795.5.10 Prognosis . . . . . . . . . . . . . . . . . . . . . . . 363 5.6.3.3 Retroperitoneal Operation . . . . . . . 3805.5.11 Surgical and Endovascular 5.6.3.4 Direct Transperitoneal Principle . . . . . . . . . . . . . . . . . . . . . . . 364 Procedure [7] . . . . . . . . . . . . . . . . . . . 3805.5.11.1 Aortoiliac Angioplasty and 5.6.4 Instrumentation . . . . . . . . . . . . . . . . . 381 Stenting . . . . . . . . . . . . . . . . . . . . . . . . 364 5.6.4.1 Standard Laparoscopic5.5.11.1 Unilateral and Bilateral Instruments . . . . . . . . . . . . . . . . . . . . 381 Aortofemoral By-pass . . . . . . . . . . . 365 5.6.4.2 Specific Laparoscopic5.5.11.2 Unilateral or Bilateral Aortoiliac Instruments for Vascular By-pass . . . . . . . . . . . . . . . . . . . . . . . . . 366 Laparoscopy . . . . . . . . . . . . . . . . . . . . 3815.5.11.3 Aortic Exclusion and Bilateral 5.6.5 Complications . . . . . . . . . . . . . . . . . . 382 Aortoiliac or Bilateral 5.6.5.1 Intraoperative Complications . . . . 382 Aortofemoral Prosthetic 5.6.5.2 Early Postoperative Reconstruction . . . . . . . . . . . . . . . . . 367 Complications . . . . . . . . . . . . . . . . . . 3825.5.11.4 Unilateral or Bilateral 5.6.6 Current Indications and Results . . 383 Thoracoiliofemoral By-pass . . . . . . 367 5.6.7 Conclusions . . . . . . . . . . . . . . . . . . . . 3845.5.11.5 Aortoiliac Endarterectomy . . . . . . . 368 References . . . . . . . . . . . . . . . . . . . . . . 3845.5.11.6 Iliofemoral By-pass . . . . . . . . . . . . . . 3685.5.11.7 Femoro-femoral Cross-over 5.7 Aortouniiliac Endoprosthesis By-pass . . . . . . . . . . . . . . . . . . . . . . . . . 368 and Femoro-femoral Crossover5.5.11.8 Unilateral or Bilateral for AAA Repair . . . . . . . . . . . . . . . . . 387 Axillofemoral By-pass . . . . . . . . . . . 369 5.7.1 Introduction . . . . . . . . . . . . . . . . . . . . 3875.5.11.9 Retrograde Femoral 5.7.2 Definition . . . . . . . . . . . . . . . . . . . . . . 387 Embolectomy . . . . . . . . . . . . . . . . . . . 369 5.7.3 Indications . . . . . . . . . . . . . . . . . . . . . 3875.5.11.10 New Surgical Trends . . . . . . . . . . . . . 370 5.7.4 Contraindications . . . . . . . . . . . . . . . 3885.5.11.11 Aortobifemoral Video-assisted 5.7.5 Preoperative Management . . . . . . . 388 By-pass with Hand-Port System . . 371 5.7.6 Procedure . . . . . . . . . . . . . . . . . . . . . . 3885.5.11.12 Aortobifemoral Totally 5.7.7 Results and Complications . . . . . . . 389 Laparoscopic By-pass 5.7.8 Patency of the Femoro-femoral with Coggia’s Technique . . . . . . . . . 372 Crossover By-pass . . . . . . . . . . . . . . 390 References . . . . . . . . . . . . . . . . . . . . . . 373 5.7.9 Local Wound Complications, Graft Infection and Morbidity . . . 3915.6 Aortobifemoral By-pass: 5.7.10 Conclusion . . . . . . . . . . . . . . . . . . . . . 395 Laparoscopy-Assisted and References . . . . . . . . . . . . . . . . . . . . . . 395 Totally Laparoscopic Operative Procedures . . . . . . . . . . . . . . . . . . . . . 3755.6.1 Introduction . . . . . . . . . . . . . . . . . . . . 375 Visceral Arteries5.6.2 Operative Procedures . . . . . . . . . . . . 3755.6.2.1 Laparoscopy-Assisted Operative 6.1 Occlusive Disease of the Coeliac Procedures with Vascular and Superior Mesenteric Arteries . 401 Suturing by the Minimally 6.1.1 Definition . . . . . . . . . . . . . . . . . . . . . . 401 Invasive Route . . . . . . . . . . . . . . . . . . 375 6.1.2 Epidemiology . . . . . . . . . . . . . . . . . . . 401 6.1.3 Aetiology . . . . . . . . . . . . . . . . . . . . . . . 401
  • 17. XXII Contents 6.1.4 Symptoms . . . . . . . . . . . . . . . . . . . . . . 402 6.3.5.1 Thrombosis . . . . . . . . . . . . . . . . . . . . . 422 6.1.5 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . 402 6.3.5.2 Embolism . . . . . . . . . . . . . . . . . . . . . . 422 6.1.5.1 Recommended European References . . . . . . . . . . . . . . . . . . . . . . 423 Standard Diagnostic Steps of Investigation . . . . . . . . . . . . . . . . . 402 6.1.5.2 Additional Useful Diagnostic Lower Extremity Arteries Procedures . . . . . . . . . . . . . . . . . . . . . 403 6.1.6 Therapy . . . . . . . . . . . . . . . . . . . . . . . . 403 7.1 Lower Limb Arterial 6.1.6.1 Surgery . . . . . . . . . . . . . . . . . . . . . . . . . 404 Recanalization . . . . . . . . . . . . . . . . . . 427 6.1.6.2 Angioplasty . . . . . . . . . . . . . . . . . . . . . 406 7.1.1 Introduction . . . . . . . . . . . . . . . . . . . . 427 6.1.7 Conclusion . . . . . . . . . . . . . . . . . . . . . 408 7.1.2 Problems and Questions . . . . . . . . . 427 References . . . . . . . . . . . . . . . . . . . . . . 408 7.1.2.1 Solved Problems . . . . . . . . . . . . . . . . 428 7.1.2.2 Unsolved Problems . . . . . . . . . . . . . . 428 6.2 Visceral Artery Aneurysms . . . . . . 411 7.1.2.3 Permanent Problems . . . . . . . . . . . . 430 6.2.1 Introduction . . . . . . . . . . . . . . . . . . . . 411 7.1.2.4 Arising Questions . . . . . . . . . . . . . . . 430 6.2.2 Epidemiology . . . . . . . . . . . . . . . . . . . 411 7.1.3 Conclusions . . . . . . . . . . . . . . . . . . . . 432 6.2.3 Aetiology . . . . . . . . . . . . . . . . . . . . . . . 411 References . . . . . . . . . . . . . . . . . . . . . 433 6.2.4 Symptoms . . . . . . . . . . . . . . . . . . . . . . 412 6.2.5 Complications . . . . . . . . . . . . . . . . . . 412 7.2 Femorodistal By-pass Surgery . . . . 437 6.2.6 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . 413 7.2.1 Introduction . . . . . . . . . . . . . . . . . . . . 437 6.2.7 Therapy . . . . . . . . . . . . . . . . . . . . . . . . 413 7.2.2 General Considerations . . . . . . . . . . 437 6.2.7.1 Surgery . . . . . . . . . . . . . . . . . . . . . . . . . 413 7.2.3 Operative Indications . . . . . . . . . . . . 438 6.2.7.2 Endovascular Therapy . . . . . . . . . . . 414 7.2.4 Technical Considerations . . . . . . . . 438 6.2.8 Prognosis . . . . . . . . . . . . . . . . . . . . . . . 414 7.2.4.1 Proximal Anastomotic Site . . . . . . . 438 References . . . . . . . . . . . . . . . . . . . . . . 415 7.2.4.2 Graft Material . . . . . . . . . . . . . . . . . . . 439 7.2.4.3 Distal Anastomotic Site 6.3 Acute Ischaemia of the Visceral (Fig. 7.2.3) . . . . . . . . . . . . . . . . . . . . . . 441 Arteries . . . . . . . . . . . . . . . . . . . . . . . . 417 7.2.5 Special Considerations . . . . . . . . . . . 442 6.3.1 Acute Intestinal Ischaemia . . . . . . . 417 7.2.6 Graft Surveillance . . . . . . . . . . . . . . . 443 6.3.1.1 Basics . . . . . . . . . . . . . . . . . . . . . . . . . . 417 7.2.7 Results . . . . . . . . . . . . . . . . . . . . . . . . . 443 6.3.2 Acute Thrombotic or Embolic 7.2.7.1 Survival . . . . . . . . . . . . . . . . . . . . . . . . 443 Arterial Occlusion . . . . . . . . . . . . . . 417 7.2.7.2 Graft Patency and Limb Salvage . . 443 6.3.2.1 Epidemiology/Aetiology . . . . . . . . . 417 7.2.7.3 Quality of Life . . . . . . . . . . . . . . . . . . 445 6.3.2.2 Symptoms . . . . . . . . . . . . . . . . . . . . . . 417 References . . . . . . . . . . . . . . . . . . . . . . 445 6.3.2.3 Complications . . . . . . . . . . . . . . . . . . 418 6.3.2.4 Diagnosis . . . . . . . . . . . . . . . . . . . . . . 418 7.3 Acute Ischaemia of the Lower 6.3.2.5 Treatment . . . . . . . . . . . . . . . . . . . . . . 419 Extremities . . . . . . . . . . . . . . . . . . . . . 449 6.3.3 Mesenteric Venous Thrombosis . . 419 7.3.1 Synonyms . . . . . . . . . . . . . . . . . . . . . . 449 6.3.3.1 Epidemiology/Aetiology . . . . . . . . . 419 7.3.2 Definition . . . . . . . . . . . . . . . . . . . . . . 449 6.3.3.2 Symptoms . . . . . . . . . . . . . . . . . . . . . . 420 7.3.3 Epidemiology . . . . . . . . . . . . . . . . . . . 449 6.3.3.3 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . 420 7.3.4 Aetiology . . . . . . . . . . . . . . . . . . . . . . . 449 6.3.3.4 Therapy . . . . . . . . . . . . . . . . . . . . . . . . 420 7.3.4.1 Embolism . . . . . . . . . . . . . . . . . . . . . . 449 6.3.4 Intestinal Ischaemia 7.3.4.2 Thrombosis . . . . . . . . . . . . . . . . . . . . . 450 after Aortoiliac Surgery . . . . . . . . . . 420 7.3.4.3 Trauma . . . . . . . . . . . . . . . . . . . . . . . . . 451 6.3.4.1 Epidemiology/Aetiology . . . . . . . . . 420 7.3.5 Symptoms . . . . . . . . . . . . . . . . . . . . . . 451 6.3.4.2 Symptoms . . . . . . . . . . . . . . . . . . . . . . 421 7.3.5.1 Pain . . . . . . . . . . . . . . . . . . . . . . . . . . . . 451 6.3.4.3 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . 421 7.3.5.2 Paraesthesia . . . . . . . . . . . . . . . . . . . . 451 6.3.4.4 Treatment . . . . . . . . . . . . . . . . . . . . . . 421 7.3.5.3 Paralysis . . . . . . . . . . . . . . . . . . . . . . . . 451 6.3.5 Acute Renal Ischaemia . . . . . . . . . . . 422 7.3.5.4 Pallor . . . . . . . . . . . . . . . . . . . . . . . . . . 452
  • 18. Contents XXIII7.3.5.5 Pulselessness . . . . . . . . . . . . . . . . . . . . 452 7.5 Buerger’s Disease of the Lower7.3.6 Complications . . . . . . . . . . . . . . . . . . 452 Extremities . . . . . . . . . . . . . . . . . . . . . 4717.3.7 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . 452 7.5.1 Synonym . . . . . . . . . . . . . . . . . . . . . . . 4717.3.7.1 Recommended European 7.5.2 Definition . . . . . . . . . . . . . . . . . . . . . . 471 Standard Diagnostic Steps 7.5.3 Epidemiology . . . . . . . . . . . . . . . . . . . 471 of Investigation . . . . . . . . . . . . . . . . . 452 7.5.4 Aetiology . . . . . . . . . . . . . . . . . . . . . . . 4717.3.7.2 Additional Useful Diagnostic 7.5.5 Symptoms . . . . . . . . . . . . . . . . . . . . . . 472 Procedures . . . . . . . . . . . . . . . . . . . . . 453 7.5.6 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . 4737.3.8 Treatment . . . . . . . . . . . . . . . . . . . . . . 453 7.5.6.1 Recommended European7.3.8.1 Conservative Treatment . . . . . . . . . 453 Standard Diagnostic Steps7.3.8.2 Surgery . . . . . . . . . . . . . . . . . . . . . . . . . 453 of Investigation . . . . . . . . . . . . . . . . . 4737.3.8.3 Thrombolytic Therapy . . . . . . . . . . . 455 7.5.7 Treatment . . . . . . . . . . . . . . . . . . . . . . 4767.3.9 Differential Diagnosis . . . . . . . . . . . 457 7.5.7.1 Conservative Treatment . . . . . . . . . 4767.3.10 Prognosis . . . . . . . . . . . . . . . . . . . . . . . 457 7.5.7.2 Surgery . . . . . . . . . . . . . . . . . . . . . . . . . 476 References . . . . . . . . . . . . . . . . . . . . . . 457 7.5.7.3 Differential Diagnosis . . . . . . . . . . . 477 7.5.7.4 Prognosis . . . . . . . . . . . . . . . . . . . . . . . 4777.4 Lower Extremity Aneurysms . . . . . 459 References . . . . . . . . . . . . . . . . . . . . . . 4777.4.1 Basic Concepts . . . . . . . . . . . . . . . . . . 4597.4.2 Popliteal Aneurysms (PA) . . . . . . . . 459 7.6 Popliteal Artery Entrapment7.4.2.1 Definition . . . . . . . . . . . . . . . . . . . . . . 460 and Popliteal Adventitial Cystic7.4.2.2 Epidemiology/Aetiology . . . . . . . . . 460 Disease . . . . . . . . . . . . . . . . . . . . . . . . . 4797.4.2.3 Symptoms . . . . . . . . . . . . . . . . . . . . . . 460 7.6.1 Definition . . . . . . . . . . . . . . . . . . . . . . 4797.4.2.4 Complications . . . . . . . . . . . . . . . . . . 460 7.6.2 Epidemiology/Aetiology . . . . . . . . . 4797.4.2.5 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . 460 7.6.3 Symptoms . . . . . . . . . . . . . . . . . . . . . . 4797.4.2.6 Treatment . . . . . . . . . . . . . . . . . . . . . . 461 7.6.4 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . 4807.4.2.7 Prognosis . . . . . . . . . . . . . . . . . . . . . . 462 7.6.4.1 Recommended European7.4.3 Aneurysms of the Common Standard Diagnostic Steps Femoral Artery . . . . . . . . . . . . . . . . . 462 of Investigation . . . . . . . . . . . . . . . . . 4807.4.3.1 Definition . . . . . . . . . . . . . . . . . . . . . . 462 7.6.5 Treatment . . . . . . . . . . . . . . . . . . . . . . 4817.4.3.2 Epidemiology/Aetiology . . . . . . . . . 462 7.6.5.1 Recommended European7.4.3.3 Symptoms . . . . . . . . . . . . . . . . . . . . . . 463 Standard Surgical Procedures . . . . 4817.4.3.4 Diagnosis . . . . . . . . . . . . . . . . . . . . . . 464 7.6.6 Special Remarks . . . . . . . . . . . . . . . . . 4837.4.3.5 Treatment . . . . . . . . . . . . . . . . . . . . . . 464 References . . . . . . . . . . . . . . . . . . . . . . 4847.4.3.6 Prognosis . . . . . . . . . . . . . . . . . . . . . . 4667.4.4 Aneurysms of the Superficial 7.7 Vascular Trauma of the Lower Femoral Artery . . . . . . . . . . . . . . . . . 466 Limb . . . . . . . . . . . . . . . . . . . . . . . . . . . 4857.4.4.1 Definition . . . . . . . . . . . . . . . . . . . . . . 466 7.7.1 The Problem . . . . . . . . . . . . . . . . . . . . 4857.4.4.2 Epidemiology/Aetiology . . . . . . . . . 467 7.7.1.1 Encountering Vascular Injury . . . . 4867.4.4.3 Symptoms . . . . . . . . . . . . . . . . . . . . . . 467 7.7.1.2 How Can Ischaemia of the7.4.4.4 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . 467 Lower Limb be Detected7.4.4.5 Treatment . . . . . . . . . . . . . . . . . . . . . . 467 or Ruled Out Reliably? . . . . . . . . . . . 4867.4.4.6 Prognosis . . . . . . . . . . . . . . . . . . . . . . 467 7.7.2 Mechanisms of Injury . . . . . . . . . . . 4887.4.5 Aneurysms of the Distal 7.7.2.1 Sharp Injury . . . . . . . . . . . . . . . . . . . . 488 Branches . . . . . . . . . . . . . . . . . . . . . . . 468 7.7.2.2 Blunt injury . . . . . . . . . . . . . . . . . . . . . 4887.4.5.1 Epidemiology/Aetiology . . . . . . . . . 468 7.7.2.3 Iatrogenic . . . . . . . . . . . . . . . . . . . . . . 4907.4.5.2 Clinical Symptoms . . . . . . . . . . . . . . 468 7.7.3 Consequences of Arterial Injury7.4.5.3 Diagnosis . . . . . . . . . . . . . . . . . . . . . . 468 of the Lower Limb . . . . . . . . . . . . . . 4937.4.5.4 Therapy . . . . . . . . . . . . . . . . . . . . . . . . 468 7.7.3.1 Compartment Syndrome . . . . . . . . 493 References . . . . . . . . . . . . . . . . . . . . . 468
  • 19. XXIV Contents 7.7.3.2 False Aneurysms and Arterio- 9.1.1 Introduction . . . . . . . . . . . . . . . . . . . . 525 Venous Fistulas . . . . . . . . . . . . . . . . . 494 9.1.1.1 Scope of the Problem . . . . . . . . . . . . 525 7.7.4 The Management of Vascular 9.1.2 Incidence and Morbidity Trauma (With Special Reference of Amputation . . . . . . . . . . . . . . . . . . 525 to the Knee Joint) . . . . . . . . . . . . . . . 494 9.1.3 Classification and Indications . . . . 526 7.7.5 Bulleted Summary . . . . . . . . . . . . . . 497 9.1.3.1 Emergency Amputation . . . . . . . . . 526 References . . . . . . . . . . . . . . . . . . . . . . 497 9.1.3.2 Elective Amputations . . . . . . . . . . . . 526 9.1.4 Determination of Amputation Level . . . . . . . . . . . . . . . . . . . . . . . . . . . 527 Diabetic Foot 9.1.4.1 Transcutaneous Oxygen Tension (PtCO2) Measurement . . . . . . . . . . . 528 8.1 Diabetic Foot . . . . . . . . . . . . . . . . . . . 501 9.1.4.2 Clearance of [133Xe] . . . . . . . . . . . . . 528 8.1.1 Definition . . . . . . . . . . . . . . . . . . . . . . 501 9.1.5 Preoperative Management . . . . . . . 528 8.1.2 Epidemiology . . . . . . . . . . . . . . . . . . . 501 9.1.6 Surgical Techniques of 8.1.2.1 Foot Ulcers . . . . . . . . . . . . . . . . . . . . . 501 Amputation . . . . . . . . . . . . . . . . . . . . 528 8.1.2.2 Amputation . . . . . . . . . . . . . . . . . . . . . 501 9.1.6.1 Toe Amputation . . . . . . . . . . . . . . . . . 528 8.1.2.3 Social and Economic Costs . . . . . . . 502 9.1.6.2 Ray Amputation . . . . . . . . . . . . . . . . 529 8.1.3 Aetiology . . . . . . . . . . . . . . . . . . . . . . . 503 9.1.6.3 Transmetatarsal Amputation . . . . . 530 8.1.3.1 Pathogenesis of the Neuropathic 9.1.6.4 Syme’s Amputation Ulcer . . . . . . . . . . . . . . . . . . . . . . . . . . . 503 (Ankle Disarticulation) . . . . . . . . . . 531 8.1.3.2 Pathogenesis of the Ischaemic 9.1.6.5 Below-knee Amputation . . . . . . . . . 532 Ulcer . . . . . . . . . . . . . . . . . . . . . . . . . . . 505 9.1.6.6 Above-knee Amputation . . . . . . . . . 533 8.1.4 Complications: Neuro- 9.1.6.7 Amputation of the Upper Osteoarthropathy . . . . . . . . . . . . . . . 506 Extremity . . . . . . . . . . . . . . . . . . . . . . 534 8.1.4.1 Definition . . . . . . . . . . . . . . . . . . . . . . 506 9.1.7 Postoperative Considerations 8.1.4.2 Epidemiology . . . . . . . . . . . . . . . . . . . 506 and Rehabilitation . . . . . . . . . . . . . . . 534 8.1.4.3 Aetiology . . . . . . . . . . . . . . . . . . . . . . . 507 9.1.8 Complications . . . . . . . . . . . . . . . . . . 535 8.1.4.4 Symptoms/Investigations/ References . . . . . . . . . . . . . . . . . . . . . . 535 Diagnosis/Treatment . . . . . . . . . . . . 507 8.1.5 Diagnosis/Investigations . . . . . . . . . 507 8.1.5.1 Clinical Examination . . . . . . . . . . . . 507 Venous Diseases 8.1.5.2 Circulation . . . . . . . . . . . . . . . . . . . . . 508 8.1.5.3 Paraclinical Evaluation . . . . . . . . . . 509 10.1 Chronic Venous Insufficiency . . . . 539 8.1.5.4 Classification Systems . . . . . . . . . . . 509 10.1.1 Introduction . . . . . . . . . . . . . . . . . . . . 539 8.1.6 Differential Diagnosis . . . . . . . . . . . 509 10.1.2 Functional Anatomy and 8.1.7 Infections . . . . . . . . . . . . . . . . . . . . . . . 510 Physiology of the Venous System . . 539 8.1.7.1 Introduction . . . . . . . . . . . . . . . . . . . . 510 10.1.2.1 Superficial Veins . . . . . . . . . . . . . . . . 539 8.1.7.2 Pathophysiology . . . . . . . . . . . . . . . . 511 10.1.2.2 Deep Veins . . . . . . . . . . . . . . . . . . . . . 539 8.1.7.3 Microbiology . . . . . . . . . . . . . . . . . . . 512 10.1.2.3 Perforating Veins . . . . . . . . . . . . . . . . 539 8.1.7.4 Clinical Presentation . . . . . . . . . . . . 512 10.1.3 Chronic Venous Insufficiency . . . . 539 8.1.7.5 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . 513 10.1.3.1 Definition . . . . . . . . . . . . . . . . . . . . . . 539 8.1.7.6 Severity Classification . . . . . . . . . . . 514 10.1.3.2 Epidemiology/Aetiology . . . . . . . . . 540 8.1.7.7 Treatment . . . . . . . . . . . . . . . . . . . . . . 515 10.1.3.3 Symptoms . . . . . . . . . . . . . . . . . . . . . . 541 8.1.8 Treatment of the Diabetic Ulcer . . 517 10.1.3.4 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . 543 References . . . . . . . . . . . . . . . . . . . . . . 518 10.1.3.5 Treatment . . . . . . . . . . . . . . . . . . . . . . 545 10.1.3.6 Conclusion . . . . . . . . . . . . . . . . . . . . . 549 References . . . . . . . . . . . . . . . . . . . . . . 549 Amputations 10.2 Deep Venous Thrombosis . . . . . . . . 551 9.1 Amputation of Extremities . . . . . . . 525 10.2.1 Epidemiology/Aetiology . . . . . . . . . 551
  • 20. Contents XXV10.2.2 Symptoms . . . . . . . . . . . . . . . . . . . . . . 551 12.1.6 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . 58010.2.3 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . 551 12.1.6.1 Examination . . . . . . . . . . . . . . . . . . . 58010.2.3.1 Clinical Signs . . . . . . . . . . . . . . . . . . . 551 12.1.6.2 Laboratory Investigations10.2.3.2 Laboratory Tests and Imaging . . . . 552 and Imaging . . . . . . . . . . . . . . . . . . . . 58010.2.3.3 Recommended European 12.1.7 Treatment . . . . . . . . . . . . . . . . . . . . . . 581 Standard . . . . . . . . . . . . . . . . . . . . . . . 552 12.1.7.1 Treatment According to the Type10.2.4 Treatment . . . . . . . . . . . . . . . . . . . . . . 552 of the Malformation . . . . . . . . . . . . . 58110.2.4.1 Conservative Treatment of DVT . . 552 12.1.7.2 Conservative Treatment . . . . . . . . . 58210.2.4.2 Invasive Treatment of DVT . . . . . . 553 12.1.7.3 Surgery . . . . . . . . . . . . . . . . . . . . . . . . . 58310.2.4.3 Prevention of DVT . . . . . . . . . . . . . . 556 12.1.8 Prognosis . . . . . . . . . . . . . . . . . . . . . . . 58310.2.5 Differential Diagnosis . . . . . . . . . . . 556 References . . . . . . . . . . . . . . . . . . . . . . 58310.2.6 Prognosis . . . . . . . . . . . . . . . . . . . . . . . 557 References . . . . . . . . . . . . . . . . . . . . . . 557 Angioaccess SurgeryLymphatics 13.1 Vascular Access to Patients in Haemodialysis . . . . . . . . . . . . . . . . . . 58711.1 Lymphoedema . . . . . . . . . . . . . . . . . . 561 13.1.1 Introduction . . . . . . . . . . . . . . . . . . . . 58711.1.1 Introduction . . . . . . . . . . . . . . . . . . . . 561 13.1.2 Urgent (Acute) Haemodialysis . . . . 58711.1.1.1 Capillary Microcirculation . . . . . . . 561 13.1.2.1 External A–V Shunt . . . . . . . . . . . . . 58711.1.1.2 Capillary Circulation and Limb 13.1.2.2 Subclavian Catheters . . . . . . . . . . . . 588 Oedema . . . . . . . . . . . . . . . . . . . . . . . . 562 13.1.2.3 Jugular Catheters . . . . . . . . . . . . . . . . 58811.1.2 Definition of Lymphoedema . . . . . 563 13.1.2.4 Femoral Catheters . . . . . . . . . . . . . . . 58911.1.3 Aetiology/Epidemiology . . . . . . . . . 563 13.1.3 Chronic Haemodialysis . . . . . . . . . . 58911.1.3.1 Primary Lymphoedema . . . . . . . . . . 563 13.1.3.1 Internal A–V Shunt (A–V11.1.3.2 Secondary Lymphoedema . . . . . . . . 565 Fistula) . . . . . . . . . . . . . . . . . . . . . . . . . 58911.1.4 Symptoms . . . . . . . . . . . . . . . . . . . . . . 566 13.1.3.2 Arteriovenous Grafts . . . . . . . . . . . . 59111.1.5 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . 566 References . . . . . . . . . . . . . . . . . . . . . . 59411.1.5.1 History and Examination . . . . . . . . 56611.1.5.2 Laboratory Tests . . . . . . . . . . . . . . . . 56711.1.5.3 Imaging . . . . . . . . . . . . . . . . . . . . . . . . 567 Multidisciplinary Vascular Issues11.1.6 Treatment . . . . . . . . . . . . . . . . . . . . . . 56811.1.6.1 Conservative Treatment . . . . . . . . . 568 14.1 Infections in Vascular Surgery . . . . 59711.1.6.2 Surgery . . . . . . . . . . . . . . . . . . . . . . . . . 568 14.1.1 Introduction . . . . . . . . . . . . . . . . . . . . 597 References . . . . . . . . . . . . . . . . . . . . . . 570 14.1.2 Pathogenesis of Infection . . . . . . . . 597 14.1.2.1 Pathogen Virulence . . . . . . . . . . . . . 597 14.1.2.2 Host Response . . . . . . . . . . . . . . . . . . 598Arteriovenous Malformations 14.1.2.3 Device Factors . . . . . . . . . . . . . . . . . . 598 14.1.3 Microbiology and Diagnosis . . . . . 59812.1 Arteriovenous Malformations . . . . 573 14.1.4 Imaging . . . . . . . . . . . . . . . . . . . . . . . . 59912.1.1 Synonyms . . . . . . . . . . . . . . . . . . . . . . 573 14.1.5 Antimicrobial Therapy . . . . . . . . . . . 59912.1.2 Definition . . . . . . . . . . . . . . . . . . . . . . 573 14.1.6 Prevention . . . . . . . . . . . . . . . . . . . . . . 60012.1.2.1 Terminology . . . . . . . . . . . . . . . . . . . . 573 14.1.6.1 Primary Prophylaxis . . . . . . . . . . . . . 60012.1.3 Epidemiology . . . . . . . . . . . . . . . . . . . 573 14.1.6.2 Local Antibiotic Prophylaxis . . . . . 60212.1.3.1 Classification . . . . . . . . . . . . . . . . . . . 573 14.1.6.3 Secondary Prophylaxis . . . . . . . . . . . 60212.1.4 Aetiology . . . . . . . . . . . . . . . . . . . . . . . 575 14.1.6.4 Other Measures of Prevention . . . . 60212.1.4.1 Embryology and Anatomy . . . . . . . 575 14.1.7 Infections in Specific Vascular12.1.5 Symptoms . . . . . . . . . . . . . . . . . . . . . . 576 Implants . . . . . . . . . . . . . . . . . . . . . . . 60212.1.5.1 Vascular Bone Syndrome . . . . . . . . 576 14.1.7.1 Prosthetic Graft Infections (PGI) . . 60212.1.5.2 Specific Vascular Malformations . . 577
  • 21. XXVI Contents 14.1.7.2 Peripheral Vascular Stent 14.4.1 Aortic Arch Aneurysms Infections (PVSIs) . . . . . . . . . . . . . . . 604 in Coarctation of the Aorta . . . . . . 639 14.1.7.3 Prosthetic Carotid Patches 14.4.1.1 Epidemiology/Aetiology . . . . . . . . . 639 Infections (PCPIs) . . . . . . . . . . . . . . 607 14.4.1.2 Treatment . . . . . . . . . . . . . . . . . . . . . . 640 14.1.7.4 Arterial Closure Devices 14.4.2 Intramural Haematoma . . . . . . . . . . 640 Infections . . . . . . . . . . . . . . . . . . . . . . 608 14.4.2.1 Synonyms . . . . . . . . . . . . . . . . . . . . . . 640 14.1.7.5 Venal Caval Filter Infections . . . . . 609 14.4.2.2 Definition . . . . . . . . . . . . . . . . . . . . . . 640 14.1.7.6 Infections of Haemodialysis 14.4.2.3 Epidemiology/Aetiology . . . . . . . . . 640 Prosthetic Grafts and 14.4.2.4 Symptoms . . . . . . . . . . . . . . . . . . . . . . 640 Autologous Arteriovenous 14.4.2.5 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . 640 Fistulas (HPGFIs) . . . . . . . . . . . . . . . 609 14.4.2.6 Treatment . . . . . . . . . . . . . . . . . . . . . . 640 References . . . . . . . . . . . . . . . . . . . . . . 611 14.4.2.7 Differential Diagnosis . . . . . . . . . . . 641 14.4.2.8 Prognosis . . . . . . . . . . . . . . . . . . . . . . . 641 14.2 Vascular Problems in Urological 14.4.3 Obstructed Aortic Arch . . . . . . . . . . 641 Surgery . . . . . . . . . . . . . . . . . . . . . . . . 615 14.4.3.1 Synonyms . . . . . . . . . . . . . . . . . . . . . . 641 14.2.1 Introduction . . . . . . . . . . . . . . . . . . . . 615 14.4.3.2 Epidemiology/Aetiology . . . . . . . . . 641 14.2.2 Vascular Lesions 14.4.3.3 Symptoms . . . . . . . . . . . . . . . . . . . . . . 641 on Preoperative Evaluation . . . . . . 615 14.4.3.4 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . 641 14.2.2.1 Abdominal Aortic Aneurysm 14.4.3.5 Treatment . . . . . . . . . . . . . . . . . . . . . . 642 (AAA) . . . . . . . . . . . . . . . . . . . . . . . . . 615 14.4.4 Recurrent Obstruction of the 14.2.2.2 Renal Tumours Involving Aortic Arch . . . . . . . . . . . . . . . . . . . . 642 the Vena Cava . . . . . . . . . . . . . . . . . . 616 14.4.5 Takayasu’s Arteritis . . . . . . . . . . . . . . 643 14.2.3 Unexpected – Iatrogenic 14.4.5.1 Synonyms . . . . . . . . . . . . . . . . . . . . . . 643 Vascular Injuries . . . . . . . . . . . . . . . . 618 14.4.5.2 Definition . . . . . . . . . . . . . . . . . . . . . . 643 14.2.3.1 Venous Injuries . . . . . . . . . . . . . . . . . 618 14.4.5.3 Epidemiology/Aetiology . . . . . . . . . 643 14.2.3.2 Arterial Injuries . . . . . . . . . . . . . . . . . 619 14.4.5.4 Symptoms . . . . . . . . . . . . . . . . . . . . . . 644 14.2.4 Bulleted Summary . . . . . . . . . . . . . . 620 14.4.5.5 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . 644 References . . . . . . . . . . . . . . . . . . . . . . 620 14.5.5.6 Treatment . . . . . . . . . . . . . . . . . . . . . . 644 14.5.5.7 Prognosis . . . . . . . . . . . . . . . . . . . . . . . 645 14.3 Vascular Trauma in Orthopaedic 14.4.6 Aortic Arch Atherosclerotic Surgery . . . . . . . . . . . . . . . . . . . . . . . . 623 Aneurysm . . . . . . . . . . . . . . . . . . . . . . 645 14.3.1 Introduction . . . . . . . . . . . . . . . . . . . . 623 14.4.6.1 Epidemiology/Aetiology . . . . . . . . . 645 14.3.2 Basic Principles 14.4.6.2 Symptoms . . . . . . . . . . . . . . . . . . . . . . 645 in Microvascular Surgery . . . . . . . . 623 14.4.6.3 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . 646 14.3.2.1 Basic Microvascular Techniques . . 624 14.4.6.4 Treatment . . . . . . . . . . . . . . . . . . . . . . 646 14.3.3 Application of Microvascular 14.4.6.5 Prognosis . . . . . . . . . . . . . . . . . . . . . . . 647 Surgery to Trauma Orthopaedics . . 626 14.4.7 Atheromas and Penetrating 14.3.3.1 Replantation . . . . . . . . . . . . . . . . . . . . 626 Atherosclerotic Ulcerations of 14.3.3.2 Major Limb Revascularization the Aortic Arch . . . . . . . . . . . . . . . . . 648 and Replantation . . . . . . . . . . . . . . . . 630 14.4.7.1 Definition . . . . . . . . . . . . . . . . . . . . . . 648 14.3.3.3 Open Fractures – Type IIIb 14.4.7.2 Symptoms . . . . . . . . . . . . . . . . . . . . . . 648 and IIIc . . . . . . . . . . . . . . . . . . . . . . . . 634 14.4.7.3 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . 648 14.3.4 Vascular Complication 14.4.7.4 Treatment . . . . . . . . . . . . . . . . . . . . . . 648 in Orthopaedic Patients . . . . . . . . . 635 14.4.8 Aortic Arch Thrombosis . . . . . . . . . 649 References . . . . . . . . . . . . . . . . . . . . . . 635 14.4.8.1 Epidemiology/Aetiology . . . . . . . . . 649 14.4.8.2 Symptoms . . . . . . . . . . . . . . . . . . . . . . 649 14.4 Treatment of Aortic Arch 14.4.8.3 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . 649 Diseases . . . . . . . . . . . . . . . . . . . . . . . . 639 14.4.8.4 Treatment . . . . . . . . . . . . . . . . . . . . . . 649 14.4.9 Aortic Arch Trauma . . . . . . . . . . . . . 650
