ABC.of.Interventional.Cardiology 2004

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  • 1. ABC OF INTERVENTIONAL CARDIOLOGY Edited by Ever D GrechTeAm YYePG Digitally signed by TeAm YYePG DN: cn=TeAm YYePG, c=US, o=TeAm YYePG, ou=TeAm YYePG, email=yyepg@msn.com Reason: I attest to the accuracy and integrity of this document Date: 2005.04.21 09:57:08 +0800
  • 2. ABC OFINTERVENTIONAL CARDIOLOGY
  • 3. For Lisa, Alexander, and Frances
  • 4. ABC OFINTERVENTIONAL CARDIOLOGY Edited by EVER D GRECH Consultant Cardiologist, South Yorkshire Cardiothoracic Centre, Northern General Hospital, Sheffield, UK
  • 5. © BMJ Publishing Group 2004All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording and/or otherwise, without the prior written permission of the publishers. First published in 2004 by BMJ Publishing Group Ltd, BMA House, Tavistock Square, London WC1H 9JR www.bmjbooks.com British Library Cataloguing in Publication Data A catalogue record for this book is available from the British Library ISBN 0 7279 1546 0 Cover shows coloured arteriogram of arteries of the heart. With permission from Science Photo Library. Typeset by BMJ Electronic Production and Newgen Imaging Systems Printed and bound in Spain by GraphyCems, Navarra
  • 6. Contents Contributors vi Preface vii Acknowledgements viii1 Pathophysiology and investigation of coronary artery disease 1 Ever D Grech2 Percutaneous coronary intervention. I: History and Development 5 Ever D Grech3 Percutaneous coronary intervention. II: The procedure 8 Ever D Grech4 Chronic stable angina: treatment options 12 Laurence O’Toole, Ever D Grech5 Acute coronary syndrome: unstable angina and non-ST segment elevation myocardial infarction 16 Ever D Grech, David R Ramsdale6 Acute coronary syndrome: ST segment elevation myocardial infarction 19 Ever D Grech, David R