  • 22. Contents XXVII14.4.9.1 Synonyms . . . . . . . . . . . . . . . . . . . . . . 650 14.4.11.7 Treatment . . . . . . . . . . . . . . . . . . . . . . 65514.4.9.2 Definition . . . . . . . . . . . . . . . . . . . . . . 650 14.4.11.8 Differential Diagnosis . . . . . . . . . . . 65514.4.9.3 Epidemiology/Aetiology . . . . . . . . . 650 14.4.11.9 Prognosis . . . . . . . . . . . . . . . . . . . . . . . 65514.4.9.4 Symptoms . . . . . . . . . . . . . . . . . . . . . . 650 14.4.12 Ehlers–Danlos Syndrome . . . . . . . . 65514.4.9.5 Complications . . . . . . . . . . . . . . . . . . 651 14.4.12.1 Synonyms . . . . . . . . . . . . . . . . . . . . . . 65514.4.9.6 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . 651 14.4.12.2 Definition . . . . . . . . . . . . . . . . . . . . . . 65614.4.9.7 Treatment . . . . . . . . . . . . . . . . . . . . . . 651 14.4.12.3 Epidemiology/Aetiology . . . . . . . . . 65614.4.9.8 Differential Diagnosis . . . . . . . . . . . 651 14.4.12.4 Symptoms . . . . . . . . . . . . . . . . . . . . . . 65614.4.9.9 Prognosis . . . . . . . . . . . . . . . . . . . . . . . 652 14.4.12.5 Complications . . . . . . . . . . . . . . . . . . 65614.4.10 Ascending Aortic Dissection . . . . . 652 14.4.12.6 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . 65614.4.10.1 Synonyms . . . . . . . . . . . . . . . . . . . . . . 652 14.4.12.7 Treatment . . . . . . . . . . . . . . . . . . . . . . 65614.4.10.2 Definition . . . . . . . . . . . . . . . . . . . . . . 652 14.4.12.8 Differential Diagnosis . . . . . . . . . . . 65614.4.10.3 Epidemiology/Aetiology . . . . . . . . . 652 14.4.12.9 Prognosis . . . . . . . . . . . . . . . . . . . . . . . 65614.4.10.4 Symptoms . . . . . . . . . . . . . . . . . . . . . . 653 14.4.13 Noonan Syndrome . . . . . . . . . . . . . . 65614.4.10.5 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . 653 14.4.13.1 Synonyms . . . . . . . . . . . . . . . . . . . . . . 65614.4.10.6 Differential Diagnosis . . . . . . . . . . . 654 14.4.13.2 Definition . . . . . . . . . . . . . . . . . . . . . . 65614.4.11 Marfan’s Syndrome . . . . . . . . . . . . . . 654 14.4.13.3 Epidemiology/Aetiology . . . . . . . . . 65614.4.11.1 Synonyms . . . . . . . . . . . . . . . . . . . . . . 654 14.4.13.4 Symptoms . . . . . . . . . . . . . . . . . . . . . . 65614.4.11.2 Definition . . . . . . . . . . . . . . . . . . . . . . 654 14.4.13.5 Complications . . . . . . . . . . . . . . . . . . 65714.4.11.3 Epidemiology/Aetiology . . . . . . . . . 654 14.4.13.6 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . 65714.4.11.4 Symptoms . . . . . . . . . . . . . . . . . . . . . . 654 14.4.13.7 Treatment . . . . . . . . . . . . . . . . . . . . . . 65714.4.11.5 Complications . . . . . . . . . . . . . . . . . . 654 14.4.13.8 Differential Diagnosis . . . . . . . . . . . 65714.4.11.6 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . 655 References . . . . . . . . . . . . . . . . . . . . . . 657
  • 23. XXIX List of ContributorsAcosta, Stefan, MD, PhD Barbas, Maria José, MDDepartment of Vascular Surgery Hospital Garcia de OrtaMalmö General Hospital Servico de Angiologia e Cirurgia VascularMalmö, Sweden Almada, Portugal(E-mail: stefan.acosta@telia.com) (E-mail: jose.barbas@clix.pt)Angelides, Nicos S., MD Bastounis, Elias A., MD, PhDCardiovascular and Thoracic Unit First Department of SurgeryNicosia General Hospital Athens University Medical SchoolNicosia, Cyprus Athens, Greece(E-mail: n_angelides@hotmail.com (E-mail: ebastoun@med.uoa.gr)Anagnostopoulos, Constantine E., MD, ScD Bell, Sir Peter, MDDepartment of Cardiothoracic Surgery University of LeicesterAthens University Medical School Department of SurgeryAthens, Greece Robert Kilpatrick Buildingand Leicester Royal InfirmaryColumbia University Leicester, UKSt. Luke’s/Roosevelt Hospital New York (E-mail: peterrfbell@ntlworld.com)New York, USA(E-mail: cea8@columbia.edu) Benedetti-Valentini, Fabrizio, MD Department of Vascular SurgeryAnagouras, Dimitrios C., MD, FETCS University of Rome “La Sapienza”Department of Cardiothoracic Surgery Rome, ItalyUniversity of Athens School of Medicine (E-mail: chvs.rm@flashnet.it)Attikon Hospital CenterAthens, Greece Berg, Patrick, MD(E-mail: dangouras@yahoo.com) Department of Vascular Surgery Centre Hospitalier LuxembourgBalas, Panagiotis E., MD (E-mail: berg.patrick@chl.lu)P. Psihico, Greece(E-mail: pbalas@otenet.gr) Bergqvist, David, MD, PhD, FRCS Department of Surgical SciencesBalzer, Klaus, MD Uppsala University, HospitalDepartment of Vascular Surgery Uppsala, SwedenEvanglisches Krankenhaus Mülheim (E-mail: david.bergqvist@surgsci.uu.se)Mülheim/Ruhr, Germany(E-mail: klaus.balzer@evkmh.de)
  • 24. XXX Contributors Biasi, Giorgio M., MCHiR, FACS, FRCS Carmo, Michele, MD Department of Surgical Sciences and Intensive Care Division of Vascular Surgery School of Medicine, University of Milan-Bicocca Ospedale S. Carlo Borromeo San Gerardo Hospital University of Milan Monza, Italy Milan, Italy (E-mail: giorgio.biasi@unimib.it) (E-mail: michele.carmo@unimi.it) Björck, Martin, MD, PhD Cau, Jérôme, MD Department of Vascular Surgery Vascular Surgery Service Academic Hospital Uppsala University Hospital Jean Bernard Uppsala, Sweden Poitiers, France (E-mail: martin@bjorck.pp.se) (E-mail: j.cau@chu-poitiers.fr) Black, Stephen A., MD Chamogeorgakis, Themistocles, MD Regional Vascular Unit Department of Cardiothoracic Surgery St. Mary’s Hospital University of Athens School of Medicine London, UK Attikon Hospital Center (E-mail: drsablack@hotmail.com) Athens, Greece (E-mail: thchamogeorgakis@yahoo.com) van Bockel, J. Hajo, MD, PhD Department of Vascular Surgery Cormier, Jean-Michel, MD Leiden University Medical Centre Division Vascular Surgery Leiden, The Netherlands St. Joseph-Hospital (E-mail: bockel@lumc.nl) Paris, France (E-mail: jm.cormier-vasc@wanadoo.fr) Brooks, Marcus J., MD Regional Vascular Unit Daenens, Kim, MD St. Mary’s Hospital Department of Vascular Surgery London, UK University Hospital Gasthuisberg (E-mail: marcus.brooks@btinternet.com) Leuven, Belgium (E-mail: kim.daenens@uz.kuleuven.ac.be) Cairols, Marc, MD Servei d’Angiologia I Cirurgia Vascular Dallatana, Raffaello, MD Hospital Universitari de Bellvitge Division of Vascular Surgery University of Barcelona Ospedale S. Carlo Borromeo Barcelona, Spain Milan, Italy (E-mail: mcairols@csub.scs.es) (E-mail: rdallatana@libero.it) Camesasca, Valter, MD Daskalopoulos, Marios E., MSC, DIC, MD School of Medicine Department of Vascular Surgery University of Milan-Bicocca University of Athens Medical School San Gerardo Hospital Athens, Greece Monza, Italy (E-mail: daskalopoulos@mail.com) (E-mail: valter.camesasca@inwind.it)
  • 25. Contributors XXXIDaskalopoulou, Stella S., MsC, DIC, MD, FASA Febrer, Guillaume, MDDepartment of Vascular Surgery Department of Vascular SurgeryUniversity of Athens Medical School University HospitalAthens, Greece Poitiers, Franceand Department of Clinical Biochemistry and Surgery (E-mail: guillaume.febrer@gmail.com)Royal Free HospitalLondon, UK Fernandes e Fernandes, José, MD(E-mail: stelladaskalopoulou@mail.com) Professor of Surgery and Chief of Service Department of Vascular SurgeryDe Angelis, Gianni A. T., MD Hospital Santa Maria and Faculty of MedicineDivision of Vascular Surgery Director Instituto Cardiovascular de LisboaOspedale S. Carlo Borromeo Lisbon, PortugalUniversity of Milan (E-mail: jmfernandes@fm.ul.pt; ffernandes@icvl.pt)Milan, Italy(E-mail: deangelis.gianni@libero.it) Fourneau, Inge, MD Department of Vascular SurgeryDefraigne, Jean-Olivier, MD University Hospital GasthuisbergDepartment of General and Human Biochemistry Leuven, Belgiumand Physiology, Centre Hospitalier Universitaire (E-mail: inge.fourneau@uz.kuleuven.ac.be)du Sart TilmanUniversity of Liège, Belgium Fraedrich, Gustav, MD(E-mail JO.Defraigne@ulg.ac.be) Department of Vascular Surgery Medical University of InnsbruckDeleo; Gaetano, MD Innsbruck, AustriaSchool of Medicine (E-mail: gustav.fraedrich@uibk.ac.at)University of Milan-BicoccaSan Gerardo Hospital Froio, Alberto, MDMonza, Italy Vascular Surgery Unit(E-mail: gaetano.deleo@unimib.it) University of Milano-Bicocca San Gerardo HospitalDimakakos, Panos B., MD Monza, ItalyVascular Department-B (E-mail: alberto.froio@unimib.it)Surgical ClinicAretaeion Hospital Geelkerken, Robert H., MDUniversity of Athens, Medisch Spectrum TwenteAthens, Greece Enschede, The Netherlands(E-mail: bxei@aretaieio.uoa.gr) (E-mail: r.geelkerken@ziekenhuis-mst.nl)Dzsinich, Csaba, MD, PhD Georgopoulos, Sotiris E.Department of Cardiovascular Surgery First Department of SurgerySemmelweis University Athens University Medical SchoolBudapest, Hungary Athens, Greece(E-mail: csdzsinich@erseb.sote.hu) (E-mail: sgeorg@med.uoa.gr)Farghadani, Hirad, MDDepartment of Vascular SurgeryCentre Hospitalier Luxembourg(E-mail: hiradfarghadani@hotmail.com)
  • 26. XXXII Contributors Gerasimidis, Thomas, MD Heikkinen, Maarit A., MD Professor of Vascular Surgery Division of Vascular Surgery Head of the Fifth Surgical Clinic Tampere University Hospital and Tampere University Aristotle University of Thessaloniki Tampere, Finland Hippokrateio Hospital (E-mail: mheik@netti.fi) Thessaloniki, Greece (E-mail: gerasimi@med.auth.gr) Horrocks, Michael, MD Academic Department of Surgery Giamarellou, Helen, MD, PhD Royal United Hospital 4th Department of Internal Medicine and Infectious Bath, UK Diseases (E-mail: profhorrocks@btclick.com) Athens University Medical School University General Hospital “ATTIKON” Horsch, Svante, MD Athens, Greece Department of Vascular and Endovascular Surgery (E-mail: hgiama@ath.forthnet.gr) Krankenhaus Porz am Rhein Porz, Germany Giannopoulos, Aris M., MD (E-mail: prof.horsch@khporz.de) First Urology Department University of Athens Kakisis, John D., MD Medical School, Laiko Hospital 3rd Department of Surgery Athens, Greece Attikon Hospital (E-mail: agiannop@med.uoa.gr) Athens, Greece (E-mail: kakisis@yahoo.gr) Golematti, Spyretta, MD, PhD Biomedical Simulations and Imaging Laboratory Karamanos, Dimitrios Faculty of Electrical and Computer Engineering Vascular Surgeon National Technical University of Athens Fifth Surgical Clinic Athens, Greece Aristotle University of Thessaloniki (E-mail: sgolemati@biosim.ntua.gr) Hippokrateio Hospital Thessaloniki, Greece Gossetti, Bruno, MD (E-mail: dkaramanos@in.gr) Department of Vascular Surgery Policlinico Umberto 1° Katsilambros, Nicholas, MD University of Rome “La Sapienza” First Department of Propaedeutic Medicine Rome, Italy Athens University Medical School Laiko University Hospital Goulao, J., MD Athens, Greece Hospital Garcia de Orta (E-mail: laennec@techlink.gr) Servico de Angiologia e Cirurgia Vascular Almada, Portugal Kiskinis, Dimitrios A., MD, PhD (E-mail: joaogoulao@hotmail.com) Papageorgiou General Hospital Department of Vascular Surgery Guillou, Matthieu, MD Aristotle University of Thessaloniki Department of Vascular Surgery Thessaloniki, Greece Hospital Jean Bernard (E-mail: kiskinis@med.auth.gr) Poitiers, France (E-mail: matt.guillou@gmail.com)
  • 27. Contributors XXXIIIKlocker, Josef, MD Laurito, Antonella, MDDepartment of Vascular Surgery Department of Vascular Surgery and Service ofMedical University of Innsbruck Nuclear MedicineInnsbruck, Austria Policlinico Umberto I, “La Sapienza” University(E-mail: josef.klocker@uib.ac.at) Rome, ItalyKonstantinidis, Konstantinos Lecis, Alexandre, MDVascular Surgeon Department of Vascular SurgeryFifth Surgical Clinic University Hospital Jean BernardAristotle University of Thessaloniki Poitiers, FranceHippokrateio Hospital (E-mail: a.lecis@aliceadsl.gr)Thessaloniki, Greece Lens, Vincent, MDKostakis, Alkiviadis, MD Department of Radiology and NeuroradiologyDepartment of Surgery Centre Hospitalier LuxembourgAthens University Medical School (E-mail: lens.vincent@chl.lu)Laiko Peripheral General HospitalAthens, Greece Liapis, Christos D., MD, FACS, FRCS(E-mail: akostak@med.uoa.gr) Department of Vascular Surgery University of Athens Medical SchoolKotsis, Thomas E., MD Athens, GreeceVascular Department-B (E-mail: liapis@med.uoa.gr)Surgical Clinic Aretaeion HospitalSchool of Medicine, University of Athens Liloia, Angela, MDAthens, Greece Department of Surgical Sciences and Intensive(E-mail: kotsisth@otenet.gr) Care, School of Medicine University of Milan-BicoccaKtenidis, Kiriakos, MD, PhD, EBSQ-VASC. San Gerardo HospitalPapageorgiou General Hospital Monza, ItalyAss.Prof. Dr. K. Ktenidis (E-mail: angela.liloia@tiscali.it)Aristotle University of Thessaloniki1st Department of Surgery-Vascular Surgery Limet, Raymond R., MDThessaloniki, Greece Department of Cardiovascular Surgery(E-mail: kiriakos@dr-ktenidis.gr) University Hospital of Liège CHU Sart-TilmanLamont, Peter, MD, FRCS-EBSQ-VASC Liège, BelgiumConsultant Vascular Surgeon (E-mail: rlimet@ulg.ac.be)Bristol Royal InfirmaryBristol, UK Lindahl, Anne-Karin, MD(E-mail: Peter.Lamont@ubht.swest.nhs.uk) Sykehuset Asker og Baerum HF, Norway (E-mail: annekarin.lindahl@helse-sor.no)Largiadèr, Jon, MDUniversitätsspital Zurich Ljungman, Christer, MD, PhDZurich, Switzerland Department of Surgical Sciences, Section Surgery(E-mail: jon.largiader@gefaesschirurgie-zuerich.ch) Academic University Hospital Uppsala, Sweden (E-mail:krister.liungman@akademiska.se)
  • 28. XXXIV Contributors Makrilakis, Constantinos, MD Mataigne, Frédéric, MD First Department of Propaedeutic Medicine Department of Radiology and Neuroradiology Athens University Medical School Centre Hospitalier Luxembourg Laiko University Hospital (E-mail: mataigne.frederic@chl.lu Athens, Greece (E-mail: kmakrila@med.uoa.gr) Melas, N., MD First Department of Surgery and Vascular Surgery Mallios, Alexandros Aristotle University of Thessaloniki Resident in Surgery Papageorgiou General Hospital Fifth Surgical Clinic Thessaloniki, Greece Aristotle University of Thessaloniki Hippokrateio Hospital Menezes, J. Daniel, MD Thessaloniki, Greece Servico de Angiologia e Cirurgia Vascular Hospital Garcia de Orta Mambrini, Simone, MD Almada, Portugal Unit of Vascular and Endovascular Surgery (E-mail: dmenezes@hgo.min-saude.pt) University Hospital “San Martino” Genoa, Italy Mercandalli, Giulio, MD (E-mail: danasim@libero.it) Division of Vascular Surgery Ospedale S. Carlo Borromeo Mansilha, Armando, MD University of Milan Porto, Portugal Milan, Italy (E-mail: mansilha@netcabo.pt) (E-mail: gmercandalli@hotmail.com) Mantas, Dimitrios, MD Metcalfe, James, MD Department of Surgery Academic Department of Surgery Athens University Medical School Royal United Hospital Laiko Peripheral General Hospital Bath, UK Athens, Greece (E-mail: metcalfe_james@hotmail.com) (E-mail: dvmantas@gmail.com) Metz René, MD Marchand, Christophe, MD Department of Neurology Vascular Surgery Service Centre Hospitalier Luxembourg University Hospital Jean Bernard (E-mail: metz.rene@chl.lu) Poitiers, France (E-mail: c.marchand@chu-poitiers.fr) Mikhailidis, Dimitri P., MD, FASA, FFPM, FRCP, FRCPATH Martinelli, Ombretta, MD Department of Clinical Biochemistry Department of Vascular Surgery (Vascular Disease Prevention Clinics) Policlinico Umberto I° and Department of Surgery, Royal Free Hospital University of Rome “La Sapienza” London, UK Rome, Italy (E-mail: MIKHAILIDIS@aol.com) Massa, Rita, MD Mitropoulos, Fotios, MD, PhD Department of Vascular Surgery and Service of Nuclear Department of Cardiothoracic Surgery Medicine, Policlinico Umberto I° University of Athens School of Medicine University of Rome “La Sapienza” Attikon Hospital Center Rome, Italy Athens, Greece (E-mail: rita-massa@lycos.com) (E-mail: fotiosmitropoulos@yahoo.com)
  • 29. Contributors XXXVMoreno, Rosa M., MD Piazzoni, Claudia, MDHospital Clinico Universitario San Carlos Department of Surgical Sciences and Intensive CareMadrid, Spain School of Medicine(E-mail: rmoreno.hcsc@salud.madrid.org) University of Milan-Bicocca San Gerardo HospitalNachbur, Bernhard, MD, FMH Monza, ItalyIttingen, Switzerland (E-mail: claudia.piazzoni@unimib.it)(E-mail: nachbur@bluewin.ch) Poulakou, Garyphallia, MDNevelsteen, Andre, MD, PhD, FRCS 4th Department of Internal Medicine and InfectiousDepartment of Vascular Surgery Diseases, Athens University Medical SchoolUniversity Hospital Gasthuisberg University General Hospital “ATTIKON”Leuven, Belgium Athens, Greece(E-mail: Andre.Nevelsteen@uz.kuleuven.ac.be) (E-mail: gpoul@med.uoa.gr)Nikita, Konstantina S., MD Pozzi, Grazia, MDBiomedical Simulations and Imaging Laboratory Department of Surgical Sciences and Intensive Care,Faculty of Electrical and Computer Engineering School of MedicineNational Technical University of Athens University of Milan-BicoccaAthens, Greece San Gerardo Hospital(E-mail: knikita@cc.ece.ntua.gr) Monza, Italy (E-mail: grazia.pozzi@libero.it)Nyman, Rickard, MD, PhDDepartment Diagnostic Radiology Riera, S, MDAcademic University Hospital Servei d’Angiologia I Cirurgia VascularUppsala, Sweden Hospital Universitari de Bellvitge(E-mail: Rickard.nyman@akademiska.se) Barcelona, Spain (E-mail: mvelazquez@torrespardo.com)Palombo, Domenico, MDUnit of Vascular and Endovascular Surgery Ricco, Jean-Baptiste, MD, PhDUniversity Hospital “San Martino” Vascular Surgery ServiceGenoa, Italy University Hospital Jean Bernard(E-mail: domenico.palombo@hsanmartino.it) Poitiers, France (E-mail: jb-ricco@wanadoo.fr)Parsson, Hakan N., MDDepartment of Surgery Rokkas, Chris K., MDUppsala University Department of Cardiothoracic SurgeryHelsingborgs Lasarett University of Athens School of MedicineHelsingborg, Sweden Attikon Hospital Center(E-mail: hakan.parsson@helsingborgslasarett.se) Athens, Greece (E-Mail: ckrokkas@yahoo.com)Pedro, Luis Mendes, MDFaculty of Medicine Saarinen, Jukka P., MDUniversity of Lisbon Division of Vascular SurgeryConsultant in Vascular Surgery Tampere University Hospital and Tampere UniversityHospital de Santa Maria Medical SchoolLisbon, Portugal Tampere, Finland(E-mail: lmendespedro@clix.pt) (E-mail: jukkaps@koti.soon.fi)
  • 30. XXXVI Contributors Salenius, Juha-Pekka, MD Skalkeas, Gregory D., Division of Vascular Surgery Professor Emeritus, Academician Tampere University Hospital and Tampere University President of the Foundation Medical School of Biomedical Research of the Academy of Athens Tampere, Finland Athens, Greece (E-mail: Juha-Pekka.Salenius@uta.fi) (E-mail: gdskalkeas@bioacademy.gr) Sampaio, Sérgio, MD Sosa, Tomislav, MD (deceased) Porto, Portugal University Hospital Merkur (E-mail: sergiommsampeio@hotmail.com) Zagreb, Croatia Saratzis, A., MD Soucacos, Panayotis N., MD, FACS Department of Vascular Surgery Department of Orthopaedic Surgery Aristotle University of Thessaloniki University of Athens, School of Medicine Thessaloniki, Greece “K.A.T.” Accident Hospital (E-mail: a_saratzis@yahoo.gr) Athens, Greece (E-mail: soukakos@panafonet.gr) Saratzis, Nikos A., MD Department of Vascular Surgery Stamou, Sotiris, MD, PhD Aritstotle University of Thessaloniki Department of Cardiothoracic Surgery Thessaloniki, Greece Athens University Medical School (E-mail: saratzis@germanosnet.gr) Athens, Greece (E-mail: sstamou@otenet.gr) Schmitz, Serge, MD Department of Vascular Surgery Stravodimos, Konstantinos G., MD Centre Hospitalier Luxembourg First Urology Department (E-mail: schmitzs@hotmail.com) University of Athens, Medical School Laiko Hospital Schulte, Stefan, MD, PhD Athens, Greece Department of Vascular Surgery (E-mail: kgstravod@yahoo.com) Krankenhaus Porz am Rhein Porz, Germany Stumpo, Regina, MD (E-mail: stefan.schulte@khporz.de) Department of Vascular Surgery Policlinico Umberto 1° Sechas, Michael N., MD, FACS University of Rome “La Sapienza” Athens, Greece Rome, Italy (E-mail: mnsechas@yahoo.gr) Tentolouris, Nicholas, MD Sefranek, Vladimir, MD, PhD First Department of Propaedeutic Medicine Slovak Institute of Cardiovascular Diseases Bratislava Athens University Medical School Bratislava, Slovakia Leiko University Hospital (E-mail: vsefranek@susch.sk) Athens, Greece (E-mail: ntentol@med.uoa.gr) Settembrini, Piergiorgio G., MD Division of Vascular Surgery Toumpoulis, Ioannis K., MD Ospedale S. Carlo Borromeo Department of Cardiothoracic Surgery University of Milan University of Athens School of Medicine Milan, Italy Attikon Hospital Center (E-mail: piergiorgio.settembrini@unimi.it) Athens, Greece (Email: toumpoul@otenet.gr)
  • 31. Contributors XXXVIITsapogas, Panagiotis, MD Wanhainen, Anders, MD, PhDFirst Department of Propaedeutic Medicine Department Diagnostic RadiologyAthens University Medical School Academic Hospital UppsalaLeiko University Hospital Uppsala, SwedenAthens, Greece (E-mail: andwan@algonet.se)(E-mail: paianpeian@yahoo.gr) Wolfe, John H. N., MDVidjak, Vinko, MD Regional Vascular UnitUniversity Hospital Merkur St. Mary’s HospitalZagreb, Croatia London, UK(E-mail: vinko.vidjak@zg.htnet.hr) (E-mail: john.wolfe@St-marys.nhs.uk)
  • 32. Vascular Surgery and the Vascular Patient
  • 33. 3 1.1 The History of Vascular Surgery in Europe Panagiotis E. BalasTo study the texts of the illustrious personalities of the past. GALEN classical physicians, such as Hippocrates (fifth century 1.1.1 Introduction b.c.), Aurelius Celsus (first century a.d.), Galen (second century a.d.) and Paulus Aegineta (sixth century a.d.),Writing the history of a medical specialty necessitates described various methods of treating varicose veins byextensive historical and bibliographic research and the ligation, cauterization and even stripping of the dilatedcollection of data from various other sources such as in- long saphenous vein [14, 38]. The Greek Antyllus of theformation from medical people. The author must be ex- third century a.d., the most famous surgeon of antiquity,perienced in collecting, evaluating and crosschecking the applied the well-known Antyllus’ method, an opera-historical data in a scientific way to preserve objectivity. tion for aneurysm in which he applied two ligatures toUndertaking this task of presenting the history of vascu- the artery and cut between them. This was the acceptedlar surgery in Europe is difficult within the allotted time method of dealing with aneurysms until the work of Jonconstraints, which necessarily are in conflict with being Hunter in the eighteenth century. Antyllus was the firstcomprehensive and objective. to recognize two forms of aneurysm: the developmental, My major concern however is that by studying and caused by dilatation, and the traumatic, following arterialworking exclusively in the field of angiology and vascular trauma [38].surgery for almost 40 years, by participating in the foun- The famous surgeon-philosopher René Leriche (1879–dation of relevant scientific societies and by organizing 1955) credits four people who, with their ideas, practicecongresses and other activities at home and abroad, I was and findings, influenced the development and evolutionpart of the evolution of this medical field during the last of knowledge in order to establish vascular surgery andhalf of the twentieth century and this could lead to a lack to a certain extent its destination in Europe and the worldof objectivity. Therefore, my goal is to maintain the objec- all over. These four people were Ambroise Paré, Williamtivity of this work while avoiding, as far as possible, any Harvey, Jean-Louis Petit and John Hunter [38].bias due to continental, national and personal scientificand professional preoccupations and interests. In this historical review, the development, evolution Ambroise Paréand recognition of the specialty of vascular surgery in In 1546, Ambroise Paré performed the first arterial liga-Europe, including references to the associated medical tion during leg amputation in the midst of a combat andspecialties, will be presented, followed by an account of said “without having seen this attempt by any other person,the various national contributions to this field. nor heard or read but God advised me to tie the artery of the amputee”. He also introduced the first arterial forceps, the “bec de corbin”. 1.1.2 The Origin and the Foundations of European Vascular Surgery William Harvey William Harvey (1578–1657), an Englishmen, went toThe first interventions of Man on the blood vessels are the University of Padova, the most prestigious Institute atlost in the depth of history, although some descriptions that time, and he studied under Hieronymus Fabricius. Inexist in ancient Indian and Greek texts. All the great 1603, Fabricius, an ardent anatomist, published the first
  • 34. 4 1.1 The History of Vascular Surgery in Europe treatise on the valves of the heart and the great veins of The end of the eighteenth and the beginning of the the body, entitled De venarum ostiolis and observed the nineteenth century marked a golden age in which many one-way valves in veins, but had not figured out exactly surgeons contributed to knowledge on vascular diseases what their role was [10]. Harvey became Professor of and surgery. There follows a brief description of their Anatomy and Surgery at St. Bartholomew’s Hospital in contributions. Hallowel applied the first arterial suture, an London and, after 9 years of experimentation on living idea proposed by Lambert around 1770. In 1774 Morel, a animals and cadavers, proved that the blood was circulat- ing in a circuit system including the heart, arteries and veins. The connection between arteries and veins through the capillaries was discovered later by the Italian Marcello Malpighi, by using the microscope. He presented his find- ings in 1628 in his book Exercitatio Anatomica de Motu Cordis et Sanguinis in Animalibus (An Anatomical Study on the Motion of the Heart and Blood in Animals) (Figs. 1.1.1 and 1.1.2). Thus 1300 years after the Greek physician Galen had concluded that the cardiovascular system carried blood and not air, Harvey disclosed the circulation [38]. John Hunter John Hunter was born in 1728 in Scotland and at the age of 23 arrived at St. Bartholomew’s Hospital to work with Percivall Pott. He worked on comparative and human anatomy and described the exposition of the arteries in the human body. His books and publications had a pro- found impact on the medical and surgical practice of that time. He described, famously, the very proximal ligation of the femoral artery, for the preservation of the collat- eral branches, in the treatment of popliteal aneurysm. One such surgical specimen is exhibited at the renowned museum of the Royal College of Surgeons of England in London. In 1757, William Hunter, John’s older brother, described and properly analysed the development of ar- terio-venous aneurysms [38]. Jean-Louis Petit Jean-Louis Petit (1731) was the first surgeon to study hae- mostasis [38]. The famous English surgeon Sir Astley Cooper, at Guy’s Hospital, made two important contributions: a success- ful ligation of the common carotid artery for aneurysm in 1805 and in 1817 his attempt to treat an aneurysm of Fig. 1.1.1 William Harvey, Exercitatio Anatomica de Motu Cor- the iliac artery by ligation, for the first time, of the aorta dis et Sanguinis in Animalibus [Anatomical Exercise on the Mo- above the bifurcation. He was also the first to use the ex- tion of the Heart and Blood in Animals]. Edition, Roterdami, A traperitoneal approach to the abdominal aorta, which pud Arnoldum Leers A 1661. (From author’s personal collec- tion) was reintroduced by C. Rob in 1963 [56].
  • 35. 1.1.2 The Origin and the Foundations of European Vascular Surgery 5military surgeon, applied the haemostatic tourniquet to The pioneer of vascular surgery in Russia was N. I.the extremities in the battlefield. During the eighteenth Pirogov who, in 1865, developed surgical approachescentury 123 studies had been conducted on aneurysms to the aorta and peripheral arteries, arguing against theand their treatment with arterial ligation and the discus- dogmatic views that a vascular suture was not promis-sion on this topic continued until the middle of the twen- ing. P. Girsztowt of Warsaw recommended in 1868 thetieth century [38]. excision of the large varicose veins. Eugene Koeberle, The pathologist Rudolf Virchow, the “Pope of German a surgeon in Strasburg, invented a simple haemostaticmedicine”, described in 1852 the existence of arterial em- clamp and applied it in surgery in 1868. It was the firstbolism. He also coined the terms thrombosis and embo- operation actually ushering in our present technique oflism and later described the aetiological triad of venous clamping and tying, which was carried out and popular-thrombosis known as Virchow’s triad. In 1859 Karl Huet- ized by J. Pean with a clamp he invented in 1869 [38].er in Germany reported the first case of venous gangrene N. V. Ekk, an outstanding Russian surgeon and physiolo-of the extremities [25]. gist in Pavlov’s laboratory in St. Petersburg, performed inFig. 1.1.2 This illustration depicts one of William Harvey’s experiments included in the book Exercitatio Anatomica de Motu Cordiset Sanguinis in Animalibus. Harvey shows that venal blood flows only towards the heart. He ligatured an arm to make obvious theveins and their valves, then pressed blood away from the heart and showed that the vein would remain empty because it was blockedby the valve
  • 36. 6 1.1 The History of Vascular Surgery in Europe 1877 the first experimental vascular anastomosis between 1906, Carrel wrote the following instructions which are the portal vein and the inferior vena cava (Ekk’s fistula) still valid a century later: “The vessels must be handled [54]. Rudolf Matas, born in Louisiana USA and trained in very gently and the endothelium must be protected…No the USA (with additional training in Paris and Barcelo- dangerous metallic forceps are used. Great care is exer- na), made history in 1888 by performing the first endoan- cised to obtain accurate and smooth approximation eurysmorraphy for a traumatic aneurysm of the brachial of the endothelium of the vessel without invagination. artery [22]. In 1895 the Russian surgeon I. F. Sabaneyev Sutures should be made with very fine needles while made the first attempt in the world to remove an embolus the wall is somewhat stretched. Stenosis or occlusion from the femoral artery while the Russian R. R. Vreden only occurs as a result of faulty technique” [24]. Carrel performed in 1897 the first retrograde embolectomy of received the Nobel Prize in Physiology and Medicine in the aorta with limited success [54]. In 1896 the Lyon 1912 for his spectacular experimental work [24]. During veterinarian M. Jaboulay proposed in the journal Lyon the ceremony of presentation of the Prize, the President Medical an inverted suture of the arteries, known as the of the Committee J. Ackerman among other things also mattress-suture. Interestingly, this suture technique was said “To the great intelligence you have received from clinically applied 50 years later by A. Blalock in Balti- your mother country, France, to whom humanity owes more, USA [23]. In 1897 the Turkish Cemil Topuzlu so many great things, is united the energy and resolve of Pacha, Pean’s pupil, repaired an axillary artery with five your adapted country. Your miraculous operations are stitches [3]. Jaboulay’s technique was improved by one of the evident result of this happy collaboration…”. With his his pupils, Alexis Carrel, who in 1902 published the tech- associate C. A. Lindbergh (famed for making the first solo nique of suturing the vessels in Lyon Medical. Also during airplane transatlantic flight in 1927) he developed in 1935 this period Carrel performed outstanding research work the first mechanical heart, a pump for circulating blood in Lyon on arterial suturing and transplantation of arter- or fluids through preserved organs, namely the precursor ies and organs. He successfully performed the first experi- of the extra-corporeal circulation which is in use today mental cardiac homo-transplantation in the world, trans- [24]. C. A. Lindbergh wrote in 1974 “medical scientists planting the heart of an animal to the neck of another by evaluating his work in the light of modern developments joining the carotid arteries (!). He published his work in have said that he was fifty to a hundred years ahead of his the journal Lyon Medical in 1902 [24]. Carrel left Lyon time” [24]. in 1904 for Canada and the USA later, following politi- In 1901, the Austrian Erwin Payr performed a vascu- cal-religious turmoil due to his testimony of a miracle at lar anastomosis with absorbable magnesium rings. Also Lourdes. In Chicago as Director of the Hull Laboratory arterial suturing was applied experimentally by Stich and of Physiology at the University of Chicago in collabora- Makkas (Germany) and many others [38]. In 1902 Tuffier tion with Charles C. Guthrie, he mastered his suturing attempted the resection of a syphilitic aneurysm of the techniques as the well-known Carrel’s Triangulation ascending aorta but the patient died on the 13th day. Joe Techniques, and also the venous patch grafts made to Goyanes of Madrid in 1929, after excision of a popliteal enlarge the diameter of arteries. Later as Director of the aneurysm, used an adjacent segment of popliteal vein to Department of Experimental Surgery, at the Rockefeller successfully bridge the defect (the first in situ vein graft) Institute for Medical Research in New York, he worked [27]. Six months later Erich Lexer at the University Hos- on the preservation of arterial and venous segments for pital in Konigsberg, Germany performed excision of an replacement of arteries and veins. He performed canine axillary aneurysm and restored the arterial continuity by transections and end-to-end anastomosis of the descend- using a segment of the great saphenous vein [43]. This ing aorta, or inserted a segment of preserved vena cava case was reported in the prestigious journal Archiv für between the divided segments of the aorta. He also Klinische Chirurgie which was read assiduously by promi- experimented with the insertion of a paraffined tube as an nent surgeons in Europe and in the United States. Among internal shunt within the aortic lumen in order to prolong them was the American William S. Halsted, the famous the time of safe occlusion [24]. In addition to transplant- first Professor of Surgery at the Johns Hopkins Medical ing vessels and organs, Carrel worked on tissue cultures School and Hospital, who had trained in Europe and, be- and organ preservation. The Norwegian R. Ingebrigtsen sides pioneering radical surgery of breast cancer, was also participated in this work and performed later interesting interested in vascular surgery, establishing a school of ex- scientific work on arteriovenous fistulae in his country. In perimental vascular surgery. He studied various types of
  • 37. 1.1.3 Europe, Cradle of the World’s Vascular Surgery 7arterial ligatures, among which was banding to achieveprogressive arterial occlusion in order to reduce the size ofdistal aneurysms. In 1892 he successfully ligated the firstpart of the subclavian artery for the treatment of a hugedistal aneurysm. Georges Labey, in 1911, performed thefirst successful arterial embolectomy of the extremities inthe world [41], although there is information that in thesame year the Hungarian surgeon J. Bakay performed adirect femoral embolectomy (D. Dzsinich, personal com-munication). In 1914 in Innsbruck, Austria, Hans vonHaberer was the first surgeon to excise a false aneurysmof the carotid artery and to restore its continuity by anend-to-end anastomosis. He also published a monographon “Kriegsaneurysmen” reporting on 72 operated casesof aneurysms [26]. During the First World War the pioneer Polish vascu-lar surgeon Romuald Weglowski recommended the directarterial reconstruction of arterial injuries, also using ve-nous grafts for arterial bridging [57]. Vojislav Soubbotich,a pioneer vascular surgeon in Serbia during the Balkanwars (1912–14), performed repair, instead of ligation, ofthe injured vessels and of the post-traumatic aneurysmsby using circular and lateral sutures, an experience com-mented on favourably by R. Matas [45, 59]. It is ironic thatnearly 40 years passed before similar efforts were success-ful during the latter part of the Korean conflict [55]. Friedrich Trendelenburg, in Leipzig Germany, intro-duced an operation for varicose veins and in 1907 at-tempted a pulmonary embolectomy; however, he saw hispupil W. Kirchner perform a successful embolectomy in1924, which was popularized later by many surgeons in Fig. 1.1.3 A copy of the original aortograph performed by Rey-Europe and the USA [40]. I was fortunate to attend the naldo dos Santos in 1929, kindly given to the author by his sonfirst pulmonary embolectomy under extra-corporeal cir- Joao Cid dos Santos in Lisbon in 1969culation by Denton Cooley and A. Bell in 1960 at SaintLuke’s Hospital in Houston, Texas. The great breakthrough in the diagnosis of arterial dis- vein was performed by the Russian N. A. Bogoraz in 1935eases was the introduction of arteriography, namely the (cited by A. N. Filatov) [54].opacification of the arterial lumen, disclosing the abnor-malities and even the occlusion of the artery, by intra-ar-terial injection of a liquid opacified by X-rays, which was 1.1.3 Europe, Cradle of the World’sfirst performed by J. Coapody in 1925 [13]. In Lisbon in Vascular Surgery1926 Egaz Moniz, a Portuguese neurosurgeon, performedthe first intra-carotid injection of thorium dioxide for theopacification of the carotid artery in a case of brain tu- European vascular surgery has been developed by themour [49]. Reynaldo dos Santos, a professor of urology in work of the above-mentioned pioneers and by EuropeanLisbon, had performed the first translumbar aortography surgeons and medical angiologists since the 1930s andin 1929 [20] (Fig. 1.1.3). after the Second World War. During the second part of The first successful replacement of a semi-occluded the twentieth century vascular surgeons were trained infemoral artery with a segment of the large saphenous Europe and many in the USA.
  • 38. 8 1.1 The History of Vascular Surgery in Europe 1.1.3.1 The Nursery of Vascular Surgery in the occlusion of the terminal aorta, a condition which Europe in the 1930s was the René was coined Leriche syndrome [38]. For the treatment of Leriche School in Strasburg, France occlusion of the abdominal aorta he performed lumbar sympathectomies with or without excision of the occlud- The identity of vascular surgery as a specialty in the major ed aortic segment. Certainly he thought that the proper field of surgery, not only in Europe but also internation- treatment should be resection of the occluded aorta and ally, started emerging in the 1930s in the famous School its replacement with an arterial substitute, as Carrel has of René Leriche in Strasburg. In this Clinic many young done experimentally, but no arterial substitute for Man European surgeons and the American Michael E. De- was available at the time [37]. He performed with R. Fon- Bakey had their training and were indoctrinated with the taine, his successor in Strasburg, stellate ganglion block impressive ideas and experience of Leriche concerning for the release of arterial spasm in pulmonary embolism, the pathophysiology and treatment of arterial diseases. in angina pectoris and in vasospastic conditions, such as Among Leriche’s pupils were Michael E. DeBakey (USA), Raynaud’s syndrome (Fig. 1.1.5). These methods were Nicolas Christeas (Greece) (both were my teachers), Joao used for many years in our angiological practice [46]. Cid dos Santos (Portugal) and the French René Fontaine, In 1947 René Leriche proposed the establishment of the Jean Kunlin and others (Fig. 1.1.4). specialty of vascular surgery by stating “Arterial surgery René Leriche, from Lyon, became director of a surgi- is a special discipline of general surgery. The diagnostic cal clinic in Strasburg and later in Paris. He described investigation and the operations exist and the material is Fig. 1.1.4 An historic picture of Leriche and his pupils in Strasburg in 1938. First row from left to right: (starting third from left) M. E. DeBakey (USA), René Leriche, N. Christeas (Greece), C. Eliades (Greece), J. Kunlin (France). Second row: from left to right: Joao Cid dos Santos (Portugal). (Picture from author’s personal collection)
  • 39. 1.1.3 Europe, Cradle of the World’s Vascular Surgery 9abundant” [38]. His proposal was realized in the Euro-pean Union countries after 57 years, in 2004 [42]. It is important to mention that many prominent Amer-ican vascular surgeons had obtained their “portions” oftraining in Europe before the Second World War, e.g. Mi-chael E. DeBakey, or after the war, e.g. Denton A. Cooley.The author owes a personal debt of gratitude to their twocardiovascular centres for the training he received. Theyare the Methodist Hospital-Texas Medical Center of Mi-chael E. DeBakey and the St. Luke’s Hospital-Texas HeartInstitute of Denton A. Cooley. A very large series of Euro-pean surgeons was trained and many hundreds of Euro-pean cardiovascular surgeons have visited these centres,obtaining experience in vascular and/or cardiac surgery,bringing it back to their home institutions. Most of thesetrainees and many other cardiovascular surgeons from allover the world became members of the M. E. DeBakey In- Fig. 1.1.5 Leriche performing operation with Christeas on histernational Cardiovascular Society which I established in left. Strasburg 1938. (Picture from author’s personal collection)Fig. 1.1.6 Audience to the President of the Hellenic Republic, Professor Constantinos Tsatsos. From left to right : H. Eascott (UK),E. Malan (Italy), The President, M. E. DeBakey (USA), A. Senning (Switzerland), P. Balas (Greece)
  • 40. 10 1.1 The History of Vascular Surgery in Europe Athens, Greece in 1976 (Fig. 1.1.6). Also, a similar Society use of heparin for prevention of thrombosis, performed of Denton A. Cooley was established. in 1947 the first successful thrombo-endarterectomy of Many prominent American vascular surgeons were the femoral artery with a silver ophthalmic spatula [40] born in Europe and, after immigrating to the USA, devel- (Fig. 1.1.7). oped leading vascular centres. Among them are the fol- During the next few years, open disobliteration was lowing: R. Linton born in Scotland, who was Director of performed mainly by French surgeons, such as Bazy, Re- Vascular Service in the Massachusetts General Hospital boul and Huguier. Despite initial enthusiasm, it was ap- in Boston; Emeriick Szilagyi, born in Hungary, who was parent that the long-term results were not satisfactory. Director of Vascular Service in the Henry Ford Hospital, However, this technique revived following the introduc- in Detroit; and Gega de Takats, also born in Hungary, who tion of patch graft angioplasty and extension of disoblit- was Director of the Vascular Service in the University of eration of long occluded arterial segments by introducing Illinois, Chicago. Henry Haimovici from Tulcea Romania the metallic ring strippers for semi-closed thrombo-end- grew up and went to Medical School in Marseille, France. arterectomy. This was done first by the Americans Can- He moved to New York and became Head of Vascular non and Baker and later by the Russian B. V. Petrovsky Surgical Service Montefiore Hospital and Medical Cen- in 1959 [54] and in 1966 by the German J. Vollmar [61] ter. It is very interesting that after his donation in 1976 using their own metallic ring strippers. Jean Kunlin, Ler- the Rumanian Vascular Surgical Society was established. iche’s pupil, performed the first femoro-popliteal autolo- John Dormandy, born in Hungary, was Consultant Vas- gous saphenous venous by-pass in Paris in 1948 [36]. cular Surgeon at St. George Hospital, London, UK. Peter Gloviczki, born in Hungary, is Professor and Chairman of the Department of Vascular Surgery, Mayo Clinic, Roch- ester, Minnesota, USA. Christopher K. Zarins, born in Latvia, is Director of Vascular Service in Stanford Univer- sity Medical Center, Stanford, California. C. Rob moved from St. Mary’s Hospital in London, UK to the USA and became Chairman of the Department of Surgery at the Rochester University Medical School in Rochester, New York. In these centres many European surgeons were trained in vascular surgery, bringing about a reciprocal exchange of knowledge and experience among the sur- geons and vascular surgical centres of Europe and the USA, starting from the old continent. 1.1.3.2 Reference to European Surgeons who Through their Pioneering Work Developed Vascular Surgery in their Continent with International Influence Clarence Crafοord, Director of Cardiovascular Surgery at the Karolinska Hospital in Stockholm, was a pioneer in performing pulmonary embolectomies and in 1944 performed the first successful correction of coarctation of the aorta. After the excision of the stenotic segment of the aorta he performed an end-to-end anastomosis, using Carrel’s triangulation technique [9]. In Russia V. F. Gu- dov, in 1945, designed and applied clinically the first vas- cular suturing apparatus [54]. Joao Cid dos Santos, taking Fig. 1.1.7 Jean Natali (France, left) and Joa Cid dos Santos (Por- advantage of the development of arteriography and the tugal) in the early 1970s
  • 41. 1.1.3 Europe, Cradle of the World’s Vascular Surgery 11 In Paris Jacques Oudot performed experimental work Columbia-Presbyterian Hospital, by Arthur Voorhees,in vascular surgery and the preservation of arterial ho- who conceived the idea by chance on observing that silkmografts with the assistance of Jean Natali, who later be- sutures placed in a canine heart became completely cov-came one of the leaders of French vascular surgery [50]. ered with connective tissue. L. V. Lebedev and L. L. PlotkinIn 1950 Oudot was the first to replace the occluded ab- in Leningrad in 1959 developed arterial prostheses fromdominal aorta with a preserved aortic bifurcated homo- synthetic lavsan and later from fluorolon [54]. The mostgraft. Later on, due to occlusion of the right leg of the celebrated of Russian vascular surgeons Β. V. Petrovsky,graft, he performed, also for the first time, a cross-over il- Founder and Director until his mid-eighties of the Alliac–iliac by-pass with an arterial homograft [51, 53]. René Union Research Center of Surgery (AURCS) in MoscowFontaine in 1951, established in Strasburg the first arterial and past Minister of Public Health of the USSR, per-bank in Europe, followed by similar banks in many Eu- formed in 1947 the first successful resection of post-trau-ropean centres. The Russian N. I. Makhow performed in matic aneurysm in Europe [54] (Fig. 1.1.8).1950 the world’s first implantation of femoral lymphatic In 1959, the German pioneer in cardiovascular surgerychannels into the femoral vein of a patient with second- Georg Heberer was the first in Europe to perform an inter-ary lymphoedema [54]. vention on a post-traumatic rupture of the thoracic aorta In 1951 Charles Dubost in Paris performed the monu- [5]. R. van Dongen, a prominent Dutch vascular surgeonmental operation of excision of an abdominal aortic aneu- and I. Boerema’s pupil, designed a specific table and usedrysm and replacement with a 14-cm-long preserved seg- a special needle for aortography in the 1950s and later onment of thoracic aorta [21]. In 1953 at St. Mary’s Hospital published an impressive book with illustrations of vascu-in London, UK, H. H. G. Eastcott together with Professor lar procedures [31, 60] (Fig. 1.1.9).Charles Rob performed reconstruction of the occluded In 1959 Karl Victor Hall, Professor of Surgery at theleft carotid artery – the first time this had been done in National Hospital of Oslo, applied in Europe, at about theEurope [23]; a similar procedure had been performed a same time as Cartier in Canada, in situ venous by-passfew months earlier by M. E. DeBakey in Houston, Texas in the lower extremities. He later developed Hall’s valve[18]. G. Arnulf in Lyon France published a book on carot- stripper [30]. In 1962 A. V. Pokrovsky in Moscow was theid surgery [1]. In 1952, at St. Thomas’ Hospital in London, first in the world to use retroperitoneal thoraco-abdomi-Sir John Kinmonth, who was a pioneer in the study andtreatment of lymphatic diseases, introduced lymphangi-ography to image the lymphatic vessels of the extremities[35]. The Czech J. Dvorak and his collaborators were thefirst in Europe to manufacture cloth arterial prostheses ofknitted terylene followed by other kinds of material [12].These prostheses were first used in 1951 at New York’s Fig. 1.1.9 Presentation of a Diploma of Honorary Distinction of IUA, by P. Balas, Secretary of the Union (left), to R. J. A. M. van Dongen in Amsterdam in 1986 during the Eighth Course ofFig. 1.1.8 B. V. Petrovsky, Russia Vascular Surgery organized by the honouree
  • 42. 12 1.1 The History of Vascular Surgery in Europe nal access to the thoraco-abdominal aorta and visceral sound was moving. This hypothesis was tested in 1845. arteries [54]. The Japanese Shige and Satomiga applied the Doppler ef- In 1953 F. Cockett in London described the perfora- fect to the diagnostic investigation of the cardiovascular tor veins in the leg as Cockett’s perforators [15] and also system using ultrasound techniques. The resulting valu- iliac compression syndrome in 1965 [16]. This syndrome able tools for the study of the cardiovascular system in- was also described by R. May in Innsbruck [14]. Around clude Doppler ultrasonography, which uses audio and 1954 the first vascular surgical clinics of England were set graphic measurements to hear and measure blood flow, up in London, one by C. Rob and F. Eascott at St. Mary’s and duplex ultrasonography, with or without colour im- Hospital and the other by F. Cockett and J. Kinmonth at St. aging. Thomas’ Hospital; another was established in Manchester In the early 1950s, Swedish physicians, following the by Michael Boyd (F. B. Cockett, communication by cor- work of the Swede Gunnar Bauer in 1940, developed respondence, 2004). both ascending and descending phlebography and they A famous Polish vascular surgeon Jan Nielubowicz, in also started the use of heparin for the treatment of venous co-operation with Waldemar Olszewski, introduced in thrombosis [4]. 1967 the surgical lymphatico-venous shunt in patients Sven Ivar Seldinger, a radiologist at the Karolinska with secondary lymphoedema [52]. Later a Scandinavian Hospital in Stockholm, applied in 1952 a technique for plastic surgeon T. Ipsen and colleagues performed, with peripheral arteriography; the procedure is now coined the use of a microscope, a lymph–venous anastomosis with his name [56] and is used at present for all endovas- [32]. After the introduction of microvascular surgery in cular procedures. In the 1960s the Swedes Carl Arnodi, the USA by Julius Jacobson II in 1960 [33], this field was Knut Haeger, Goran Nylander and others contributed to extended in Europe by the work of Victor Krylov in the the study of venous disorders of the lower extremities (G. early 1970s at AURCS in Moscow [2] and by M. Gazi Yas- Hagmueller, communication by correspondence 2004). argil in Switzerland [19]. James S. T. Yao, working as research fellow at the vas- E. Malan, Director of a Cardiovascular Institute in cular laboratory W. T. Irving at St. Mary’s Hospital in Milan, proposed a “classification of the vascular mal- London in 1968, did pioneering work in the study of pe- formations” and established in the 1970s and 1980s an ripheral arterial circulation by using strain gauge plethys- important centre of vascular surgery in Italy. In 1967 in mography and ultrasound Doppler and developed the an- Athens, Greece, P. Balas performed the first replantation kle/brachial blood pressure index (ABI), which has been of a completely amputated upper extremity in Europe, and still is used extensively [62]. In the 1960s I. Boerema, which is functioning satisfactorily up to the present date father of modern hyperbaric medicine, applied hyper- [11]; this was followed by a successful case carried out by baric oxygen therapy in cases of critical limb ischaemia the Swiss Bruno Vogt in 1979. Jorg Vollmar in Germany and gangrene and in anaerobic infections of the extremi- developed a rigid endoscope in 1969 to inspect the lu- ties, and he also performed minor procedures in the hy- minal surface after closed arterial endarterectomy [61]. perbaric facility in the University Hospital in Amsterdam The Czech V. Michal in 1973–78 developed procedures [7] (Fig. 1.1.10). However, the largest and very impres- for vasculogenic impotence (femoro-pudendal by-pass, sive hyperbaric medical facility in Europe, and probably internal iliac thrombo-endarterectomy and direct arterial the world, was established in AURCS in Moscow in 1975, anastomosis to the cavernous body) [48]. where Victor Krylov performed carotid endarterectomy and B. A. Konstantinov and others performed cardiac op- erations in 1998. In 1998 I visited this centre, which was 1.1.3.3 Medical and Interventional Vascular under the direction of a senior professor specializing in Contributions to the Development hyperbaric medicine and included many sections such of Vascular Surgery in Europe and Worldwide as surgical, obstetrics, gynaecology and others [2] (Fig. 1.1.11). Christian Doppler was a mathematician born in Salzburg, In the early 1970s in London V. V. Kakkar made a Austria. In 1842 he wrote a paper entitled “Concerning breakthrough in the prevention of venous thrombo- the colored light of double stars”, the substance of which embolism by introducing the subcutaneous injection of is now known as the Doppler effect. He hypothesized that a low dose of heparin for the prophylaxis of deep vein the pitch of a sound would change if the source of the thrombosis (DVT) [34].
  • 43. 1.1.3 Europe, Cradle of the World’s Vascular Surgery 13 eral arteriography; the procedure is now coined with his name [58]. In 1971 E. Zeitler, a German radiologist, started popu- larizing in Europe the American Charles Dotter’s tech- nique of transcutaneous arterial disoblitaration. Andreas Gruntzig of the Angiological Clinic of Alfred Bollinger in Zurich, Switzerland, after his work with Zeitler, devel- oped in 1974 the monumental method of arterial dilata- tion by using a balloon catheter for dilatation of the pe- ripheral and coronary arteries, introducing percutaneous transluminal angioplasty (PTA) [28]. In 1976 Gruntzig performed the first PTA on the coronary arteries with the back-up of cardiac surgeons [28]. In 1977 Felix MahlerFig. 1.1.10 Hyperbaric Chamber, University Hospital of Am- from the Department of Angiology of the University ofsterdam Berne was the first to perform PTA of the renal arter- ies, for renovascular hypertension, with the back-up of vascular surgeons. The application of Gruntzig’s method A. Nikolaides contributed through original works to (PTA) was one of the greatest breakthroughs in the treat-the study of venous diseases [6]. ment of cardiovascular diseases in the twentieth century. S. I. Seldinger, a radiologist at the Karolinska hospital The radiologist I. K. Rabkin at AURCS in Moscow per-in Stockholm, applied in 1952 a technique for periph- formed the first transcatheter intravascular procedure inFig. 1.1.11 Performance of minor surgery in the chamber
  • 44. 14 1.1 The History of Vascular Surgery in Europe the USSR and was the first in the world to perform, in 1984, dilatation and endovascular prosthetic grafting of an external iliac artery [54]. N. L. Volodos was the world pioneer in devising and clinically applying endoprosthe- ses in the aorta and iliac arteries in the Ukraine in 1985, before J. Parodi [54]. Claude Mialhe from France was a world pioneer, performing in 1995 endovascular abdomi- nal aortic aneurysm repair by using a modular stent graft [47], followed immediately by Wolf J. Stelter in Frankfurt, Germany (personal communication, 1964). The Leicester group under Sir Peter Bell and the radiologist A. Bolia contributed to the advancement of endoluminal treat- ment by applying subintimal angioplasty to the lower extremities [8]. In the 1970s Herbert Ehringer in Vienna introduced intravenous thrombolysis for arterial occlu- sions. The German angiologist Hans Hess in Munich in the early 1980s introduced intra-arterial thrombolysis in peripheral arterial occlusive disease, followed by the Fig. 1.1.12 Presentation by P. Balas, President of the ESVS, of a Swede D. D. Do (1987). Diploma of Honorary Member of the Society to Roger Green- halgh (UK) during the Congress of the Society in Berlin in 1993 1.1.4 European Vascular Surgical and Angiological Societies ies, who formed the Council of Vascular Surgeons in the and Congresses EU (Aosta group), a statute was attested by a notary and was drawn, defining the specialty of vascular surgery and Since the 1970s the following events have played an es- the objectives of the Council, signed by the following: M. sential role in the development of European vascular sur- D’Addato (Italy), P. C. Maurer (Germany), H. G. Nicaise gery. The European Society of Vascular Surgery (ESVS) (France), R. Vanmaele (Belgium), J. Barbosa (Portugal), J. was founded by leading vascular surgeons R. Greenhalgh, Buth (The Netherlands), P. L. Harris (UK), M. A. Cairols Sir Peter Bell (UK), P. Fiorani (Italy), H. Mhyre (Norway), (Spain), P. Balas (Greece) and W. P. Paaske (Denmark). H. Van Urk (The Netherlands) and others. The inaugural The Council approached the European Union of Medical meeting of the Society was held in May 1987, with the Specialists (UEMS) and after long discussions, together first President being Hans Myhre, during the Internation- with the help of the ESVS, a Division of Vascular Surgery al Symposium of the Charing Cross Hospital in London; in the Section of General Surgery of the UEMS was es- it was organized by Greenhalgh, who had written the first tablished in 1992 in Edinburgh. The Division organized constitution of the Society. Preceding the formation of a European Board of Vascular Surgical Qualification the Society, the European Journal of Vascular Surgery was (EBSQ-VASC) to provide a European certification in vas- started by a European Editorial Board chaired by Green- cular surgery for the vascular surgeons of the countries halgh and became the official journal of the Society [44] of the EU, following proper assessment. The first assess- (Fig. 1.1.12). ment took place in Venice in 1966 and subsequently each Concerning the establishment of vascular surgery as an year in conjunction with the annual meeting of the ESVS. independent specialty in the European Union (EU), cred- Following successful examinations a diploma is provided it has to be given, among others, to Domenico Palombo, with the title Fellow of the European Board of Vascular an Italian vascular surgeon who organized a meeting of a Surgery [44]. On 15 October 2004 vascular surgery was working group of representatives of vascular surgical so- recognized by the UEMS as an independent specialty in cieties of the 12 EU countries at that time, in St. Vincent the EU (Fig. 1.1.13). People who over the years contribut- (Aosta-Italy) on March 1991, to discuss the perspectives ed to the recognition of the specialty were R. Greenhalgh of European vascular surgery. Through many meetings (UK), P. Harris (UK), J. Buth (The Netherlands), W. P. of representatives of European vascular surgical societ- Paaske (Denmark), C. Liapis (Greece), F. Benedetti-Val-
  • 45. 1.1.4 European Vascular Surgical and Angiological Societies and Congresses 15Fig. 1.1.13 Creation of Section of Vascular Surgery, 15 October2004. From left: F. Benedetti-Valentini, President UEMS Sectionof Vascular Surgery; R. Greenhalgh, President European Boardof Surgery and UEMS Representative, Surgical Specialties; H.Halila, President UEMS; and C. Liapis, President ESVSentini (Italy), J. Fernandes e Fernandes (Portugal), J. Wolfe(UK), G. Biasi (Italy), D. Bergqvist (Sweden) and others Fig. 1.1.14 P. Balas, President of the Congress of the ESVS in[44]. Athens in 1992 and P. Fiorani (Italy), President of ESVS and Mrs A crucial factor in the development and evolution of P. Fioranithe field of endovascular therapies for peripheral arte-rial diseases in Europe was the establishment in 1992 inBordeaux, France, of the International Society of Endo- Biasi (Italy), P. Maurer (Germany), H. Boccalon, L. Castel-vascular Surgery. Among the eight founders members lani (France), D. Clement (Belgium), A. Nicolaides (UK),of the Society four were Europeans: P. Balas (Greece), P. L. Norgren (Sweden) and others. In 1988 The Mediterra-Bergeron (France), J. Busques (France) and J. Bleyn (Bel- nean League of Angiology and Vascular Surgery (MLAVS)gium) [17]. During the Congress of the European Society was established by P. Balas (Greece), A. Strano, G. Biasifor Vascular Surgery (ESVS 1992), which I had organized (Italy), L. Castellani (France), A. Angelides (Cyprus), E.in Athens (Fig. 1.1.14), we organized with Edwards Diet- Hussein (Egypt), J. Fernandes e Fernandes (Portugal) andrich, from the Arizona Heart Institute, a spectacular satel- representatives from other European countries, underlite, live broadcast of endovascular procedures from his the patronage of the IUA, for the promotion of angiol-Institute to the Athens Hilton Hotel, an event that I am ogy in the Mediterranean countries [2]. The contributionconvinced was decisive for the decision of the European of the angiological schools of Fernando Martorell (Barce-Society of Vascular Surgery and its journal to change their lona, Spain), J. Merlen (Lille, France), C. Olivier (Paris),names to include the endovascular component [2]. Franco Pratesi (Florence), A. Strano (Palermo-Rome, European angiology played a pivotal role in the devel- Italy), Alfred Bollinger (Zurich) and Bent Fagrell (Stock-opment of world angiological disciplines, among which holm) should also be emphasized. In 1959 Max Ratschow,was vascular surgery. The promotion of European and an outstanding German angiologist in Heidelberg, pub-international angiology has been achieved by the Inter- lished an important book Angiologie. Among Ratschow’snational Union of Angiology (IUA) and its journal Inter- pupils were outstanding German angiologists Hans Hessnational Angiology, which started in 1982 with P. Balas and W. Schoop and the Swiss Leo Widmer (Basel). Allas Editor-in-Chief, and essential to this process has been these contributed to the development of the major fieldthe co-operation of prominent European angiologists of angiology in Europe, paving the way for the develop-and vascular surgeons such as F. Pratesi, A. Strano and G. ment of vascular surgery.
  • 46. 16 1.1 The History of Vascular Surgery in Europe The following leading European cardiovascular sur- in angiology-vascular surgery and of the vascular sur- geons George Arnulf (France), J. Kinmonth (UK), Edmon- geons. Among them were the 25 annual Charing Cross do Malan (Italy), R. Fontaine, Jean Natali (France), J. C. Symposia in London, the annual congresses of the ESVS Dos Santos (Portugal), Jean Van Der Stricht (Belgium) and in various European countries since 1988 and the inter- others were the founders of The European Chapter of the national and the European congresses of the IUA [2]. International Society for Cardiovascular Surgery in 1951 In Fig. 1.1.15, during the 15th World Congress of An- and of its official journal Journal of International Cardio- giology in Rome in 1989 are depicted the past, present vascular Surgery in the 1960s, playing a crucial role in the and the future presidents of the IUA. From left to right: development of cardiovascular surgery in Europe [29]. P. Balas (Greece), D. Clement (Belgium), P. Glovinczki Since the 1960s many international, European and na- (USA), P. Maurer (Germany), Cs. Dzsinich (Hungary), tional congresses, conferences, work-shops and other sci- A. Strano (Italy), President of the Congress, L. Castellani entific activities have been organized in Europe, contrib- (France), H. Boccalon (France), A. Schirger (USA) and uting significantly to the continuing education of trainees G. Parulkar (India). Fourteen Annual Mediterranean Fig. 1.1.15 The Presidents of the IUA, during the 15th World Congress of Angiology, Rome, 1989
  • 47. 1.1.5 Epilogue 17Congresses have been organized so far. Also, 14 Annual 1.1.5 EpilogueCongresses of the MLAVS have also been organized (Fig.1.1.16). Tables 1.1.1 and 1.1.2 present various national data This historical review is a tribute to the personalities whoconcerning vascular surgery in various European coun- contributed to some extent to the progress of vasculartries. It was possible to collect these through personal surgery in Europe, both those who are among us at pres-communications with leading vascular surgeons and/or ent and those who are fondly remembered (Fig. 1.1.17).from publications. Some omissions are due to lack of in- However, from this short historical account many impor-formation. tant persons and their work have not been mentioned due to limited space, but the interested reader can find them in other more extensive historical treatises.Table 1.1.1 National data concerning vascular surgery in Europe. (A The existence of the independent speciality of vascular sur-gery and date of establishment, B the existence of vascular surgical clinics and date of establishment, B1 number of state clinics,B2 number of university clinics, B3 total number, C date of establishment of a vascular surgical society and/or angiological society,D the publication of vascular surgical and/or angiological journals, E the publication of books on vascular surgery and/or angiology,+ existence, – existence, ? no information available)Country A B C D E B1 B2 B3Austria + (1983) 1 (1972) 4 – – + –Bulgaria + (1994) 1 (1964) – 7 – + –Croatia ? 9 (1964) 13 19 + (1996) – ?Cyprus + (1987) – – – – – –Czech Republic + (1986) 3 1 4 ? + +Denmark + (2004) 4 5 9 – – –Germany + (1978) ? ? 100 + (1984) + +Greece + (1989) 2 4 6 + (1982) + +Hungary + ? ? ? + + +Iceland – 1 (1994) – – – – –Ireland – 1 (Late 50s) – – + (With UK) – –Italy + (1974) 28 79 107 + ? +Norway + (1986) – – – + (1990) + –Poland + (2001) – – – + (2001) + +Serbia + (1992) 1 (1989) – – – – –Slovak Republic + (1988) 1 (1978) – – – – –Spain + (1978) 1 (1963) – 42 ? + +Switzerland + (2002) – – – + (1989, 2000) + +The Netherlands – – – – + (1981) – –Turkey – 1 (1961) – – + (1982) + +UK + (1966) ? ? ? + – +Ukraine – 1 (1972) ? ? + (2001) + +
  • 48. 18Table 1.1.2 Dates that various vascular surgical procedures started. (A Excision of aneurysms, A1 thoracic, A2 abdominal, A3 peripheral, B carotid endarterectomy,C arterial endarterectomy, D aortic by-pass, E femoro-popliteal by-pass, E1 with vein, E2 with plastic arterial prosthesis. F venous reconstruction, G endovascularaneurysm repair, G1 abdominal, G2 thoracic, G3 peripheral, ? no information available). The dates indicate the first performed operation A B C D E F G A1 A2 A3 E1 E2 G1 G2 G3Austria ? ? ? 1962 ? 1958 1952 ? ? ? ? ?Bulgaria 1960 ? ? 1962 ? ? ? 1962 1974 ? ? ?Cyprus 1988 1978 ? 1981 ? ? ? ? ? 2000 ? ? 1.1 The History of Vascular Surgery in EuropeCzech Republic Early 60s Early 60s ? Early 60s Early 60s ? Middle 50s 1958 1979 1994 ? ?Greece Early 70s 1958 1964 1963 Early 70s 1963 1962 1961 ? 1996 Early 2000 1997Hungary 1954 ? ? 1969 1949 1967 1951 ? 1986 1997 ? ?Iceland ? 1967 ? 1973 ? 1960 ? ? ? ? ? ?Ireland ? 1953 ? 1956 ? 1959 ? 1954 ? ? ? ?Norway 1979 1956 ? 1958 1955 ? ? ? ? 1995 ? ?Poland ? 1957 ? 1963 1958 ? Late 50s Late 50s 1992 Last years Last years ?Russia 1947 1958 ? ? ? 1959 ? ? 1999 ? ? ?Serbia ? 1966 ? 1965 ? 1966 1956 ? 1970 ? ? ?Slovak Republic ? 1968 ? 1961 1953 1964 ? 1960 1981 ? ? ?Spain 1962 ? ? 1963 ? ? 1959 ? ? ? ? ?Switzerland 1957 1966 ? ? ? ? ? ? ? ? ? ?The Netherlands Yes ? ? Yes ? Yes ? ? ? 1994 ? ?Turkey ? 1961 ? ? ? ? ? ? ? ? ? ?
  • 49. 1.1.5 Epilogue 19 I trust that the new generations of vascular surgeons, inspired by the achievements of the important and lead- ing personalities in angiology and vascular surgery of the past, will continue to carry the torch of progress of vascular surgery with enthusiasm and vision, to pioneer scientific work and carry out excellent medical practice for the benefit of our fellow humans afflicted by vascular diseases. Acknowledgements I greatly appreciate the following colleagues for providing important historical data concerning the development and evolution of vascular surgery in their countries: • V. Anastasov, Plovdiv, Bulgaria • Nicos Angelides, Nicosia, Cyprus • Sir Peter Bell, Leicester, UK • Patrice Bergeron, Marseille, France • David Bergqvist, Uppsala, Sweden • Giorgio Biasi, Milan, Italy • Andrea Brunner, Nuremberg, Germany • Murat Byazit, Turkey • Josep M. Capdevila, Barcelona, Spain • Lazar B. Davidovic, Belgrade, Serbia • R. J. A. M. van Dongen, Amsterdam, The Netherlands • Csaba Dzsinich, Budapest, Hungary • H. H. G. Eastcott, London, UK • Bert Eiklboom, Utrecht, The Netherlands • Georg Hagmueller, Vienna, Austria • William P. Hederman, Dublin, Ireland • A. V. Gavrilenko, Moscow, RussiaFig. 1.1.16 The President of the MLAVS, P. Balas, presenting a • Roman Jaworski, Wroclaw, PolandDiploma of Honorary Member to G. Biasi (Italy), former Secre- • Kiriaki Kalligianni, Athens, Greecetary of the League • Milan Krajicek, Praha, Czech Republic • William MacGowan, Dublin, Ireland. • Zygmunt Mackiewicz, Bydgoszcz, Poland • Nikolay Muz, Ukraine • Hans O. Myhre, Trondheim, Norway • Bernhard Nachbur, Ittigen, Switzerland • Jean Natali, Paris, France • Anatoly Pokrovsky, Moscow, Russia • V. Riambou, Barcelona, Spain • Einar Stranden, Oslo, Norway • Vladislav Treska, Plezen, Czech RepublicFig. 1.1.17 Galene’s Dictum in Greek (To study the texts of the • James Yao, Chicago, USAillustrious personalities of the past) • F. Zernovicky, Bratislava, Slovak Republic I would also like to thank my friends Professor Julius Ja- cobson, II, New York, N. Y., USA and Mr. L. H. Brown, Athens, Greece, for their editorial assistance.
  • 50. 20 1.1 The History of Vascular Surgery in Europe References 20. Dos Santos R, Lamas A, Pereirgi CJ (1929) L’arteriographie 1. Arnulf G (1957) Pathologie et chirurgie des carotids. Mas- des members de l’aorte et ses branches abdominal. Bull Soc son et Cie, Paris Nat Chir 55:587 2. Balas P (2003) Memoirs of an angiologist and vascular sur- 21. Dubost C, Allary M, Oeconomos N (1951) A propos du trait- geon. Zita, Athens ement des aneurysmes de l’aorte. Ablation de l’aneurysme, 3. Batirel HF, Yuksel M (1997) Our surgical heritage. Ann retablissment de la continuité par greffe de l’aorte humaine Thorac Surg 64:1201–1203 conservée. Mem Acad Chir 77:381 4. Bauer G (1940) Venographic study of thromboembolic 22. Eascott HHG (1969) Arterial surgery. Lippincott, problems. Acta Chir Scand 84 (Suppl) 61:1–75 Philadelphia 5. Becker HM (2000) In memoriam Prof. Dr. Georg Heberer. 23. Eascott HHG, Pickering GW, Rob CG (1954) Reconstruc- Gefasschirurgie 5:4–5 tion of internal carotid artery in a patient with intermittent 6. Bergqvist D, Comerota JA, Nicolaides A, Scurr JH (1994) attacks of hemiplegia. Lancet ii:994–996 Prevention of venous thromboembolism. Med-Orion, 24. Edwards WS (1974) Alexis Carrel. Visionary surgeon. London Charles C Thomas, Springfield 7. Boerema I (1961) An operating room for high oxygen pres- 25. Encyclopaedia Britannica On line. Virchow (12/9/2004) sure. Surgery 47:291–298 www.britannica.com. 8. Bolia A, Miles KA, Brennan J, Bell PRF (1990) Percutane- 26. Fraedrich G (2004) From Hippocrates to Palmaz-Schatz. ous transluminal angioplasty of occlusions of the femoral The history of carotid surgery. Eur J Vasc Endovasc Surg and popliteal arteries by subintimal dissection. Cardiovasc 28:455 Intervent Radiol 13:357 27. Goyanes J (1929) Nuenos trabajos de cirugia vascular. Sub- 9. Bjork VO (1984) Clarence Crafoord (1900–1984) The lead- stitucion plastica de las arterias por las venas, o atrerioplas- ing European thoracic surgeon died. J Cardiovasc Surg tica venosa, applicada como nuevo metodo, al tratamiento 25:473 de los aneurismas. El Siglo Med Sept pp 346–561 10. Caggiati M, Rippa M, Bonati A, Pieri A, Riva A (2004) Four 28. Gruntzig A, Holff H (1974) Perkutaene rekanalisation chro- centuries of valves. Eur J Vasc Endovasc Surg 28:439–441 nischer arterieller verschluess mit einem neuen dilatations- 11. Christeas N, Balas P, Giannikas A (1969) Replantation of katheter. Dtsch Med Wochenschr 99:2502 amputated extremities. Report of two successful cases. Am J 29. Haimovici H (1977) The history of the International Car- Surg 118:68–73 diovascular Society. J Cardiovasc Surg 18:207–240 12. Chvapil M, Krajicek N (1963) Principle and construction 30. Hall KV (1962) The great saphenous vein used in situ as an of a highly-porous collagen-fabric vascular graft. J Surg Res arterial shunt after extirpation of the vein valves. Surgery 5:358–364 51:492–495 13. Coapody J (1925) Arterienphotographien vermittels, Lipi- 31. Heberer G, van Dongen RJAM (1989) Vascular surgery. odol. Klin Wehnschr 4:2327 Springer, Berlin Heidelberg New York 14. Cockett FB (1990) A historical outline of varicose vein sur- 32. Ipsen T, Pless J, Fredriksen PB (1990) Experience with mi- gery up to the present day. Flebolinfologia 1:3–5 crolymphaticovenous anastomoses for the treatment of ob- 15. Cockett FB, Jones DE (1953) The ankle blow-out syndrome. structive lymphedema. Plast Reconstr Surg 85:562–571 A new approach to the varicose ulcer problem. Lancet [Jan 33. Jacobson J, II, Suarez EL (1960) Microsurgery in anastomo- 3] 1:17–23 sis of small vessels. Surgical Forum XI:243 16. Cockett FB, Thomas ML (1965) The iliac compression syn- 34. Kakkar VV, Spindler J, Flute PT et al (1972) Efficacy of the drome. Br J Surg 52:816–821 low doses of heparin in prevention of deep venous throm- 17. Criado F (1998) ISES: the first five years 1992–1997. J Endo- bosis in blind randomized trail. Lancet 2:101 vasc Surg 5:XXI–XXII 35. Kinmonth JB (1952) Lymphangiography in man; a meth- 18. DeBakey ME (1975) Successful carotid endarterecto- od of outlining lymphatic trunks at operation. Clin Sci my for cerebrovascular insufficiency. J Am Med Assoc 11:13–20 233:1083–1085 36. Kunlin J et al (1951) Le traitement de l’ischémie artéritique 19. Donaghy RMP, Yasargil MG (1967) Micro-vascular surgery. par la greffe veineuse longue. Rev Chir 15:206–235 Mosby, St Louis; Georg Thieme, Stuttgart 37. Landry P (1999) Biographies, William Harvey. www.blu- pete.com/Literature/Biographies/Science/Harvey.htm
  • 51. References 2138. Leriché R (1923) Des oblitérations artérielles hautes (oblit- 50. Natali J (1992) L’apport de Jacques Oudot a la chirurgie de la eration de la terminaison de l’aorte) comme causes des in- bifurcation aortique. Ann Chir Vasc 6:185–192 suffisances circulatoires des membres inferieurs. Bull Mem 51. Natali J (2002) The Lèriche Memorial Lecture. In: The 50th Soc Chir Paris 49:401–404 International Congress of the European Society for Cardio-39. Leriche R (1940) De la resection du carefour aorto-iliaque vascular Surgery, June 20–23, 2001, Budapest, Hungary. En- avec double sympathectomie lombaire pour thrombose ar- docardiovascular WEB Magazine 6:7–17 teritique de l’aorte: le syndrome de l’obliteration termino- 52. Nielubowicz J, Olszewski W (1968) Surgical lymphatico-ve- aortique par arterite. Presse Med 48:601 nous shunts in patients with secondary lymphoedema. Br J40. Leriche R (1943) Physiologie pathologique et chirurgie des Surg 55(6):440 artères des membres. Masson et Cie, Paris 53. Oudot J (1951) La greffe vasculaire dans les thromboses du41. Leriche R (1947) Les embolectomies de l’artere pulmonaire carrefour aortique. Presse Med 59:234 et des artères des membres. Masson Cie, Paris 54. Pokrovsky A, Bogatov YP ( 2000) Vascular surgery in Rus-42. Leriche R (1947) Rapport. Sur la desobstraction des throm- sia. J Angiol Vasc Surg 6(3):8–20 boses artérielles anciennes, par M. Jean Cid dos Santos (de 55. Rich NM, Clagett PG, Salander JM, Piscevic S (1983) The Lisbone). Mem Acad Chir 73:409–411 Matas/Soubbotitch connection. Surgery 93:17–1943. Lexer E (1907) Die ideale operation des arteriellen und des 56. Rob C (1963) Extraperitoneal approach to the abdominal arteriell-venosen aneurysma. Arch Klin Chir 83:459 aorta. Surgery 53:87–8944. Liapis CD, Paaske WP (2004) Status of vascular surgery in 57. Schumacker HB (1987) Romuald Weglowski: neglected pio- Europe. Elsevier, Amsterdam neer in vascular surgery. J Vasc Surg 6:95–9745. Matas R (1903) An operation for the radical cure of aneu- 58. Seldinger SI (1953) Catheter replacement of the needle in rism based upon arteriography. Ann Surg 37:161–196 percutaneous arteriography. A new technique. Acta Radiol46. Mellière D (2000) Petite histoire du traitement des maladies 39:368–376 artérielles et de ses pionniers. Europeene D’ Editions, Paris 59. Soubbotitch V (1913) Military experience of traumatic an-47. Mialhe C, Amicabile C (1995) Traitement endovasculaire eurysms. Lancet 2:720 des aneurysmes de l’aotre sous-renal par endoprothese 60. Van Dongen RJAM (1970) Photographic atlas of recon- Stentor, Serie preliminaire. J Mal Vasc 20:290–295 structive arterial surgery. Stenfert Kroesse, Leiden48. Michal V, Kramar R, Pospichal J (1974) Femoro-pudendal 61. Vollmar J, Storz L (1974) Vascular endoscopy: possibilities by-pass, internal iliac thromboendarterectomy and direct and limits of its clinical application. Surg Clin North Am arterial anastomosis to the cavernous body in the treatment 54:111–122 of impotence. Bull Soc Int Chir 33:343–350 62. Yao JST, Hobbs JT, IrvineWT (1968) Ankle pressure mea-49. Moniz E (1934) L’angiographie cerebrale. Masson et Cie, surement in arterial diseases of the lower extremities. Br J Paris Surg 55:859–860
  • 52. 23 1.2 Development of Atherosclerosis for the Vascular Surgeon Jean-Olivier Defraigne and adventitia. Endothelial cells (EC) lineate the intima 1.2.1 Introduction and are in contact with the blood flow. Smooth muscle cells (SMC) are encountered in the media. Based on theirAtherosclerosis is a complex disease involving various fibre content and on cell composition, two main types ofvascular segments and blood vessels such as the aorta, arteries are distinguished. Besides collagen fibres, elasticcarotid, coronary and/or peripheral arteries. Taken to- arteries contain a high proportion of elastic fibres in thegether, the thrombotic or thromboembolic complications media. Located proximally to the heart, these arteriesarising from this systemic process (stroke, myocardial in- store energy within their wall during the heart systole.farction and gangrene) are the leading causes of morbid- Thereafter, during the diastole period, they recoil and re-ity and mortality in United States, Europe and also Asia. instate this energy, thus transforming pulsatile flow into a A high plasma cholesterol level is known to be a major continuous one. In contrast, more distal arteries exhibit arisk factor for the development of atherosclerotic lesions. larger amount of SMC in the media. These latter arteriesAs a consequence, atherosclerosis is too often considered provide the resistive properties to the arterial tree, thusas a simple overload of lipids within the intimal layer of contributing to vascular tone [14].blood vessels [3]. Nevertheless, a revolution in the con- Molecular signals and complex interactions betweencept of atherosclerosis occurred after the recognition that EC and SMC are implicated in the preservation of nor-the intrinsic vascular wall cells are not merely passive re- mal blood flow and vascular patency [42]. Regarding itssponders to inflammatory stimuli but can elaborate vari- total surface and its metabolic activities, the endotheliumous mediators implicated in the initiation of an inflam- may be considered as a whole organ [7]. EC indeed pro-matory process [41, 42]. Thus, although it is clear that duce and release several mediators implicated in the localthe accumulation of lipids in macrophages and smooth control and regulation of vascular tone, blood flow, ves-muscle cells is a prominent aspect of the disease, numer- sel patency and SMC activities (Table 1.2.1). By express-ous sequential cellular events leading to an inflammatory ing cell adhesion molecules, EC also regulate cell trafficdisease of the blood vessels play a central role in athero- through the vascular wall. ECs are implicated in bloodgenesis. coagulation, notably by acting on platelet aggregation. Untreated or poorly treated atherosclerosis has signifi- For example, in response to local thrombotic events,cant medical consequences. So, better knowledge of both EC secrete vasodilating substances such as prostacyclinthe atherosclerotic disease course and of factors favour- (PGI2), prostaglandin E2 (PGE2), nitric oxide (NO) anding the onset of complications will help in improving not endothelial-dependent relaxing factor (EDRF). In ad-only medical treatment but also the selection, indications dition, as listed in Table 1.2.1, EC are also implicated inand adequacy of surgical interventions. matrix product elaboration, as well as immunological and growth regulatory functions. 1.2.2 Physiopathology of Atherosclerosis 1.2.2.2 Initiation of Atherosclerosis and Role of Endothelial Dysfunction1.2.2.1 Normal Blood Vessel Morphology Atherosclerotic lesions develop progressively with a suc-From the lumen to the external side, normal arteries are cession of events leading to the constitution of mature le-made up of three concentric layers named intima, media sions named atheromatous plaques (Fig. 1.2.1). These lat-
  • 53. 24 1.2 Development of Atherosclerosis for the Vascular Surgeon Table 1.2.1 Products released by endothelial cells Function Products secreted Elaboration of matrix components Fibronectin, laminin, collagen (type I, II, III, IV), proteoglycans Control of vascular tonus NO, prostacyclin (PGI2), prostaglandin E2 (PGE2), angiotensin-converting enzyme (ACE), thromboxane (TXA2), leukotrienes, endothelin-1 Control of cell proliferation Platelet-derived growth factor (PDGF), endothelial-derived growth factor (EDGF), fibroblast growth factor (FGF), insulin-like growth factor-1 (IGF-1), transforming growth factor-β (TGF-β), granulocyte-monocyte-colony stimulating factor (GM-CSF) Control of coagulation Von Willebrand factor (vWF), thromboplastin, platelet activating factor (PAF), plasminogen activator inhibitor 1 and 2 (PAI-1 and PAI-2), high molecular weight kininogen (HMWK), thombomodulin, antithrombin III, heparan sulfate, adenosine diphosphatase, tissue plasminogen activator, protein C Control of inflammatory processes Interleukins-1, -6, -8, leukotrienes B4, C4, D4, E4, cell adhesion molecules (CAM), major and immunological function histocompatibility complex II (MHC II) Fig. 1.2.1 Steps and processes observed during atheromatous plaque formation and maturation
  • 54. 1.2.2 Physiopathology of Atherosclerosis 25ter are composed mainly of: (1) cells (monocyte-derived To explain the process of developing atherosclerosis,macrophages, T lymphocytes and SMC); (2) connective several theories have been proposed. For example, thetissue and extracellular matrix (collagen, proteoglycans, plaque cluster could result from the monoclonal prolifer-fibronectin and elastic fibres); and (3) lipid deposits ation of modified SMC originating from a single progeni-(crystalline cholesterol, cholesteryl esters and phospho- tor (monoclonal theory) [2]. Another theory considers thelipids). Due to varying proportions of these components, role of a small accumulation of SMC, which acts as a pri-a spectrum of lesions may be observed, giving rise to sta- mordial stage of stem cells prone to playing a role in theble, fibrous or vulnerable plaques. The fatty streak form- development of atherosclerosis (intimal cell hypothesis)ing yellow streaks on the luminal surfaces of blood vessels [49]. Although some isolated cases are perhaps relevant,is often considered to be a lesion preceding the develop- none of these theories is able to completely explain all thement of a more advanced plaque [46]. Aside from SMC aspects of ongoing atherosclerosis. This suggests that theand T lymphocytes, monocyte-derived macrophages are eventual onset of atherosclerosis is also determined bya major component of this highly cellular lesion that rep- superimposed extrinsic factors such as increased choles-resents a primitive inflammatory response. Nevertheless, terol levels, smoking, etc.the relationship between fatty streaks and the ultimate Whereas, as mentioned previously, EC normally ex-development of atherosclerosis is not completely elu- press anticoagulant and vasodilatative properties, incidated. For examples, fatty streaks may be observed in some circumstances (ischaemia, stimulation by humoralfetuses and in children and may regress spontaneously. factors, influence of various pathological processes), ECIn addition, they are more frequent in females whereas may modify their activities and exhibit procoagulant andatherosclerosis is more frequent in males. vasoconstrictive properties (Fig. 1.2.2). In this latter per-Fig. 1.2.2 Consequences of endothelial dysfunction. Normal endothelium displays antiaggregant, anticoagulant and vasodilatativeproperties, along with inhibition of cell proliferation. After exposure to various agents causing endothelial dysfunction, these func-tions are modified toward procoagulant and vasoconstrictive activities together with stimulation of cell recruitment and prolifera-tion. (LDL Low density lipoprotein, PAF platelet activating factor, PAI-1 plasminogen activator inhibitor-1, PGI2 prostacylin, TXA2thromboxane A2, SMCs smooth muscle cells)
  • 55. 26 1.2 Development of Atherosclerosis for the Vascular Surgeon spective, numerous observations of animal models and the first to be expressed after stimulation and initiates the in clinical situations led to the concept of the response- process of leukocyte rolling. In a second step, ICAM-1 to-injury hypothesis, which takes into account the differ- and probably VCAM-1 are expressed, thus contributing ent steps involved in atherosclerosis. A first version of to stronger and permanent adhesion. These latter inter- this hypothesis proposed that endothelial denudation or actions precede the leukocyte infiltration of the intima, abrasion was the initial event. At the present time, rather starting the atherosclerotic process. than endothelial denudation, endothelial dysfunction is Adhesion of circulating monocytes to the surface of the considered a keystone in the triggering and progression EC is effectively an early event in the development of an of the atherosclerotic process [41, 42]. So, injury to the atherosclerotic plaque. In response to a chemoattractant endothelium layer and to underlying SMC initiate a pro- (monocyte chemoattractant protein-1, MCP-1, produced tective compensatory response, ultimately altering the by EC), monocytes adhere to, and insinuate themselves normal homeostatic properties of endothelium. During between, the tight junctions of the EC, to enter the suben- these compensatory responses, aside the release of growth dothelial space [33, 40]. Inside the intima, they transform factors and cytokines, expression of adhesion molecules and differentiate into a phagocyte state (macrophages). on the endothelial surface is simultaneously increased, They ingest modified lipids [primarily oxidized lipids resulting in increased adhesiveness for leukocytes and coming from low-density lipoprotein (LDL), see below] platelets. So increased vascular permeability, altered and attempt to remove these lipids from the intima. As control of the vascular tone and altered balance between their lipid content increases, these macrophages take on a pro- and antithrombotic factors follow EC dysfunction. foamy appearance (“foam cells”) and accumulate locally. Finally, a chronic inflammatory response is installed, The process of “scavenging” lipoproteins by macrophages leading to healing or to a fibroproliferative response and also leads to the release of cytokines, which stimulate eventually to an advanced, complicated lesion. smooth muscle migration and proliferation (see below). Immune mechanisms also appear to play a role in the process. Albeit in small numbers in human plaques, T 1.2.2.3 Evolution of the Atherosclerotic Plaque lymphocytes (implicated in the cell-mediated immune response) are present in both young and advanced fibrous Adhesion and Migration of White Blood Cells lesions. A suggested role for T lymphocytes during ath- erogenesis is help in mobilizing macrophages, which is Cellular adhesion molecules (CAMs) are implicated in similar to their role in immune responses [14, 26]. the interactions between EC and circulating leukocytes, monocytes or T lymphocytes. After injury, the adhesive- ness of the EC increases progressively and several adhe- Influence of Haemodynamic Factors sion molecules are sequentially expressed on the luminal surfaces of EC, such as members of the immunoglobu- Haemodynamic forces imposed on the endothelium in- lin super family VCAM-1 (vascular cell adhesion mol- fluence its biological response. High shear stress (tangen- ecule-1), ICAM-1 (intercellular adhesion molecule-1) or tial drag force) appears to reduce the incidence of early membrane glycoprotein E-selectin [11, 42]. VCAM-1 is intimal lesions by affecting the migration, proliferation the ligand for VLA-4 (very-late forming antigen-4) and and biological functions of ECs [31, 51]. For example, ICAM-1 binds to LFA-1 or Mac-1. The latter are integ- it has been shown that cultured ECs submitted to a flow rins present at the surface of different kinds leukocytes. still present an alignment parallel to the direction of flow. E-selectin is involved in interaction with leukocytes and When high shear stress is applied, change in the endo- platelets, since E-selectin binds P-selectin and to L-selec- thelial cytoskeleton is observed and the actin microfila- tin, expressed by platelets and leukocytes, respectively ment bundles are aligned. In contrast, the latter remain [7]. dense and nonaligned in areas where shear stress is low The pattern of expression of each CAM (onset after in- and the flow nonlaminar and turbulent. In addition, high jury, time course and duration, and degradation) is vari- shear stress increases the production of vasodilating and able, thus conferring a specific role to each of them and anti-aggregating prostacyclin (PGI2). These findings im- providing an insight into the understanding of their spe- ply a mechanism that may contribute to increased ath- cific role in leukocyte adhesion. For example, E-selectin is erogenicity in areas of low shear stress. Moreover, mitotic
  • 56. 1.2.2 Physiopathology of Atherosclerosis 27division of EC is more frequent in areas of turbulent flow factor (HB-EGF), vascular endothelial cell growth factorthan in contiguous areas [50]. (VGEF)]. All of these have been detected in atheroscle- At atherosclerotic lesion-prone sites of the circulatory rotic plaques [29, 42, 43]. In response to these chemoat-system, the expression of VCAM on the endothelium tractants, SMC migrate from the media to the intima.can be altered by abrupt changes in the direction and Migrating SMC are morphologically different from theforce of local blood flow. An element responsive to shear native SMC found in the media and their growth andstress has been identified in the regulatory region of sev- proliferation are stimulated. Where denudation of endo-eral genes (one coding for platelet-derived growth factor, thelium is noted, other factors are also implicated. Co-PDGF) and promotes the expression of adhesion mol- agulation factors and other products released by plateletsecules as well as other molecular factors that participate forming micro-thrombi also contribute to the evolutionin atherogenesis. It is supposed that a transcription factor of the plaque [39]. Simultaneously, neo microvasculariza-produced in response to abnormal shear forces can in- tion originating from the vasa vasorum develops withinduce the expression of genes contributing to the develop- the plaque and the vessel wall, and allows local delivery ofment of atherosclerosis. As a consequence, intimal lesions substances contributing to the evolution of the atheroma.preferably develop in areas of low levels of shear stress. Like PDGF, thrombin released by focal haemorrhages in If one considers laminar flow in a straight, un-branch- the plaque area is a modulator of SMC activity [24].ing segment of a vessel, the flow velocity is greatest at the So whereas EC dysfunction is the key factor initiat-centre of the vessel and, because of friction, is least at the ing the plaque, SMC are implicated in its progressionblood–endothelium interface. Depending on fluid viscos- [43]. Nevertheless, the rate of SMC proliferation withinity, mean velocity and blood vessel diameter, bifurcations the plaques is not uniform and slow progression mayand other geometric changes result in turbulent flow, be observed for a long period of time, interspersed withwith random and erratic flow profiles. The velocity vec- transient bouts of increased cell proliferation. Within thetor of blood flow in these areas becomes nonlinear. These plaques, local cytostatic mediators such as transformingchanges in haemodynamic factors that occur at bifurca- growth factor-β (TGF-β) and interferon-γ (IFN-γ) maytions account for the topographical distribution of ath- be implicated in the regulation of cell proliferation [32].erosclerosis [14, 58]. So in the vessels particularly prone As the plaque matures, SMC display high secreting activi-to atherosclerosis (coronary arteries, major branches of ties, producing various constituents of the extracellularthe aortic arch, abdominal aorta, major visceral and low-er extremity branches), the plaque localizations are notstrictly randomly determined. In the carotid territory forexample, plaque formation occurs frequently at the originof the proximal internal carotid artery. The area of the ca-rotid sinus opposite the flow divider between the externaland internal carotid arteries exhibits lower shear stressand is thus subjected to changes in haemodynamic forcesthat promote atherosclerosis. Maximal intimal thicknessoccurs on the side opposite the flow divider and intimalthickening is minimal on the inner wall while flow re-mains laminar. Such data may be transposed to other vas-cular territories.The Role of Smooth Muscle Cells (SMC)Leukocytes and ECs produce and release numerous cy-tokines and potent mitogens [interleukin-1 (IL-1), tu-mour necrosis factor-α (TNF-α), macrophage-colony Fig. 1.2.3 Atherosclerotic plaque. This mature plaque is charac-stimulating factor (M-CSF)] or growth factors [fibroblast terized by a fibrous cap and by the presence of cholesterol cleftsgrowth factor (FGF), heparin-binding epidermal growth in the vessel wall
  • 57. 28 1.2 Development of Atherosclerosis for the Vascular Surgeon matrix (such as type I and type III collagen, elastin and pounds. Besides effects on lipid metabolism (stimulation proteoglycans). As a consequence, more mature plaques of lipolysis and increase in LDL levels), nicotine con- are characterized by increased fibrous and less cellular ar- tributes to the conversion of SMC from a contractile to chitecture [42, 58] (Fig. 1.2.3). a synthetic phenotype. Increased levels of fibrinogen, in- creased platelet activity and blood viscosity together with decreased prostacyclin levels also contribute to altering the vascular wall. 1.2.3 Contributive Factors to Endothelial Homocysteinemia is an autosomal recessive disease Dysfunction and Plaque Formation that is the consequence of a deficiency of the enzyme cystathione β-synthase [5]. Elevated levels of homocys- Several potential factors leading to endothelial dysfunc- teine are correlated with an increased risk of coronary tion have been identified and include smoking, diabetes heart disease, stroke and peripheral vascular disease [52]. mellitus, hypertension, increased plasma level of oxidized Homocysteine causes EC dysfunction, SMC proliferation modified lipoprotein (LDL, low density lipoprotein), hy- and collagen production. Increased LDL oxidation and per homocysteinemia, infectious microorganisms (Her- inhibition of endogenous anticoagulant activity are asso- pes virus or Chlamydia pneumoniae), or combinations of ciated features of the disease. these or other factors. 1.2.3.2 The Oxidized LDL Hypothesis 1.2.3.1 Miscellaneous Factor Low density lipoproteins (LDL) are plasma particles that Hypertension is associated with increased vascular per- contain in association with protein several types of lip- meability resulting in enhanced migration of lipoproteins ids with a predominance of phospholipids, free and es- and macromolecules into the intima. In the presence terified cholesterol, for a total of about 1200 unsaturated of hypertension, cyclic strain and pulsatile stretching fatty acid chains. In the presence of high levels of LDL of the vessel wall are increased, which lead to repeti- – a well-recognized risk factor for developing athero- tive, circumferential, pulsatile pressure distension being sclerosis – influx of cholesterol and LDL into the intima conferred to the vascular wall [57]. In response to cyclic is increased. In addition to binding to connective tissue strains, signal transduction pathways in ECs are activated elements (such as proteoglycans), accumulated LDL is with resulting changes in morphology and proliferation. progressively oxidized [36–38, 56] (Fig. 1.2.4). This in- As mentioned previously, expression of cellular adhesion creased oxidation gives rise to the production of several molecules (ICAM-1 for example) is increased. In addi- toxic products. For example, free radicals chain reaction tion, production of toxic oxygen species (hydrogen per- within the lipid chains form hydroperoxides that easily oxide, superoxide anion, hydroxyl radical) is increased by break down, generating aldehydes (malonaldehyde, 4-hy- hypertension, with reduction of endothelial nitric oxide droxynonenal) and other toxic substances that can react release resulting in increased peripheral resistance [9]. with lysine moieties in the B-apoprotein part of the LDLs. Cyclic strains also affect the arterial sub endothelium, Other toxic products include for example 7-β-hydroper- with changes in SMC shape, orientation and proliferation oxycholesterol, 7-ketocholesterol, lysophosphatidylcho- and the secretion of extracellular matrix contributing to line, oxidized fatty acid and epoxy sterols [18]. the development of atherosclerotic lesions. Notably, col- Native (nonoxidized) LDLs are collected by the ex- lagen production is increased when SMC are submitted tremely specific LDL receptors, and then cleared by a to cyclic strains. Finally, angiotensin II promotes SMC nonatherogenous process. In contrast, the oxidatively hypertrophy and its levels are frequently elevated during modified LDLs are not recognized by these receptors. hypertension. They are metabolized in an unregulated way by scaven- Smoking is damaging for the vascular wall, result- ger receptors expressed by the macrophages present in ing in swelling and luminal surface projections of ECs the vascular wall and derived from the circulating mono- [53]. Cigarette smoke contains several potentially toxic cytes, as mentioned previously [48]. Removal and seques- compounds including nicotine, aromatic hydrocarbons, tration of modified LDLs by macrophages may be consid- sterols, aldehydes, nitriles, cyclic ethers and sulfur com- ered a protective role minimizing the effects of modified
  • 58. 1.2.3 Contributive Factors to Endothelial Dysfunction and Plaque Formation 29Fig. 1.2.4 Role of LDL oxidation in atheromatous plaque formation. After oxidation, LDLs exert toxic effects on endothelial cellswith resultant expression of cell adhesion molecules and release of growth factors. Oxidized LDL also stimulates smooth muscle cellproliferation. After endocytosis of oxidized LDL, macrophages transform into foam cells. (E-selectin Endothelial selectin, GM-CSFgranulocyte-monocyte-colony stimulating factor, ICAM-1 intercellular adhesion molecule-1, LDL low density lipoprotein, Lyso-PClysophosphatidylcholine, MCP-1 monocyte chemoattractant protein-1, ox-chol oxidized cholesterol VCAM-1 vascular cell adhesionmolecule)LDL. Nevertheless, this route is atherogenous, since the increases the inward movement of lipoprotein within theinternalization of LDL by macrophages leads to the for- artery, leading to a positive feedback. This induces a vi-mation of lipid peroxides and facilitates the transforma- cious cycle favouring development and progression of thetion of macrophages into foam cells [60]. Vitamins C and plaque. Second, autoantibodies directed toward modifiedE protect LDLs against oxidation and protective effects of LDLs are produced. Along with scavenging of LDL, im-vitamin E supplementation have been suggested in some mune complexes taken up by macrophages stimulate thereports [17]. release of cytokines and growth factors by macrophages, In addition to their ability to injure macrophages, oxi- thus contributing to stimulation of SMC migration anddized LDLs contribute to the perpetuation of the inflam- proliferation.matory reaction and to progression of the plaque, mainly Diabetes is often associated with an accelerated coursefor two reasons [35]. First, oxidized LDLs are implicated and a diffuse character of atherosclerosis, especially inin the recruitment and proliferation of monocytes and peripheral arteries, with devastating cardiovascular com-lymphocytes, notably via upregulation of gene expression plications. In this case, the nonenzymatic glycosylationfor MCP-1 and for M-CSF. This inflammatory response process of LDL impairs binding of LDL to its receptor and
  • 59. 30 1.2 Development of Atherosclerosis for the Vascular Surgeon increases the formation of foam cells [22]. This process is these latter cells [4]. Once immunologically activated by facilitated since vascular permeability is increased subse- T lymphocytes, these macrophages massively release ma- quent to alteration of the components of the extracellu- trix metalloproteases (such as collagenases, elastases and lar matrix and to thickening of the basement membrane stromelysins) [16]. Although metalloproteases probably [54]. exert a regulatory action by breaking down extracellular matrix formation during the early stage of plaque for- mation, these serine and cysteine proteases degrade the various components of the extracellular matrix, further 1.2.4 Plaque Instability destabilizing the plaques [15, 27, 44]. Simultaneously, and Complicated Plaques production of tissue-factor procoagulant and other hae- mostatic factors further increase the possibility of throm- Generally, atherosclerotic plaques remains asymptomatic bosis. because of the development of a collateral circulation her- Along with intrinsic factors, extrinsic factors also in- alded by chronic or subacute episodes of hypoxia and be- fluence the plaque stability. Low or oscillatory shear stress cause of a compensatory enlargement of the blood vessel, promotes plaque complication. Cyclic blood pressure thus trying to maintain adequate blood flow and constant changes may cause circumferential bending of eccentric lumen diameter (vascular remodelling) [23]. Increasing soft plaques, which may weaken them. In addition, large the vessel size is effective until the narrowing is approxi- deposits of calcium found on atheromatous plaques can mately less than 40% of the normal lumen [59]. be directly mediated by interaction with collagen. This However, during its maturation process the plaque massive calcification of the plaque alters the elastic prop- may become vulnerable and predisposed to ulceration erties and has significant haemodynamic consequences. and/or rupture [12, 19]. Once a plaque becomes ulcer- ated and disrupted, the coagulation cascade is initiated, with formation of platelet-rich white thrombi, that differ 1.2.5 Classification of Atherosclerotic Plaques from the red thrombi formed in regions of stasis or low flow. Despite simultaneous endogenous thrombolysis, the initial small mural thrombus may evolve to a major, The American Heart Association Committee on Vascu- near-occlusive thrombus. It may also embolize, resulting lar Lesions has proposed a classification of atheroscle- in distal small vessel occlusion leading eventually to mas- rotic plaques [46, 47]. This classification is based on the sive arterial occlusion. In these circumstances, acute clin- plaque’s evolution and maturation stages. Phase I lesions ical conditions may occur, with the onset of a wide range correspond to early arterial changes that will progress of symptoms including rapidly installing unstable angor in a stable fashion for several years. Phase II lesions are pectoris, myocardial infarction, transient ischaemic at- lipid-rich plaques that are prone to rupture. Phase III and tack, or toe gangrene. phase IV lesions refer to acutely complicated plaques with Several factors influencing plaque stability have been formation of a nonocclusive (phase III) or an occlusive identified, such as the extent of the lipid core, the fibrous (phase IV) thrombus. Phase V lesions consist of an orga- cap and its thickness, and the amount of inflammation nized and fibrotic thrombus. within the cap. Thin or ruptured fibrous caps with lack From a histological perspective and according to their of SMC-mediated healing, a large lipidic core (with a cell and lipid contents, different types (I, II and III) are predominance of cholesterol esters) and intense cell in- distinguished in phase II lesions. The vulnerable type IV filtration with inflammatory activity render the plaque (lesion with intermixed lipids and fibrous tissue) and Va more vulnerable [6]. In other words, dense and uniform (lesion with an increased lipid core covered by a thin fi- fibrous caps are generally associated with stable plaques. brous cap) lesions are the most relevant to acute ischaemic Usually, erosion and thinning of the plaque are uneven lesions. Disruption of a type IV or type Va lesion leads to and rupture frequently occurs at the shoulder of the le- the formation of a thrombus or “complicated” type VI le- sion where the fibrous cap is the thinnest and more sus- sion. Type VI lesions consist of confluent cellular lesions ceptible to physical forces causing rupture [21]. In the with a great deal of extracellular lipid intermixed with areas of rupture, the plaque is also massively infiltrated fibrous tissue covered by a fibrous cap. The complicated by macrophage-derived foam cells and SMC proliferation type VI is reserved for phase III and IV lesions causing seems impaired, with a high frequency of apoptosis of acute syndromes. These lesions are more the consequence
  • 60. 1.2.7 General Therapeutic Measures 31of an occlusive thrombus rather than being characterized Initial studies were performed ex vivo and focused onby a small mural thrombus. lipid assessment with nuclear magnetic resonance spec- troscopy and chemical shift imaging [45]. With the im- provement of the MRI techniques, high resolution and contrast imaging became possible and therefore allowed 1.2.6 Assessment and Evaluation of the Risk the in vivo study of different plaque components [10]. As of an Atherosclerotic Plaque shown in vivo on human carotid, coronary and periph- eral arteries, MRI allows characterization of the plaqueAs shown above, the sequence of events characterizing components, such as lipid core, neovascularization, fi-atherosclerosis is associated with an active inflammation brous cap, necrotic cores, intraplaque haemorrhage andprocess. This explains the elevation of plasma concentra- thrombus, with very high overall sensitivity and specific-tions of various markers, such as fibrinogen, C-reactive ity [28]. Correlation is excellent with histopathology inprotein and E-selectin, which may indicate ongoing ath- grading the lesion shape and type. The concentration oferosclerosis. Elevated levels of circulating metalloprote- serum markers of inflammation also correlates with MRases have also been found in patients with unstable and markers of atherosclerosis, as shown in patients pre-complicated carotid plaques [42]. senting with plaques in the aorta and common carotid Description of the various technical methods available artery [55]. The patients with MRI markers of unstableto evaluate an atherosclerotic patient presenting with clin- plaques have higher values of IL-6, C-reactive protein andical symptoms is outside the scope of this chapter and is VCAM-1 than those without MRI markers. Finally, in thereported elsewhere. Nevertheless, when considering ath- thoracic aorta, MRI and trans-oesophageal echocardiog-erosclerosis development and complications, an essential raphy cross-sectional aortic images show a strong corre-goal is to identify or recognize a vulnerable or unstable lation for estimation of the plaque composition and of theplaque prone to thrombosis and rupture. This is essential mean maximum plaque thickness [20].if one is to eventually decrease the complication rate of Along with monitoring of basic studies of atheroscle-atherosclerosis and to prevent acute complications. rotic disease, MRI may thus be used to follow the progres- Several invasive (e.g. X-ray angiography, intravascular sion of atherosclerosis in a given patient (hypercholester-ultrasound and angioscopy) and noninvasive (surface B- olemic patient for example) or to detect atherosclerosismode ultrasound and ultrafast computed tomography) prospectively and its location in a given population. Forimaging techniques may provide information on mor- example, an MRI study of asymptomatic patients fromphological characteristics of the disease, such as lumen the Framingham Heart Study (FHS) showed that ath-diameter, degree of stenosis or wall thickness [8, 34]. erosclerotic disease prevalence and burden (i.e. plaqueNevertheless, some of these techniques are limited in the volume/aortic volume) significantly increased with ageevaluation of the evolutionary tendency of atherosclero- and was higher in the abdominal aorta compared withsis. For example, measurement of luminal stenosis from the thoracic aorta.digital subtraction techniques does not adequately reflect So, in vivo, high-resolution, multi-contrast MR im-disease burden in carotid atherosclerosis. Vessel wall re- aging is a promising method for imaging vulnerablemodelling may produce normal luminal measurements plaques, characterizing plaques in term of lipid and fi-despite a large atheromatous plaque in situ. Moreover, al- brous content, and identifying the presence of thrombusthough an assessment of the relative risk associated with or calcium in all arteries including the coronary arteries.the atherosclerotic disease may be obtained with some MRI also allows serial evaluation assessment of the pro-techniques, these techniques do not give information on gression and/or regression of atherosclerosis over time.the composition of the plaque and are therefore incapableof identifying unstable plaques. In this context, noninvasive high-resolution magnetic 1.2.7 General Therapeutic Measuresresonance imaging (MRI) is an alternative for atheroscle-rotic plaque characterization, as shown by animal and hu-man studies [30]. MRI differentiates plaque components Since atherosclerosis is a systemic disease frequentlyon the basis of biophysical and biochemical parameters associated with several risk factors, hygieno-dieteticsuch as chemical composition and concentration, water measures must be recommended in addition to drugcontent, physical state, molecular motion, or diffusion… therapies. Smoking must be discontinued with the help
  • 61. 32 1.2 Development of Atherosclerosis for the Vascular Surgeon of smoking cessation programmes and antidepressant 4. Bjorkerud S, Bjorkerud B (1996) Apoptosis is abundant therapy, if necessary. Lipid-lowering drugs are especially in atherosclerotic lesions, especially in inflammatory cells indicated, with the use of HMG-CoA reductase inhibi- (macrophages and T-cells), and may contribute to the ac- tors. Statins not only decrease cholesterol levels but also cumulation of gruel and plaque instability. Am J Pathol exert pleiotropic effects on the vascular wall limiting the 149:367–380 inflammatory process within the plaques [1, 13]. Plaque 5. Boushey CJ, Beresdorf SA (1995) A quantitative assessment regression with lipid-lowering therapy has been reported of plasma homocysteine as a risk factor for vascular disease: in both the aorta and carotids. An LDL cholesterol level probable benefits of increased folic acide intakes. J Am Med less than 100 mg/dl should be attained. The incidence of Assoc 274:1049–1057 cardiac event may be minimized by appropriate control 6. Boyle JJ (1997) Association of plaque rupture and athero- of heart rate and blood pressure. Diabetic patients should sclerotic inflammation. J Pathol 181:93–99 be adequately treated and monitored. Haemoglobin A1c 7. Burrig KF (1991) The endothelium of advanced arterioscle- should be less than 7%. Dietary supplementation of vita- rotic plaques in humans. Arterio Thromb 11:1678–1689 min B12 and folic acid should be prescribed, especially in 8. Celermajer DS (1998) Noninvasive detection of atheroscle- patients with hyperhomocysteinemia [25]. Exercise de- rosis. N Engl J Med 339:2014–2015 creases LDL cholesterol and all patients should maintain 9. Chobanian AV (1983) The influence of hypertension and a regular exercise regimen. Lastly, the use of anti-platelet other hemodynamic factors in atherogenesis. Cardiovasc drugs may reduce the risk of fatal and nonfatal ischaemic Dis 26:177–196 events in patients with vascular disease. Several drugs are 10. Choi CJ, Kramer CM (2002) MR imaging of atherosclerotic available and aspirin and clopidogrel are quite effective. plaque. Radiol Clin North Am 40:887–898 11. Davies MJ, Wollf N (1993) Atherosclerosis: what is it and why does it occur? Br Heart J 69 (Suppl):S3–S11 12. Davies MJ, Richardson PD, Woolf N, Katz DR, Mann J 1.2.8 Conclusion (1993) Risk of thrombosis in human atherosclerotic plaques: role of extracellular lipid, macrophage, and smooth muscle Knowledge about atherosclerosis has increased dramati- cell content. Br Heart J 69:377–381 cally over the last 20 years. Despite significant improve- 13. Davignon J, Mabile L (2002) Mécanismes d’action des ments in medical and surgical treatment, atherosclerosis statines et leurs effets pléiotropiques. Ann Endocrinol remains a serious disabling and sometimes life-threat- 62:101–112 ening disease. Perhaps in the future the development of 14. De Palma RG, Gallagher GL (1997) In: Sidawy AN, Sumpio gene therapy will provide a new mode of therapy able to BE (eds) The basic science of cardiovascular disease. Futura, modify not only the initiation but also the progression Armonk, N.Y., pp 151–186 of the plaque. Nevertheless, at the present time, general 15. Defawe O, Colige A, Lambert C, Munaut C, Delvenne P, therapeutic, preventive and adjunctive measures are the Nusgens B, Lapière C, Limet R, Sakalihasan N (2003) TIMP- only way to limit the progression and consequences of 2 and PAI-I mRNA levels are lower in aneurysmal as com- atherosclerosis. In addition, a screening programme is pared to atheroocclusive abdominal aortas. Cardiovasc Res also useful in order to detect the unstable plaques prone 60:205–213 to rupture and to complications. 16. Dollery CM, McEwan JR, Henney AM (1995) Matrix metalloproteinases and cardiovascular disease. Circ Res References 77:863–868 1. Bellosta S, Via D, Canavesi M (1998) HMG-CoA reductase 17. Esterbauer H, Rotheneder M, Striegl G, Waeg G, Ashy A, inhibitors reduce MMP-9 secretion by macrophages. Arter- Sattler W, Jurgens G (1989) Vitamin E and other lipophilic isocler Thromb Vasc Biol 18:1671–1678 antioxidants protect LDL against oxidation. Fat Sci Technol 2. Benditt EP, Benditt JM (1973) Evidence for a monoclonal 91:316–324 origin of human atherosclerotic plaque. Proc Natl Acad Sci 18. Esterbauer H, Dieber-Rotheneder M, Waeg G, Striegl G, Ju- USA 70:1753–1756 rgens G (1990) Biochemical structural and functional prop- 3. Berliner JA, Navab M, Fogelman AM, Frank JS, Demer LL, erties of oxidized low density lipoprotein. Chem Res Toxicol Edwards PA, Watson AD, Lusis AJ (1995) Atherosclerosis: 3:77–92 basic mechanisms: oxidation, inflammation and genetics. 19. Falk E (1992) Why do plaques rupture? Circulation 86 (Sup- Circulation 91:2488–2496 pl III):III30–III42
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  • 64. 35 1.3 Lipids and Peripheral Arterial Disease Stella S. Daskalopoulou, Marios E. Daskalopoulos, Christos D. Liapis, Dimitri P. Mikhailidis 1.3.1 Introduction 1.3.2 Effect of Lipid Lowering on PADPeripheral arterial disease (PAD) is associated with a high 1.3.2.1 Prevention of PADrisk of vascular events [1, 2, 14, 18, 19, 31, 32]. This istrue whether PAD is symptomatic or asymptomatic. This A post-hoc analysis of the Scandinavian Simvastatin Sur-risk is so high that PAD is considered as a coronary heart vival Study (4S) found that new or worsening intermit-disease (CHD) equivalent [5, 13]. It follows that these tent claudication was significantly (p = 0.008) reducedpatients need to have their modifiable vascular risk fac- (by 38%) in those taking the statin when compared withtors controlled. Dyslipidaemia, a modifiable vascular risk the group assigned to placebo [30]. All the patients (n =factor, should be treated aggressively with lipid-lowering 4444) participating in this trial had CHD and were fol-drugs, according to international guidelines [5, 13, 16, 37]. lowed-up for a median of 5.4 years.The earlier low density lipoprotein-cholesterol (LDL-C) In the Program on the Surgical Control of Hyperlipid-targets {European LDL-C target <96 mg/dl (2.5 mmol/l) emias (POSCH) [9] the effect of cholesterol-lowering in-[5] and National Cholesterol Education Program (NCEP) duced by partial ileal by-pass in patients (n = 838) with aAdult Treatment Panel (ATP) III [13] LDL-C target <100 previous MI and hyperlipidaemia was assessed. The inci-mg/dl (2.6 mmol/l)} have been revised recently. Thus, the dence of new cases of claudication was significantly lowerUK guidelines set the LDL-C goal to ≤2.0 mmol/l (77 [relative risk (RR): 0.66, 95% confidence interval (CI):mg/dl) for high-risk patients (March 2004) [37]. Further- 0.20–0.90; p = 0.009] in the intervention group whenmore, the revised NCEP ATP III guidelines proposed the compared with the control (nonintervention) group 4optional target of ≤70 mg/dl (1.8 mmol/l) for very high- years after the closure of the trial.risk patients (July 2004) [16]. Other lipid variables, such as high density lipoprotein-cholesterol and triglycerides, are also important and they 1.3.2.2 Improvement of Symptomshave recently attracted more attention [11]. However, the Associated with PADguidelines still focus on LDL-C levels as the main targetfor treatment [5, 13, 16, 37]. As mentioned above, new or worsening intermittent clau- In this review, we consider the evidence showing the dication was significantly (p = 0.008) reduced (by 38%) ineffect of lipid-lowering drugs on: the active treatment group of the 4S trial [30].• Prevention of PAD In another study [24] patients (n = 354) with intermit-• Improvement of symptoms associated with PAD tent claudication were assigned to placebo or active treat-• Reduction of the risk of vascular events [e.g. myocar- ment with atorvastatin 10 mg or 80 mg daily. Maximal dial infarction (MI), stoke or revascularization] asso- walking time after 12 months of treatment did not change ciated with PAD. significantly. However, there was a significant (p = 0.025) improvement in pain-free walking time in the 80 mg group compared with placebo. A physical activity ques- tionnaire showed improvement (p = 0.011) in ambulatory ability for the 10 and 80 mg groups, whereas two quality of life questionnaires did not show significant changes.
  • 65. 36 1.3 Lipids and Peripheral Arterial Disease Another study [21] included 392 patients with an ankle tional reduction in the rate of noncoronary revasculariza- brachial pressure index (ABPI) <0.90 and 249 with ABPI tion (4.4% versus 5.2%; p = 0.006). Half of that difference 0.90–1.50. After adjusting for age, sex, ABPI, co-mor- involved a definite reduction in carotid endarterectomy bidities, cholesterol and other confounders, those taking or angioplasty (0.4% versus 0.8%; p = 0.0003). statins had significantly better walk performance indices In the Mohler et al. study [24], mentioned above, there than participants not taking statins. Positive associations was a significant (p = 0.003) reduction in vascular events were slightly attenuated after additional adjustment for after 12 months. There were 3 events in the 240 patients C-reactive protein (CRP) level but remained statistically (1.3%) assigned to atorvastatin (10 and 80 mg/day) and 9 significant for walking velocity and the summary perfor- events in the 114 patients (7.9%) assigned to placebo. mance score. These findings suggest that both the choles- Statin use has also been shown to decrease the risk of terol-lowering and non-cholesterol-lowering actions of vascular events in diabetics with and without prior MI statins may favourably influence functioning in persons [2]. with and without PAD. In a comparison of 318 PAD patients treated with The effect of short-term therapy with simvastatin on statins versus 342 patients not on lipid-lowering drugs walking performance was assessed in hypercholesterolae- there were significant changes in the event rates after mic (>220 mg/dl; 5.7 mmol/l) patients (n = 86) with PAD a mean follow-up of 39 months [1]. Sudden coronary [25]. The patients were assigned either to simvastatin 40 death, fatal MI and new coronary events were all signifi- mg (n = 43) or to a placebo (n = 43). At 6 months, the cantly reduced (p = 0.0005, p = 0.007 and p < 0.0001, re- mean pain-free walking distance increased by 90 m (95% spectively). CI: 64–116; p < 0.005) more in the simvastatin group than In the LEADER trial [22], bezafibrate had no effect on in the placebo group. Similar results were seen for the the incidence of CHD and of stroke combined. However, mean total walking distance (increased by 126 m; 95% CI: the incidence of nonfatal coronary events was reduced 101–151; p < 0.001). The ABPI at rest increased by 0.09 (RR: 0.60, 95% CI: 0.36–0.99; p = 0.05), particularly in (95% CI: 0.06–0.12; p < 0.01) and after exercise by 0.19 those aged <65 years at entry, in whom all coronary events (95% CI: 0.14–0.24; p < 0.005) in those taking simvas- may also be reduced (RR: 0.38, 95% CI: 0.20–0.72). In tatin. There was also a greater improvement in claudica- this trial plasma fibrinogen levels fell by 13% (p < 0.0001) tion symptoms among patients treated with simvastatin. in the bezafibrate group. It is well established that elevat- In the Lower Extremity Arterial Disease Event Reduc- ed plasma levels of this coagulation factor contribute to tion (LEADER) trial [22], bezafibrate 400 mg daily (n = whole-blood viscosity and to an increased risk of vascular 783 men) or placebo (n = 785 men) were compared (me- events in patients with PAD. dian follow-up of 4.6 years). Bezafibrate reduced the se- verity of intermittent claudication for up to 3 years. The changes in symptoms may be related to the angio- 1.3.3 Peripheral Vascular Surgery and Statins graphic improvement documented in several studies. Graft patency and limb salvage were improved in patients 1.3.2.3 Reduction of the Risk of Vascular taking statins before infra-inguinal by-pass surgery [18]. Events Associated with PAD Aggressive lipid lowering may reduce the high mor- tality and morbidity (mainly from coronary events) as- The Heart Protection Study (HPS) [17] confirmed that sociated with vascular surgery in PAD and other patients statin treatment reduces the risk of death and adverse [14, 29]. Coronary events are the most important cause of cardiovascular events in patients with coronary and non- long-term morbidity and mortality after peripheral vas- coronary atherosclerosis, including patients with PAD cular surgery [12, 14]. Even PAD patients without overt but without diagnosed CHD (n = 2701). There was a sig- CHD are at significant risk of long-term cardiac events. nificant reduction (approximately 25%) in the first major The effect of atorvastatin compared with placebo on vascular event (major coronary event, stroke or revascu- the occurrence of a composite of cardiovascular events af- larization) among patients with PAD, with or without pri- ter vascular surgery was assessed [12]. Patients (n = 100) or CHD (both p < 0.0001). In HPS there was a significant were randomly assigned to atorvastatin 20 mg once daily 16% [standard error (SE) 6.0, 95% CI: 5.0–26.0)] propor- (n = 50) or placebo (n = 50) for 45 days, irrespective of
  • 66. 1.3.6 Concluding Comments 37their serum cholesterol concentration. Vascular surgery uric acid (p < 0.0001) in patients with PAD treated forwas performed on average 30 days after randomization. 3–4 months [38]. The difference in the creatinine levelsDuring the 6-month follow-up, the incidence of cardiac was more pronounced in the tertile of patients with theevents was higher in the placebo compared with the ator- highest baseline creatinine levels.vastatin group [13 (26.0%) versus 4 (8.0%); p = 0.031]. Statins can reduce circulating CRP levels [6, 20]. Oth- In a case-control study, among patients (n = 2816) er lipid-lowering drugs (e.g. ciprofibrate [33], fenofibratewho underwent major vascular surgery, 160 (5.7%) died [36] and ezetimibe [7, 34]) can also decrease circulatingduring their hospital stay [32]. After adjustments, statin CRP levels. However, the potential relevance of loweringtherapy was significantly less common in the patients CRP levels to a greater or lesser extent remains unclear.who died than in controls (8% versus 25%; p < 0.001). Furthermore, recent evidence suggests that circulatingThe adjusted OR for peri-operative mortality among CRP levels may only be a moderate predictor of CHDstatin users as compared with nonusers was 0.22 (95% CI risk.= 0.10–0.47). Patients with the metabolic syndrome have a clustering of many risk factors, such as hypertension, insulin resis- tance/type 2 diabetes mellitus, dyslipidaemia and obesity [11]. Therefore, it not surprising that these patients are at 1.3.4 Additional Potential Actions increased risk of developing PAD [15, 28]. The prevalence of Lipid-lowering Drugs that may of the metabolic syndrome in PAD patients in a cross- Benefit PAD Patients sectional survey [15] was 58%.Statins exert pleiotropic effects, which may be indepen-dent of LDL-C lowering. These effects may appear even 1.3.5 Are all Statins the Same?before a change in lipid level occurs [26, 35]. Statins increase nitric oxide (NO) production andimprove endothelial function (e.g. increased flow-me- Statins are of proven efficacy in secondary prevention indiated dilatation). They have antioxidant properties and high-risk groups such as PAD patients. However, we dothey inhibit the migration of macrophages and smooth not know if all statins are equally effective. This questionmuscle cell proliferation, leading to an antiproliferative can only be answered by “head to head” comparison trialseffect and the stabilization of atherosclerotic plaques. that incorporate clinical endpoints.Statins have anti-inflammatory effects including a reduc- Potential differences between statins can convenientlytion in the circulating levels of CRP, inflammatory and be considered in the context of:proinflammatory cytokines [e.g. interleukin-6 (IL-6), IL- • LDL-C lowering potency, and8], adhesion molecules [e.g. intercellular adhesion mol- • Pleiotropic actions.ecule-1 (ICAM-1), vascular cellular adhesion molecule-1(VCAM-1)] and other acute phase proteins. They reduce So far, “head to head” comparisons clearly show that sometissue factor expression and platelet activity, whereas fi- statins are considerably more potent, in terms of LDL-Cbrinolysis can be enhanced. Statins improve microalbu- lowering, than others [10, 27]. However, potency mustminuria, renal function, hypertension and arterial wall not be considered in the decision-making process at thestiffness. A significant reduction of the carotid and femo- expense of safety and event-based evidence. What is lessral intima-media thickness was also reported early after clear is whether statins differ in properties that may notstatin treatment. be exclusively due to variations in their LDL-C-lowering In the GREACE trial, the effect [3, 4] of atorvastatin capacity, the so-called pleiotropic actions [8].on serum creatinine and uric acid in patients with CHDwas rapid and it was reversed equally rapidly if patientshappened to discontinue atorvastatin. The fall in creati- 1.3.6 Concluding Commentsnine was greater in both those with higher baseline se-rum levels of this indicator of the glomerular filtrationrate and at the higher doses of atorvastatin. Simvastatin Trial-based evidence shows that lipid-lowering treat-can also significantly reduce serum creatinine and serum ment is beneficial in patients with PAD. However, these
  • 67. 38 1.3 Lipids and Peripheral Arterial Disease patients are often under-treated despite their high risk for 6. Balk EM, Lau J, Goudas LC, Jordan HS, Kupelnick B, Kim vascular events [19, 23]. It is also not widely appreciated LU, Karas RH (2003) Effects of statins on nonlipid serum that lipid lowering can improve PAD-related symptoms. markers associated with cardiovascular disease: a systematic The time has come for those looking after PAD patients to review. Ann Intern Med 139:670–682 use aggressive preventive treatment. 7. Ballantyne CM, Houri J, Notarbartolo A, Melani L, Lipka LJ, Although statins can improve both clinical outcomes Suresh R, Sun S, LeBeaut AP, Sager PT, Veltri EP; Ezetimibe and symptoms in PAD, it is possible that further benefit Study Group (2003) Effect of ezetimibe coadministered can be obtained if LDL-C levels are lowered beyond the with atorvastatin in 628 patients with primary hypercho- “older” targets for high-risk patients [from 96–100 mg/ lesterolemia: a prospective, randomized, double-blind trial. dl (2.5–2.6 mmol/l) to 70–77 mg/dl (1.8–2.0 mmol/l)]. Circulation 107:2409–2415 However, we do not know if these “new” LDL-C targets 8. Bonetti PO, Lerman LO, Napoli C, Lerman A (2003) Statin provide further symptomatic improvement or a more ef- effects beyond lipid lowering – are they clinically relevant? fective prevention of events in PAD. These issues need to Eur Heart J 24:225–248 be resolved by appropriately designed trials. 9. Buchwald H, Bourdages HR, Campos CT, Nguyen P, Wil- liams SE, Boen JR (1996) Impact of cholesterol reduction References on peripheral arterial disease in the program on the sur- 1. Aronow WS, Ahn C (2002) Frequency of new coronary gical control of the hyperlipidemias (POSCH). Surgery events in older persons with peripheral arterial disease and 120:672–679 serum low-density lipoprotein cholesterol ≥125 mg/dl treat- 10. Cannon CP, Braunwald E, McCabe CH, Rader DJ, Rou- ed with statins versus no lipid-lowering drug. Am J Cardiol leau JL, Belder R, Joyal SV, Hill KA, Pfeffer MA, Skene 90:789–791 AM; Pravastatin or Atorvastatin Evaluation and Infection 2. Aronow WS, Ahn C (2003) Elderly diabetics with peripheral Therapy-Thrombolysis in Myocardial Infarction 22 Inves- arterial disease and no coronary artery disease have a higher tigators (2004) Intensive versus moderate lipid lowering incidence of new coronary events than elderly nondiabetics with statins after acute coronary syndromes. N Engl J Med with peripheral arterial disease and prior myocardial infarc- 350:1495–1504 tion treated with statins and with no lipid-lowering drug. J 11. Daskalopoulou SS, Mikhailidis DP, Elisaf M (2004) Preven- Gerontol A Biol Sci Med Sci 58:573–575 tion and treatment of the metabolic syndrome. Angiology 3. Athyros VG, Mikhailidis DP, Papageorgiou AA, Symeonidis 55:589–612 AN, Pehlivanidis AN,Bouloukos VI, Elisaf M (2004a) The 12. Durazzo AE, Machado FS, Ikeoka DT, De Bernoche C, Mo- effect of statins versus untreated dyslipidaemia on renal nachini MC, Puech-Leao P, Caramelli B (2004) Reduction function in patients with coronary heart disease: a subgroup in cardiovascular events after vascular surgery with atorvas- analysis of the GREek Atorvastatin and Coronary-heart-dis- tatin: a randomized trial. J Vasc Surg 39:967–975 ease Evaluation (GREACE) Study. J Clin Pathol 57:728–734 13. Expert Panel on Detection, Evaluation, and Treatment of 4. Athyros VG, Elisaf M, Papageorgiou AA, Symeonidis AN, High Blood Cholesterol in Adults (2001) Executive Sum- Pehlivanidis AN, Bouloukos VI, Milionis HJ, Mikhailidis mary of The Third Report of The National Cholesterol DP; GREACE Study Collaborative Group (2004b) Effect Education Program (NCEP) Expert Panel on Detection, of statins versus untreated dyslipidemia on serum uric acid Evaluation, And Treatment of High Blood Cholesterol levels in patients with coronary heart disease: a subgroup In Adults (Adult Treatment Panel III). J Am Med Assoc analysis of the GREek Atorvastatin and Coronary-heart- 285:2486–2497 disease Evaluation (GREACE) study. Am J Kidney Dis 14. Farkouh ME, Rihal CS, Gersh BJ, Rooke TW, Hallett JW 43:589–599 Jr, O’Fallon WM, Ballard DJ (1994) Influence of coronary 5. De Backer G, Ambrosioni E, Borch-Johnsen K, Brotons C, heart disease on morbidity and mortality after lower ex- Cifkova R, Dallongeville J, Ebrahim S, Faergeman O, Gra- tremity revascularization surgery: a population-based study ham I, Mancia G, Manger Cats V, Orth-Gomer K, Perk J, in Olmsted County, Minnesota (1970-1987). J Am Coll Car- Pyorala K, Rodicio JL, Sans S, Sansoy V, Sechtem U, Silber diol 24:1290–1296 S, Thomsen T, Wood D: Third Joint Task Force of European and Other Societies on Cardiovascular Disease Prevention in Clinical Practice (2003) European guidelines on cardio- vascular disease prevention in clinical practice. Eur Heart J 24:1601–1610
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  • 70. 41 1.4 Clotting Disorders: What Should the Vascular Surgeon Know About Hypercoagulation States in Venous Diseases? Rosa M. Moreno these cases, thrombosis is the final consequence of several 1.4.1 Introduction factors making the precise definition of its physiopatho- logical basis extremely difficult.In daily clinical practice, the vascular surgeon frequentlyhas to evaluate and manage patients who present withvenous thrombosis. Identifying the cause of this disease 1.4.2.1 Risk Factorsalong with its risk factors has several interesting implica-tions, which are reviewed in this chapter concerned with Acquired risk factors and predisposing conditions for theabnormalities in the blood clotting mechanism that gen- development of DVT have been described by an ad hocerates hypercoagulation states. team on behalf of The Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter [42] (Table 1.4.1). The factors classi- cally defined are: a previous history of DVT, immobili- 1.4.2 Venous Thrombosis zation, the postoperative state, age, heart disease, trauma to the lower limbs, a concurrent malignancy, hormoneVenous thrombosis is a significant cause of morbidity and therapy, pregnancy, the postpartum period and obesity.mortality in western countries, and is estimated to affect Familial thrombophilia, a genetic risk factor, has beenbetween 1 and 3 persons per 1000 each year [36]. A hy- known since 1965 when Egeberg [10] identified an inher-percoagulation, or hypercoagulable, state is defined as an ited tendency for thrombosis caused by an antithrombinabnormal situation of the circulating blood, in which a III deficiency in a Norwegian family.smaller stimulus is required to induce the onset of throm- It was not until almost two decades later that proteinbosis compared to the normal coagulation state. It most C [16] and protein S [44] deficiencies were identified, andcommonly manifests as thromboembolic disease, deep anomalies such as factor V Leiden thrombophilia, muta-vein thrombosis (DVT), pulmonary thromboembolism tion of the prothrombin gene or dysfibrinogenemia have(PTE) or post thrombotic syndrome. However, venous been only recently described.thrombosis can affect any body site such as the retina,veins of the arm, or the mesenteric, hepatic or cerebralveins. Acquired or Environmental Risk Factors Venous thrombosis seems to be age-related, since ratesduring childhood according to some authors are as low as Previous History of DVT1 per 100,000 annually, while the incidence could reach A previous episode of DVT in the lower limb is the most1% per year in elderly subjects [38]. The thrombotic state significant risk factor for developing a subsequent DVTis produced by an upset in the normal balance of proco- episode. Specific phlebographic findings or the results ofagulant, anticoagulant and fibrinolytic factors. noninvasive tests are considered sufficient to confirm a An inherited tendency for thrombosis, irrespective of previous DVT episode. A patient with post thromboticthe causative factor, has been denoted primary or heredi- syndrome yet no history of DVT should be suspected oftary thrombophilia. Situations in which thrombosis is ac- having undergone a previous episode.quired are known as secondary hypercoagulable states. In
  • 71. 42 1.4 Clotting Disorders: What Should the Vascular Surgeon Know About Hypercoagulation States in Venous Diseases? Table 1.4.1 Risk factors for venous thrombosis Acquired Congenital Mixed Previous thrombosis Antithrombin III deficiency Hyperhomocysteinaemia Immobilization Protein C deficiency High factor VIII levels Postoperative period Protein S deficiency High factor IX levels Age Factor V Leiden High factor XI levels Heart disease Prothrombin gene mutation Acquired PC resistance Lower limb trauma Blood group Dysfibrinogenemia Malignant tumour Methylenetetrahydrofolate reductase Hormone treatment Dysfibrinogenemia Pregnancy/postpartum Obesity Antiphospholipid syndrome Immobilization factors appear to act as triggers for coagulation, although All situations affecting the action of the calf muscular these results have not yet been published. pump are associated with DVT. Several situations are related to immobilization, such as bed rest, in turn pro- duced by conditions such as acute myocardial infarction, The Postoperative State cardiac insufficiency, respiratory insufficiency, paralysis The duration of surgery and the type of anaesthesia are or trauma, or even prolonged periods of sitting when related to the postoperative onset of DVT. These risks are travelling long distances. particularly high in patients undergoing orthopaedic pro- The duration and cause of immobilization affect the cedures [6, 19] at the level of the pelvis, hip or legs, with risk of DVT [37]. Since 1954, when Homans [18] report- risks estimated at 30% to 50%. Further variables consid- ed the first case of DVT after a long commercial flight, ered risk factors are neurosurgery procedures, any intra- this subject has generated much interest among both the abdominal procedure, and gynaecological and urological medical and general population, with the so-called tourist surgery, especially radical prostatectomy [29]. class syndrome frequently appearing in the general press. Several publications reflect the interest in this topic [27, 43]. Some have reported findings such as sudden death Age being more common in airport arrivals than departure The risk of thrombosis increases with age. This may be lounges [43]. Attention has also been paid to the possible explained by a combination of factors such as reduced influence that the length of the flight might have. Hence, mobility, diminished muscle tone, increased morbidity the risk of DVT is 50 times higher in flights of distance and the deterioration of the venous system itself. The age longer than 10,000 km compared to flights covering a dis- effect is considerable and should always be considered tance of 5000 km [27]. Other studies, some controlled, before making any clinical decision. When this risk is find no conclusive data regarding the size of possible weighed up against the undesirable effects of treatment, risks, and attribute travel-related DVT to a multifactorial the cost of screening or the disadvantages of not prescrib- predisposition [11, 26]. In 2002, the World Health Or- ing treatment, the management option selected can vary ganization launched its WRIGHT study (WHO Research tremendously depending on the patient age group. into Global Hazards of Travel) to try to more precisely define these concepts. This investigation aims to establish the mechanisms through which thrombosis is induced and identify the roles of hypoxia and hypobaria. These
  • 72. 1.4.2 Venous Thrombosis 43Heart Disease recent studies have shown a 4% to 8% increased risk ofThe severity of a heart condition seems to increase the thrombosis among women using OC, yet comparisonsrisk of developing DVT and, according to the New York between OC containing 30 μg and 50 μg have not yieldedHeart Association (NYHA) functional class, a correlative conclusive results [14]. Progestagens are also thought torisk score is assigned [37, 42]. affect the risk of thrombosis. Third-generation progesta- gens (desogestrel and gestodene) have been related to a risk of thrombosis of up to two times that of preparationsTrauma to the Lower Limbs containing second-generation progestagens [22, 51].Major trauma is an important risk factor for thrombosis, Hormone replacement therapies (HRT) based ex-which occurs in 50% to 60% of patients with cranial, or clusively on oestrogens increase the risk of endometrialspinal cord trauma and fractures of the pelvis, femur or cancer, to the extent that there is a tendency to prescribetibia [13]. oestrogen and progesterone HRT except in hysterec- tomized women. There are reports indicating a two- to fourfold increased risk of DVT in women on HRT [9,A Concurrent Malignancy 15]; this should be taken into account when evaluatingDVT is more common in patients with a malignant tu- menopausal women. It should also be kept in mind thatmour, an observation made for the first time by Trous- a large number of epidemiological studies conclude thatseau [47] in 1865. DVT can be the first sign of cancer Asian women, because of their diet rich in soy, reach theand is taken as a warning sign for malignant disease. The menopause in better condition than Occidental womenthrombogenic effect of cancer arises from the produc- and have a lower incidence of undesirable effects. More-tion of humoral factors (procoagulants), mechanical fac- over, and despite the large number of published reportstors (vein compression or local infiltration) and general focusing on isoflavones (a Medline search of the term iso-factors indicated by the presence and increased levels of flavones yields over 7500 citations), there is no mentionacute phase reactants [5]. Indirectly, thrombosis may also in the literature of an increased risk of thrombosis linkedbe induced by reduced patient mobility and diminished to the uptake of these components of soy.uptake of vitamins such as folates. Finally, thrombosismay be promoted by the treatment received by the patientincluding radiotherapy and chemotherapy [31, 49], and Pregnancy and the Postpartum Periodmay also be triggered by postsurgery fibrosis. It has been estimated that 1 in 2000 women develop The prevalence of cancer in patients with DVT has thrombosis during pregnancy. This risk increases 10been estimated at 3% to 18% by different studies. In a times when compared with nonpregnant women of theSwedish population study [34], 19% of patients with same age [23, 30]. This risk also goes up in the postpar-DVT already had a diagnosis of cancer and 1 year later tum period. Pregnancy leads to increased levels of thethis proportion had increased by 5%. blood clotting factors I, VII, VIII, IX, X, XI and XII, an The type of tissue affected may also be related to the increased platelet count and reduced protein S and anti-development of DVT [37], adenocarcinoma (especially thrombin concentrations. Further, the fibrinolytic path-mucinous) and cerebral malignant glioma being associ- way may be blocked by the increased levels of activatedated with the greatest risk. plasminogen inhibitors 1 and 2, produced in the placenta. These factors, combined with the venous stasis produced by compression by the uterus of draining leg veins, canHormone Therapy increase the risk of thrombosis during the prepartum pe-Several publications [50] have reported that oral contra- riod by up to 20 times. Some 2 months after childbirth,ceptives (OC), including those containing mini hormone fibrinolytic and coagulation systems return to their nor-doses, are linked to an increased risk of thrombosis of mal state.about fourfold. Most OC contain an oestrogen and pro-gesterone. Over the years, the amount of oestrogen hasbeen steadily reduced until the present dose of 30 μg or Obesityeven less of ethinyloestradiol. However, there is still no Severe obesity can be an independent risk factor forconvincing evidence that this dose reduction has man- developing thrombosis, especially if 175% of the idealaged to decrease the risk of thrombosis. Both early and weight is surpassed [37].
  • 73. 44 1.4 Clotting Disorders: What Should the Vascular Surgeon Know About Hypercoagulation States in Venous Diseases? Genetic Risk Factors risk of thrombosis by 3- to 8-fold in heterozygous carriers and by 50- to 80-fold in homozygous carriers [24]. Antithrombin III Deficiency This condition is produced by point mutations in the antithrombin III (AT-III) gene and shows an autosomal Prothrombin Gene Mutation 20210A dominant transmission pattern. AT-III is an α2 globulin This anomaly described in 1996 is caused by a mutation that inhibits factors XIIa, XIa, IXa, Xa, IIa and plasmin. Its in nucleotide 20210 of the prothrombin gene (guanine re- prevalence is less than 1 in 1000 people [45]. The homo- placed by adenine). The heterozygous state occurs in 1% zygous state is incompatible with life. Heterozygotes show to 4% of the general population and in up to 6% to 10% 40% to 60% the normal functional activity of AT-III. of subjects with venous thrombosis. The risk of thrombo- An acquired AT-III deficiency may occur in cases sis increases 2–3 times with respect to the population at of its reduced production (in liver disorders or follow- large, and seems to be mediated by increased prothrom- ing the administration of OC), enhanced excretion (ne- bin levels [35]. It has even been suggested that prothrom- phrotic syndrome, protein-losing enteropathy), excessive bin gene and factor V Leiden mutations occur in 63% of consumption, or disseminated intravascular coagulation families with thrombophilia [3]. (DIC). Blood Group Protein C Deficiency Non-O blood groups are associated with a 2- to 4-fold Protein C is vitamin K dependent. It acts by inactivating increased risk of venous thrombosis [21]. factors Va and VIIIa and requires the presence of pro- tein S as a cofactor, activated by thrombin and thrombo- modulin. Protein C deficiency is a hereditary disorder of Methylenetetrahydrofolate Reductase 677T autosomal dominant transmission. The prevalence [39, A variation in the gene coding for methylenetetrahydro- 46] of an asymptomatic heterozygous deficiency is low at folate reductase (MTHFR), an enzyme involved in ho- 1/300–500, with 1/16,000–36,000 showing clinical signs. mocysteine metabolism, has been associated with slightly A homozygous protein C deficiency manifests as neona- elevated homocysteine levels in the blood [12], increasing tal purpura fulminans progressing with thrombosis in the the risk of thrombosis. microcirculation and DIC. Other Plasma Anomalies Related Protein S Deficiency to the Risk of Thrombosis Protein S is a vitamin-K-dependent glycoprotein that acts as a cofactor to protein C in the degradation of factors Va Hyperhomocysteinemia and VIIIa. Its pattern of transmission is autosomal domi- Homocysteine is an amino acid that metabolizes cysteine nant. Its prevalence is similar to those of protein C and (with vitamin B6 acting as cofactor) or methionine (with AT-III deficiencies. vitamin B12 as cofactor). Its blood levels can rise as the re- sult of either a congenital deficiency in one of the enzymes involved in these processes or a nutritional deficiency of Resistance to Activated Protein C folate, vitamin B6 or vitamin B12. High blood homocyste- This anomaly is the consequence of the substitution of ine levels induce endothelial damage and are associated the amino acid arginine 506 by glutamine in the factor with an increase in tissue factor, and the enhanced ac- V molecule. This mutated factor V, designated factor V tivity of factors V and XII, and protein C. Homocysteine Leiden, is resistant to the catalytic action of activated pro- levels above 18 μmol/l are linked to an increased risk of tein C. This disorder, first described in 1993 by Dahlbäck thrombosis [32]. [8], has an autosomal dominant pattern of transmission Patients with hyperhomocysteinemia have a 3.5 times and is the most common deficiency in the general Cau- higher risk of presenting with thrombosis. This risk in- casian population linked to thrombosis. Its prevalence [4, creases by over 20-fold if the patient also has factor V 41] is high at 5% to 15%, yet it is relatively uncommon in Leiden. Treatment with folate and vitamins B6 and B12 populations of other races. Factor V Leiden increases the reduces homocysteine concentrations.
  • 74. 1.4.3 What Should a Surgeon do when Faced with Hypercoagulation? 45Antiphospholipid Antibodies 1.4.3 What Should a Surgeon do whenAntiphospholipid syndrome (APS) is a commonly ac- Faced with Hypercoagulation?quired cause of hypercoagulation. It appears in 1% to15% of the population, this rate increasing with age (to50% in patients over the age of 80 years) [28]. APS af- When confronted with an episode of DVT, several un-fects patients with lupus anticoagulant or anticardiolipin certainties immediately come to mind. First, should weantibodies. These antibodies react with endothelial cells, search for evidence of thrombophilia? How should this beplatelets and phospholipids. Recurrent venous thrombo- done and when? Also important to the vascular surgeonsis is one of its clinical manifestations [20]. Thrombotic is the question of whether to consider special therapeuticcomplications, estimated to be as high as 50%, have also options in patients who are carriers of thrombophilia.been reported after vascular reconstruction procedures[1]. A further common manifestation of APS is miscar-riage. Its diagnosis should include the identification of 1.4.3.1 Should a Search for Thrombophilialupus anticoagulant and anticardiolipin antibodies. be Undertaken? Treatment consists of eliminating risks such as avoid-ing pregnancy and taking OC. If venous thrombosis has All acquired risk factors can be controlled to a certainalready been provoked, heparin or urokinase should be extent whether at the level of prophylaxis or treatment.immediately given followed by oral anticoagulation with The major worry is evaluating a genetic hypercoagulablewarfarin adjusted to maintain the international normal- state because its presence can be well demonstrated butized ratio (INR) between 2 and 3. Patients with a history its treatment not yet well defined.of DVT or miscarriage who are pregnant should be treat- There are several arguments in favour of embarkinged with heparin throughout pregnancy and switched to on a search for thrombophilia. Its discovery could ben-oral anticoagulation after giving birth. efit relatives. Prophylaxis may be started in situations of added risk. It is well known that both pregnancy and OC are associated with factor V Leiden or a mutation in pro-High Coagulation Factor Levels thrombin gene 20210A, increasing the risk of thrombosisAugmented levels of prothrombin (factor II), factor VIII, by 4–8 times. A similar situation arises owing to the linkfactor IX, or factor XI have been linked to a high risk of with HRT or treatment with tamoxifen. In contrast, if, inthrombosis [25]. Although little is known about the aeti- an elderly patient presenting an idiopathic venous throm-ology of these abnormalities, they have been described as bosis, thrombophilia is discovered, this will avoid worrya combination of congenital and acquired alterations. and an exhaustive, sometimes unforthcoming, search for neoplastic disease.Defects in the Fibrinolytic SystemA drop in fibrinolytic activity and a predisposition to 1.4.3.2 How Should the Search be Done?thrombosis may be secondary to diminished plasmino-gen levels, to reduced activity of plasminogen activator or As mentioned previously, the most recently discoveredto the increased action of the plasminogen inhibitor. deficiencies (factor V Leiden and prothrombin gene mu- Reduced fibrinolytic activity occurs in acquired dis- tation 20210A) are highly prevalent, thus generating anease states (myocardial infarction, generalized arterio- increased number of patients whose venous thrombosissclerosis, diabetes, scleroderma, thrombocytopenic pur- could be attributed to an inherited thrombophilia. Thepura, ulcerative colitis, Crohn’s disease) [7]. first step of diagnosis will involve drawing up a careful Congenital plasminogen deficiency is transmitted in clinical record, a meticulous physical examination and aan autosomal dominant manner. Thrombotic events usu- basic laboratory routine check to characterize the severityally occur when plasminogen levels fall below 40% of of the thrombotic process, and determine the presencethose related to normal biological activity [17]. This dis- of any of the causes of hypercoagulability. Obviously, anorder is extremely rare with reports of only a few isolated objective test for the diagnosis of venous thrombosis willcases [33]. also have to be conducted. The second step will be to screen for the causes of hereditary thrombophilia, which if identified will mean
  • 75. 46 1.4 Clotting Disorders: What Should the Vascular Surgeon Know About Hypercoagulation States in Venous Diseases? adopting a specific management plan. Screening should a first episode [38]. The current consensus is that there be performed, especially if DVT appears before the age is no need to prolong treatment in the presence of these of 50 years in cases of DVT recurrence and if there is a anomalies. However, the risk of recurrence is probably family history of DVT. If one or more of these conditions high in the heterozygous population simultaneously hav- are met, a complete evaluation will be needed to rule out ing both anomalies. thrombophilia. It is also important to keep in mind that interaction between an acquired and a congenital risk factor can sub- stantially increase the risk threshold. A clear example is 1.4.3.3 Diagnosing Thrombotic Disease the increased relative risk produced when the use of OC in Patients with Thrombophilia is added to the presence of factor V Leiden [48] (RR in- creases from 6 to 35), or if HRT is added to this factor (RR All patients presenting juvenile, idiopathic, recurrent increases from 4 to 15) [40]. thrombosis with a family history of thrombosis should When these anomalies are detected in asymptomatic be assessed for possible deficiencies. Once a suspicion of carriers (relatives of the patient), in the presence of ad- thrombophilia has been established, the following factors ditional risk factors, these subjects might benefit from a may be determined during the episode of thrombosis: an- selective prophylaxis regimen. These subjects could be ticardiolipin antibodies, homocysteine, factor V Leiden rejected by insurance companies. and prothrombin gene mutation. Other factors may be Indefinite anticoagulation is only considered appro- consumed during the coagulation process or be reduced priate for patients categorized as high risk, meaning two by anticoagulant therapy, or because of hepatic insuffi- or more events; a spontaneous (without another DVT ciency or sepsis. For this reason, the clinician should wait risk factor) severe event; or a patient with a spontane- until the end of the 6-month treatment period and then ous event and documented antiphospholipid antibodies. leave a further treatment-free interval (proposed by some When patients are categorized as having moderate risk, as ideally 2 months), before determining the presence of i.e. in the absence of symptoms or if the stimulus for a the remaining possible deficiencies (protein C, protein S, thrombotic event has been identified, prophylaxis would antithrombin III). only be given in a risk situation. 1.4.3.4 Treating Thromboembolic Disease 1.4.3.5 Specific Considerations in Treating in Patients with Thrombophilia Thromboembolic Disease Related to Thrombophilia The treatment regime for a patient with DVT and pul- monary thromboembolism is usually heparin initially Antithrombin III Deficiency and oral anticoagulant for 3–6 months, adjusted to keep the INR between 2 and 3. According to several random- The treatment of this deficiency consists of infusions of ized trials, after a first episode, the incidence of recurrent fresh plasma or preferably antithrombin concentrate. venous thromboembolism is between 5% and 15% in Long-term treatment involves oral anticoagulation pro- the first year and from 20% to 30% at 4 years [2]. At the vided there have been past thrombotic episodes. Heparin same time, it should be taken into account that the risk is given during pregnancy or in other risk situations (e.g. of haemorrhage is estimated at 2% to 3% per year. This surgery, trauma, sepsis). yearly risk in young patients, with no added risks for the haemorrhage, is unimportant but may give rise to a series of contraindications for treatment in patients with mul- Protein C Deficiency tiple associated diseases and an advanced age. In general there is scarce information on thrombotic Intravenous infusion of fresh plasma can restore func- recurrence in nonselected patients. Most studies have tional levels of protein C. Heparin prophylaxis (during been based on select populations with generally very pregnancy) or treatment should be given in risk situa- high recurrence rates. For the most prevalent abnormali- tions such as after surgery, trauma or sepsis. Lifetime oral ties, factor V Leiden and prothrombin mutation 20210A, anticoagulation is required for recurrent or life-threaten- the available data fail to indicate a higher recurrence after ing thrombosis.
  • 76. References 47Protein S Deficiency 2. Anderson FA, Wheeler HB, Goldberg RJ et al (1991) A population based perspective of the hospital incidence andThe management of this deficiency is the same as for pro- case-fatality rates of deep vein thrombosis and pulmonarytein C deficiency. embolism. The Worcester DVT study. Arch Intern Med 151:933–938 3. Bertina RM (1997) Factor V Leiden and other coagula-Activated Protein C Resistance tion factor mutations affecting thrombotic risk. Clin Chem 43:1678–1683Heparin prophylaxis is given in high-risk situations for 4. Bertina RM, Koeleman RPC, Koster T et al (1994) Mutationthrombosis. Lifetime anticoagulation therapy is required in blood coagulation factor V associated with resistance tofor recurrent or life-threatening thrombosis. activated protein C. Nature 369 (117):750–753 5. Bick RL (1992) Coagulation abnormalities in malignancy: a review. Semin Thromb Hemost 18:353–369Prothrombin Gene Mutation 6. Cohen SH, Ehrlich GE, Kaufman MS, Cope C (1973) Throm- bophlebitis following knee surgery. J Bone Surg 55:106–111The treatment for this condition remains to be clearly 7. Colleen D, Juhan-Vaghe I (1988) Fibrinolysis and athero-defined. Long-term oral anticoagulation therapy is also sclerosis. Semin Thromb Hemost 14:180–183recommended in patients with recurrent thrombosis. 8. Dahlbäck B, Carlsson M, Svensson PJ (1993) Familial thrombophilia due to a previously unrecognized mecha- nism characterized by poor anticoagulant response to acti- vated protein C. Proc Natl Acad Sci USA 90:1004–1008 1.4.4 Summary 9. Daly E, Vessey MP, Hawkins MM, Carson JL, Gough P, Marsh S (1996) Risk of venous thromboembolism in users• The occurrence of venous thrombosis is the result of of hormone replacement therapy. Lancet 348:977–980 interaction between both genetic and acquired fac- 10. Egeberg O (1965) Inherited antithrombin deficiency caus- tors. ing thrombophilia. Thromb Diath Hemorrh 13:516–530• Screening should be based on characterizing patients 11. Ferrari E, Cevallier T, Chapelier A, Baudouy M (1999) Trav- according to their clinical history. el as a study. Chest 115:440–444• Tests should be undertaken 2 months after the end of 12. Frosst P, Bloom HJ, Milos R et al (1995) A candidate genetic anticoagulation therapy. risk factor for vascular disease a common mutation in meth-• Asymptomatic carriers do not require treatment yet ylenetetrahydrofolate reductase. Nat Genet 10:111–113 should undergo prophylaxis in situations of risk. 13. Geerts WH, Code KI, Jay RM, Chen E, Szalai JP (1944) A• Treatment of a first episode of DVT with proven prospective study of venous thromboembolism after major thrombophilia is the same as for the general popula- trauma. N Engl J Med 331:1601–1606 tion. 14. Gertsman BB, Piper JM, Tomita DK, Ferguson WJ, Stadel• There is a need for greater insight into all possible risk BV, Laundin FE (1991) Oral contraceptive estrogen dose factors and in particular the interactions produced and the risk of deep venous thromboembolic disease. Am J among several risk factors, since this will synergisti- Epidemiol 133:32–37 cally potentiate the risks involved. 15. Grady D, Furberg C (1997) Venous thromboembolic events• Future data will enable the physician to gauge this risk associated with hormone replacement therapy. J Am Med in each individual patient and design the tools needed Assoc 278:477 to prevent the thromboembolic state. 16. Griffin JH, Evatt B, Zimmerman TS, Kleiss AJ, Wideman C (1981) Deficiency of protein C in congenital thromboticReferences disease. J Clin Invest 68:1370–13731. Ahn SS, Kalunian K, Rosove M, Moore WS (1988) Postop- 17. Hasegawa DH, Tyler BJ, Edson JR (1982) Thrombotic dis- erative thrombotic complications in patients with the lupus ease in three families with inherited plasminogen deficien- anticoagulant: increased risk after vascular procedures. J cy. Blood 60:213–217 Vasc Surg 7:745–756 18. Homans J (1954) Thrombosis of the leg veins due to pro- longed sitting. N Engl J Med 250:148–149
  • 77. 48 1.4 Clotting Disorders: What Should the Vascular Surgeon Know About Hypercoagulation States in Venous Diseases? 19. Hull RD, Raskob GE (1986) Prophylaxis of venous throm- 35. Poort SR, Rosendaal FR, Reitsma PH, Bertina RM (1996) boembolic disease following hip and knee surgery. J Bone A common genetic variation in the 3’-untranslated region Surg 68:146–150 of the prothrombin gene is associated with elevated plasma 20. Insko EK, Haskal ZJ (1997) Antiphospholipid syndrome: prothrombin levels and an increase in venous thrombosis. patterns of life-threatening and severe recurrent vascular Blood 88:3698–3703 complications. Radiology 202:319–326 36. Porter JM, Moneta GL (1995) Classification and grading of 21. Jick H. Slone D, Westernholm B et al (1969) Venous throm- chronic venous disease. A consensus statement. J Vasc Surg boembolic disease and ABO blood type. Lancet i:539–542 21:635–645 22. Kemmeren JM, Algra A, Grobee DE (1995) Third genera- 37. Porter JM, Moneta JL (1995) Reporting standards in venous tion oral contraceptives with differing progression compo- disease: an update. J Vasc Surg 21:635–645 nents. Lancet 346:1589–1593 38. Rosendal FR (1997) Thrombosis in the young: epidemiol- 23. Kierkegaard A (1983) Incidence and diagnosis of deep vein ogy and risk factors, a focus in venous thrombosis. Thromb thrombosis associated with pregnancy. Acta Obstet Gynecol Hemost 78:1–6 Scand 62:239–243 39. Rosendaal FR, Koster T Vandenbroucke JP, Reitsma PH 24. Koster T, Rosendaal FR, De Ronde H, Briët E, Vandenb- (1995) High risk of thrombosis in patients homozygous roucke JP, Bertina RM (1993) Venous thrombosis due to a for factor V Leiden (activated protein C resistance). Blood poor anticoagulant response to activated protein C: Leiden 85:1504–1508 Thrombophilia Study. Lancet. 342:1503–1506 40. Rosendal FR, Vessey M, Rumley A et al (2002) Hormonal 25. Koster T, Blann AD, Riét E, Vandenbroucke JP, Rosendaal replacement therapy, prothrombotic mutations and the risk FR (1995) Role of clotting factor VIII in effect of von Wil- of venous thrombosis. Br J Haematol 116:851–854 lebrand factor on occurrence of deep-vein thrombosis. Lan- 41. Rees DC, Cox M, Clegg JB (1995) World distribution of fac- cet 345:152–155 tor V Leiden. Lancet 346:1133–1134 26. Kraaijenhaghen RA, HaverKamp D, Koopman MM, Pran- 42. Rutherford RB, Clagett GP, Cranley JJ, O’Donell TF, Raju S, doni P, Piovella F, Büller HR (2000) Travel and risk of ve- Zierler RE, Browse N, Nicolaides A (1988) Reporting stan- nous thrombosis. Lancet 356:1492–1493 dards in venous disease. J Vasc Surg 8:172–181 27. Lapostolle F, Surget V, Borron SW et al (2001) Severe pul- 43. Savesvaan R (1986) Sudden natural deaths associated with monary embolism associated with air travel. N Engl Med commercial air travel. Med Sci Law 26:35–38 345:779–783 44. Schwarz HP, Fischer M, Hopmeier P, Batard MA, Griffin JH 28. Manoussakis MN, Tzioufas AG, Silis MP, Pange PJ, Goude- (1984) Plasma protein S deficiency in familial thrombotic venos J, Moutsopoulos HM (1987) High prevalence of an- disease. Blood 64:1297–1300 ticardiolipin and other autoantibodies in a healthy elderly 45. Tait RC, Walker ID, Perry DJ et al (1994) Prevalence of anti- population. Clin Exp Inmunol 69:557–565 thrombin deficiency in the healthy population. Br J Haema- 29. Mayo M, Halil T, Browse NL (1971) The incidence of deep tol 87:106–112 vein thrombosis after prostatectomy. Br J Urol 43:738–742 46. Tait RC, Walker ID, Reitsma PH et al (1995) Prevalence 30. McColl MD, Ramsay JE, Tait RC et al (1997) Risk factors for of protein C deficiency in the healthy population. Thromb pregnancy associated venous thrombosis. Thromb Hemost Haemost 73:87–93 78:1183–1188 47. Trousseau A, Phegmasia Alba Dolens (1865) Clinique 31. Meier CR, Jic H (1998) Tamoxifen and risk of idiopathic ve- Médicale de l‘Hötel-Dieu de Paris. Vol. 3.Ballière, Paris, pp nous thromboembolism. Br J Clin Pharmacol 45:608–612 652–695 32. Mudd SH, Skovby F, Levy HL et al (1985) The natural histo- 48. Vandenbroucke JP, Koster T, Briët E, Reitsma PH, Bertina ry of homocystinuria due to cystathionine beta-synthetase RM, Rosendaal FR (1994) Increased risk of venous throm- deficiency. Am J Hum Genet 37:1–31 bosis in oral contraceptives users who are carriers of factor 33. Nilsson IM, Tengborn LA (1984) A family with thrombosis V Leiden mutation. Lancet 344:1453–1457 associated with high level of tissue plasminogen activator 49. Weijl NL, Rutten MF, Zwinderman AH et al (2000) Throm- inhibitor. Haemostasis 14:24–27 boembolic events during chemotherapy for germ cell can- 34. Nordstrom M, Lindblad B, Anderson H, Bergqv D, Kjellströ cer: a cohort study and review of the literature. J Clin Oncol T (1994) Deep venous thrombosis and occult malignancy: 18:2169–2178 an epidemiological study. BMJ 308:891–894
  • 78. References 4950. World Health Organization (1995) Venous thromboembol- 51. World Health Organization (1995) Effect of different pro- ic disease and combined oral contraceptives: results of inter- gestagens in low estrogen oral contraceptives on venous national multicentre case control study. World Health Orga- thromboembolic disease. World Health Organization Col- nization Collaborative Study of Cardiovascular Disease and laborative Study of Cardiovascular and Steroid Hormone Steroid Hormone Contraception. Lancet 346:1575–1582 Contraception. Lancet 346:1582–1588
  • 79. 51 1.5 Noninvasive Diagnosis of Vascular Diseases P. Berg, H. Farghadani, V. Lens, R. Metz, F. Mataigne, S. Schmitz • Platelet count: changes may precipitate or aggravate 1.5.1 Peripheral Arterial Disease the symptoms of PAD. Associated haematological dis- ease may influence treatment.1.5.1.1 Introduction • Blood glucose or haemoglobin HbA1c, urea, cre- atinine: diabetes and chronic renal insufficiency areNoninvasive vascular laboratory findings remain impor- important risk factors in PAD, for interpretations oftant in the diagnosis of peripheral arterial disease (PAD). results and for further treatment.In many circumstances they are as accurate as invasive • Lipid profile: elevated low-density lipoprotein (LDL),imaging and have the advantage of being quick and in- triglycerides and low high-density lipoprotein (HDL)expensive. The two basic modalities of evaluation are the represent major risk factors for PAD and have to beindirect methods (ankle brachial pressure index, Doppler treated. Lipid modification can be associated with sta-wave forms, treadmill exercise) that provide location and bilization or regression of femoral atherosclerosis.functional severity of disease, and the direct method of • Hypercoagulability screen and homocysteine levelsevaluation, colour duplex imaging (CDI), which provides should be performed selectively in patients with amore specific anatomical and physiological information. family history or atypical events.1.5.1.2 Physical Examination 1.5.1.4 Special Investigations, Other Than ImagingIn the majority of patients, diagnosis can usually be made Pressure and Volume Measurementson the basis of the history. Chronic arterial insufficien-cy of the lower extremity causes two very characteristic Ankle Brachial Pressure Index (ABPI)types of pain: intermittent claudication and ischaemic rest • The ABPI serves as a baseline for comparing the pa-pain. Information may be obtained in the case of sudden tient with him or herself at different times.worsening of limb perfusion in acute limb ischaemia. • Widely standard in the evaluation of patients with Physical examination should include: PAD.• Palpable pulses. • It is calculated for each extremity by dividing the high-• Audible bruits. est ankle pressure by the highest arm pressure.• Changes in colour and temperature.• Presence of ulcers or gangrene. The ABPI provides important basic information; the fol- lowing indices are consistent with the following clinical diagnoses:1.5.1.3 Basic Haematological and Biochemical Tests • 1.0–1.2: normal. • 0.5–0.9: claudication.The following blood tests are most frequently used and • <0.5: markedly decreased (often to less than 0.30).are those that should be performed for all new patients Seen in patients with rest pain, ischaemic ulcer or gan-presenting with PAD: grene [11, 29, 33].• Complete blood count (haemoglobin, haematocrit, • >1.3: abnormally high. Secondary to noncompressible white cell count). vessels due to medial calcification.
  • 80. 52 1.5 Noninvasive Diagnosis of Vascular Diseases • For calcified arteries, the use of digital pressures or • The pulse volume recording is obtained by a plethys- flow velocity recording in the pedal arteries is needed mograph connected to these devices placed at selected to supplement pressure recordings. locations of the limb [26]. • Specificity of this index is 100% for all reports. • In addition a brachial cuff reflects the undampened • Sensitivity is 92–94% [39]. cardiac contribution to arterial pulsatility. • Comparing each PVR reveals an eventual significant occlusive lesion. Segmental Limb Systolic Pressure Measurements (SLP) • The accuracy of each SLP and PVR alone is reported • Routinely used because of accurate haemodynami- to be 85%. cally significant detection of occlusive lesions between • These two measurements used together have an accu- the heart and the measuring point. racy of over 95%. • The cuffs are placed in standard locations: high-thigh, • This combination could help to recognize diabetic pa- low-thigh, below the knee, ankle and metatarsal. tients. • Direct measurement is obtained by placing a Doppler probe over the artery just below the inflated cuff, or the probe can be placed over one of the pedal arteries Doppler Velocity Waveform (VWF) giving a pressure gradient between the different cuffs. • Arterial VWF is recorded by a continuous-wave Dop- • A gradient greater than 20 mmHg suggests occlusive pler over the femoral, popliteal, posterior tibial and disease between the two cuffs. dorsalis pedis arteries. • Qualitative differences of the VWF between two adja- cent recording points identify the presence of an oc- Digital Pressure Measurement and Toe Brachial Index clusive lesion in the intervening arterial segment. • Digital pressures are useful in arterial occlusive dis- • In normal individuals the VWF is triphasic, with re- ease within the foot or hand and in instances of falsely verse flow seen. elevated ankle pressures secondary to medial calcifica- • When atherosclerotic changes are present in the ar- tion. teries, turbulence may be seen at the high-frequency • Using a small cuff (2.0 or 2.5 cm) and a photo elec- peak or on the descending phase of the forward flow. trode placed on the finger or toe as the pulse sensor, • Dampened reverse flow suggests the presence of ste- the digital pressure is obtained in the same way as for nosis and with severe stenosis or occlusion the reverse the ankle pressure. flow is absent. In addition, the systolic acceleration of • The normal toe brachial index is 0.8–0.9. the forward flow becomes flattened. • An index of 0.35 ± 0.15 is consistent with claudica- • In severe ischaemia the waveform becomes continu- tion. ous and nonpulsatile. • An index of 0.11 ± 0.10 is consistent with ischaemic • In a patent but dilated artery, the flow waveform shows rest pain [27]. a widening of the systolic forward flow. • For absolute pressure, it is generally considered that a • Visual inspection of these waveforms recorded over toe pressure less than 30 mmHg is indicative of severe the different arteries described can detect and localize ischaemia. arterial occlusive disease in most cases. • There is no difference between the mean values for • These tests are painless, inexpensive, quick and accu- diabetic and nondiabetic patients. rate enough. VWF is more accurate than SLP alone. It has been reported [20] that VWF was 97% accurate (75% for SLP alone) in detecting superficial femoral Segmental Plethysmography artery lesions with over 50% luminal narrowing and or Pulse Volume Recording (PVR) 91% accurate (54% for SLP alone) in detecting similar • Any instrument measuring the change in volume of lesions in the popliteal artery. the limb during each cardiac cycle by a plethysmo- graphic sensor may be used; for example, sphygmo- manometer, mercury-in-silastic tube strain gauge or impedance captors.
  • 81. 1.5.1 Peripheral Arterial Disease 53Functional Testing by other noninvasive tests. It provides a measure of the adequacy of the arterial oxygen supply to the tissues.Treadmill Exercise (TE) • An oxygen-sensing electrode is placed on the skin,• At rest, variation of flow in the lower limb requires an which contains a small heating unit that warms the 80% stenosis, which is due to low flow and high resis- skin to a temperature of 44°C, conducive to efficient tance of its circulation. oxygen diffusion.• Despite that, during exercise, a 20% stenosis is enough • The quantity of oxygen available for diffusion to the for significant haemodynamic changes because of high skin is a function of the arterial flow to the area and flow and low resistance of the circulation. the amount of oxygen extracted from the blood to• For practical reasons only brachial and ankle cuffs are meet the metabolic requirements of the tissues. routinely used. • When arterial occlusive disease is severe, the tissue• The standard usually used is walking at 3.5 km/h on a perfusion becomes marginal and capillary oxygen 12% incline for 5 min. The ABPI is measured before perfusion decreases as the proportion of oxygen ex- exercise, at 1 or 2 min, at 5 min and then every minute traction must increase to meet the metabolic demands until back to initial values. of the tissue.• Thus, the onset of claudication, the maximum walking • TcpO2 is usually measured at the dorsum of the foot, distance, the percentage decrease in pressure and its medial aspect of the calf, and the thigh, with a refer- absolute value during the post-exercise period (10–15 ence electrode placed in the infraclavicular region. min) and recovery time are obtained. • Comparing the values obtained at the lower extremity• In patients with multiple occlusions, the ankle pres- and the chest yields an index that can be compared to sure is often decreased to zero, with longer recovery the normal value with regard to the patient’s age, car- time than patients with a single occlusion. diac output and arterial oxygen tension. • The measurement should be done in a supine and in a sitting position; the difference between both valuesInducing Limb Hyperaemia (ILH) provides information about the microcirculatory re-• For the ILH, the pressure cuff is placed on the lower serve supply. thigh and inflated to a level of 50 mmHg above the • The results are expressed in mmHg. systolic pressure for 3–5 min. • There are important variations, essentially in older pa-• Reactive hyperaemia occurs after the pressure cuff is tients and in concomitant cardiopulmonary disease. abruptly deflated. • In general, a TcpO2 <30 mmHg suggests ischaemia• Ankle systolic pressure (AP) is then recorded at 1-min and nonhealing. As there is an admitted error range intervals until it returns to the resting level. of ±10 mmHg, it is admitted that if TcpO2 <20 mmHg,• The decrease in AP 30 s after cuff deflation is equiva- healing will not occur and if TcpO2 >40 mmHg heal- lent to that observed 1 min after walking to the point ing will be probable. of claudication on a treadmill [10, 14, 38]. • There is a high positive predictive value (77–87%) [6,• It is reported elsewhere [23] that ABPI and the tread- 34–37]. mill test are widely superior to this test; nevertheless, ILH can be proposed if the treadmill is not possible.• Unfortunately, many patients do not tolerate the dis- Laser Doppler Fluxmetry (LDF), Capillary Microscopy (CM) comfort associated with this degree and duration of • CM enables visualization of the nailfold capillaries of cuff inflation. the big toe in the sitting position and provides infor- mation about capillary morphology, density and ve- locity.Microcirculatory Investigations • LDF measurements on the pulp of the big toe give in- formation about total skin perfusion, including capil-Transcutaneous Oxygen Measurements (TcpO₂) laries, deeper vessels and arteriovenous anastomoses,• TcpO2 provides valuable metabolic data which may be which are mainly involved in thermoregulation. used to supplement the haemodynamic data provided
  • 82. 54 1.5 Noninvasive Diagnosis of Vascular Diseases • The reactive hyperaemia response after a 3-min arte- • Enhancement of vascular structure requires high con- rial occlusion can be measured to assess the reserve trast flow rates of 3–5 ml/s of 300–350 mg/ml iodic capacity of skin blood supply. contrast with a total amount of 120–150 ml. • In a Dutch multicentre study, clinical and Doppler • Irradiation is inevitable and particular precautions systolic pressure parameters were found to be inad- have to be taken to reduce the irradiation dose as equate for predicting imminent amputation, because much as possible. all patients met these criteria but only 44% of them underwent amputation. Aorta • Applications for evaluation of the aorta with CTA are: Conclusion dissection, aneurysm, traumatic injury, atherosclerot- The combination of all three techniques – TcpO2, LDF ic pathology and other inflammatory and congenital and CM – showed the highest specificity (87%), but a diseases. rather low sensitivity (46%). The conclusion is that TcpO2 • Abdominal aneurysm disease, including diagnosis measures provide microcirculatory classification and are and post-operative follow-up, is well explored by CTA, the easiest measurement to perform [36]. providing information about the extent of the aneu- rysm formation and other extraluminal pathology. • Thoraco-abdominal aortic exploration can be achieved 1.5.1.5 Imaging Techniques with CTA with the new multirow scanner in a single exploration of 20 s. Duplex Scanning • Due to its fast access, high availability and short ex- amination time, CTA is the preferred method for diag- • Colour duplex imaging incorporates real-time B-mode nosis of aortic dissection and traumatic aortic injury. imaging, and pulsed and colour Doppler. CTA gives direct visualization of the aortic trauma- • Duplex scanning can provide most of the essential an- tism. atomical information plus some functional informa- tion; for instance, velocity gradients across stenoses. • The arterial tree of the lower extremities can be visual- Renal Arteries ized, with the extent and degree of occlusive lesions • CTA is routinely used for the evaluation of renal artery accurately assessed and arterial velocities measured. stenosis, and evaluation of renal transplant donors. • It can characterize specific lesions in regard to their • Excellent information regarding renal lesions and re- suitability for endovascular treatment. Arterial recon- nal arteries can be provided with appropriate explora- structive surgery can be performed on the basis of du- tion (section thickness of 0.625–1.25 mm). plex scanning alone in some cases. • Real-time B-mode imaging is the best mode for de- termining the anatomical detail of a vessel (e.g. plaque Lower Limb CTA characterization, intimal flap, mural thrombus, diam- • New MDCT allows study of the arterial system of the eter measurements). lower extremity with only one examination. Multiple Detector Computer Tomography (MDCT) Studies Comparing MDCT and CT Angiography • Recent advances in CT scanner technology, mainly • Particular attention should be paid to the study of the multiple detector rows and high gantry rotation speed, axial native images including all the diagnostic infor- as well as developments in reformatting technique al- mation. low the CT scan to be used as a noninvasive method to • 3D reconstruction and post-processing images are explore the “deep” arterial system (including aorta and highly operator dependent. visceral arteries) as well as the lower limb arteries. • Inadvertent 3D manipulations could “create” or “ig- • CTA is a “noninvasive” imaging modality, but it still nore” pathological conditions. requires injection of contrast media.
  • 83. 1.5.1 Peripheral Arterial Disease 55Fig. 1.5.1. Male 65 years, 76-mm-diameter infrarenal abdominal aortic aneurysm (AAA), stenosis of right common iliac artery.Postoperative CTA after endovascular aneurysm repair (EVAR)Magnetic Resonance Angiography • The main limiting factor is low image resolution com- pared to CT.• MRA is a noninvasive and nonirradiating technique. • MRA is used for imaging vessels of the lower extrem-• Its limitation is mainly due to the electromagnetic ity and visceral aortic branches (renal, mesenteric ar- field, which creates the images but prohibits the use teries). of this methodology on patients wearing pacemakers • For renal arteries MRA with contrast enhancement and other ferromagnetic foreign bodies. has a reported sensitivity of 96%.• As in ultrasound, “flow images” can be acquired with- • With regard to the lower extremity vessel, MRA is a out the use of contrast medium. preoperative noninvasive tool mainly useful in plan-• Use of non nephrotoxic intravenous contrast agent ning peripheral intervention or surgery. (gadolinium) enhances the MRA result. The bolus in- jection is done at a rate of 1.5–2 ml/s.• Enhanced MRA results in reduction of flow artefacts 1.5.1.6 Conclusion and enhanced image resolution.• Gadolinium-enhanced MRA has a reported sensitivity Colour duplex imaging associated either with CT angi- that ranges from 75% to 100% for assessment of ex- ography or MR angiography allows, in most cases, con- tracranial carotid stenosis compared to conventional ventional angiography to be avoided, which should be angiography. reserved for when there is a discrepancy between non-• MRA is used to image preoperative evaluation of en- invasive imaging techniques or when an endovascular dovascular aortic repair. treatment is likely to be performed during the session.
  • 84. 56 1.5 Noninvasive Diagnosis of Vascular Diseases Fig. 1.5.2. Female 71 years, occlusion of a left femoro-popliteal by-pass, patency of a stent of the right superficial femoral artery (SFA) 1.5.2.2 Imaging Techniques 1.5.2 Disease of Arteries Supplying the Brain • Visualizing the intracerebral circulation is also more 1.5.2.1 Introduction and more accurately done by noninvasive techniques. • Three noninvasive approaches for visualizing the • Stroke represents the third leading cause of death in brain-supplying arteries will de discussed: the first industrialized countries today. based on Doppler ultrasound, the second based on • Macro-angiopathies are responsible for nearly one- magnetic resonance and finally the third based on third of all ischaemic strokes. computer tomography. • In extracranial disease, the correct diagnosis of the degree of carotid stenosis in combination with clini- cal findings is the key to deciding whether patients Doppler Ultrasound require carotid endarterectomy. • Digital subtraction intra-arterial angiography (DSA) • High-resolution ultrasound combined with colour- is mostly considered to be the gold standard but differ- coded Doppler flow analysis (Duplex sonography) ent noninvasive methods are giving quite comparable has become a clinical tool of great value permitting results [24]. bedside noninvasive diagnosis of the extracranial and intracranial vessel pathology.
  • 85. 1.5.2 Disease of Arteries Supplying the Brain 57Fig. 1.5.3. Male 74 years, asymptomatic stenosis of the right internal carotid artery (ICA). Velocity criteria correspond to a stenosisof 70–80%• The accuracy of the description of the degree of carotid • Recently, echocontrast agents have been shown to im- stenosis has been demonstrated in several studies. prove Doppler ultrasound image quality, permitting a• Each neurosonology laboratory uses several standard- better diagnosis of pseudo-occlusions and intracranial ized criteria which are refined according to the techni- vessel disease [8]. cal advances in Doppler ultrasound techniques com- • Doppler ultrasound techniques have the advantage bined with regular auto-evaluation. that they can be repeated easily and even allow con-• Velocity criteria [2], pre- and post-stenotic Doppler tinuous monitoring of the acute stroke patient [7]. spectrum and collateral flow allow the best evaluation • Transcranial Doppler can also be applied during ca- of the degree of stenosis. rotid surgery to help decide whether a shunt should be• The detection of a floating thrombus and some char- placed and verify its patency. acterization of the atheromatous plaque consistency is also used in evaluating the degree of instability of the arterial lesion. Magnetic Resonance Angiography• Microembolic signals (HITS) in the post-stenotic flow also permit the prediction of stroke risk in high-grade • The first MR angiographic images were 2D and 3D stenosis. time-of-flight (TOF) and had a low accuracy because of the tendency to often overestimate the lesion.
  • 86. 58 1.5 Noninvasive Diagnosis of Vascular Diseases Fig. 1.5.4. MR angiography of the same patient as in Fig. 1.5.2. Eighty percent stenosis of the ostium of the right ICA. Reconstruc- tion of the Circle of Willis demonstrating an absence of the segment A1 of the left anterior cerebral artery • More recently, 3D contrast-enhanced MR angiogra- Computed Tomographic Angiography phy increased confidence in MRA and shows a good correlation with conventional DSA for extracranial • Spiral CT angiography has demonstrated its clinical and intracranial vessels. effectiveness in the assessment of narrowing of the lu- • MR imaging also permits the brain parenchyma to be men of the extracranial carotid artery bifurcation and visualized and thus shows the extent of the associated is even more accurate than conventional CT angiog- vascular lesions. raphy. • MR diffusion imaging techniques are a unique win- • CT also permits extra- and intracranial vessels to be dow to see, very early after stroke, the cytotoxic oe- analysed as well as the brain parenchyma. Perfusion dema provoked by an ischaemic injury. mapping is feasible and allows one to accurately deter- • MRA combined with MR diffusion and MR perfusion mine the brain tissue at risk in acute stroke. imaging has the advantage of giving the clinician a • The practical advantages of CT imaging are the short comprehensive analysis of the stroke in evolution and scanning times with fewer motion artefacts, the easier hints at its aetiology. handling of agitated and unstable stroke patients and the wide availability of CT machines.
  • 87. 1.5.3 Diseases of the Venous Circulation 59Fig. 1.5.5. CT angiography of the same patient. Confirmation of a high-grade calcified stenosis of the right ICA1.5.2.3 Conclusion 1.5.3 Diseases of the Venous Circulation• Doppler ultrasound, MRA and CTA all show similar accuracy in the diagnosis of occlusive diseases of the 1.5.3.1 Introduction brain-supplying arteries [21].• No noninvasive technique on its own is accurate • Venous problems are common. enough to replace DSA. Especially in carotid stenosis, • They include chronic venous insufficiency and acute the combination of two techniques, with the addition deep venous thrombosis. of a third if the first two disagree, appears to be the best • Chronic venous insufficiency refers to both superficial approach. Thus, invasive DSA before carotid endarter- varicosities and postphlebitic syndrome. ectomy can be avoided in the majority of patients.• For intracranial imaging, combined MRA and CTA is equal to the accuracy of DSA in most cases [12]. 1.5.3.2 Chronic Venous Insufficiency• Transcranial Doppler ultrasound is a bedside pro- cedure, is easy to perform, and allows monitoring of Investigations brain haemodynamics, detection of microemboli as well as evaluation of collateral flow and may even en- When special tests with instruments have not satisfacto- hance vessel reopening during thrombolysis [1]. rily explained the nature of the venous disorder, the fol- lowing techniques for studying the vein can be used.
  • 88. 60 1.5 Noninvasive Diagnosis of Vascular Diseases Fig. 1.5.6. Female 21 years, symptomatic chronic venous insufficiency of the left leg. Duplex ultrasound demonstrates normal re- spiratory movements on the right side and absence of reflux after blocking respiration. Normal photoplethysmography (red curve). On the left side, prolonged reflux after Valsalva, short venous filling time Photoplethysmography • A diminished refilling time demonstrates incompetent • By this method the number of red cells is estimated venous valves, but cannot differentiate whether this in the skin capillary bed using a photoelectrical trans- incompetence is within the superficial or deep venous ducer. system. Two successive recordings may be done, with • The signals are recorded as a line tracing on a chart and without saphenous occlusion, by finger or cuff recorder or a computerized display. pressure. • It has been shown that the degree of congestion of red • If RFT is corrected after saphenous occlusion, this cells in skin capillaries bears a close relationship to the means that incompetence is due to the superficial sys- venous pressure in the limb, and thus the signal from tem. Placing the cuff successively over the thigh and the photoplethysmograph closely parallels the venous the calf may make the same comparison. This differ- pressure changes. entiates between incompetence of the short and long • With exercise, in an upright position, the venous pres- saphenous veins. sure within the limb generally falls, and it takes at least 20 s before the original pressure is regained (venous refilling time: VRT). Volume Plethysmography • In states of superficial or deep vein valvular incompe- • The limb volume closely parallels the venous pressure tence the refilling time may be decisively shortened by so that when the patient is standing still it is maximal reflux of venous blood down the limb. but afterwards, when blood has been expelled from the limb, both venous pressure and limb volume will fall.
  • 89. 1.5.3 Diseases of the Venous Circulation 61• The time taken for the volume to return to its original predictive values. Even if ascending venography has value is a good indication of valve competence. With been described as the gold standard for the diagnosis of fully competent valves, this will be at least 20 s, but DVT, Duplex ultrasonography has become the meth- when superficial or deep vein incompetence is pres- od of choice, combined with plasma D-dimer assay. ent this will be shortened according to the severity of condition. InvestigationsDoppler Flowmeter Duplex Scanning• According to the direction and speed of movement of • Duplex scanning is a practical method of assessing red cells, there is a Doppler shift in the phase of the blood flow in veins and valve cusp movements. signal which is recognized by the machine and made • It can differentiate between acute and chronic throm- apparent. bosis.• Only speed and direction are represented by the sig- • All the major deep veins of the lower limb can be as- nal, not the volume. sessed.• Abnormal flow in direction indicates that the valves • The technique is less accurate for the small veins of the are incompetent or absent. calf and cannot demonstrate the presence of thrombi• The probe is placed over the vein to be examined while in these small veins. However, in many cases this de- the patient is standing and the response to coughing, pends on the ability and the experience of the techni- to calf compression, to exercise and to an occluded sa- cian. phenous (long or short) vein is studied. • The vein is scanned in transverse and sagittal planes. • The presence of thrombosis is evaluated by the com- pressibility of the vein.Ultrasonography • In addition, a vein without thrombus should show• Ultrasonography provides a much more sophisticated Doppler evidence of flow, variation with respiration demonstration by giving an image of veins and their and increase when distal veins are compressed. valves on a display screen. It will show the movement • Recent thrombi tend to be anechoic and only later will in these structures and also the direction and speed of show characteristic internal echoes. blood flow within them.• The vein walls and lumen can be outlined and studied, clot may be recognized by absence of flow and immo- Volume Plethysmography bile vein walls, and the structure of valves and their • Pulse volume recorders are used to assess venous out- competence can be scrutinized. flow.• The anatomy of veins can be visualized preoperatively. • Two components of the curves are used: first, the Individual deep veins and their branches can be dis- circumference changes after the inflation of the cuff; tinguished and their flow pattern displayed, so that, second, the downslope of the curve after immediate for instance, incompetence in gastrocnemius vein deflation. can be recognized and the reflux within it estimated • In the case of thrombosis, the downslope will be slow. to assess its significance. In the popliteal vein this will • For calculation, two values are used: the maximum indicate the effectiveness of the musculovenous pump increase in calf volume and the maximum venous out- below the knee or, conversely, the severity of reflux in flow during the first second after deflation of the cuff. the deep veins at that level. • Both of these values are decreased in patients with DVT [4].1.5.3.3 Deep Vein Thrombosis 1.5.3.4 Conclusion• The clinical diagnosis of deep vein thrombosis (DVT) is unreliable in more than 50% of cases, and, in recent Duplex scanning of the superficial and deep veins is the years, plasma D-dimer assays have been used to predict preferred imaging technique to asses venous disorders of the presence of DVT with high sensitivity and negative the legs.
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  • 92. 65 1.6 Invasive Diagnosis of Vascular Diseases Luís Mendes Pedro and José Fernandes e Fernandes contrast, that promoted its clinical utilization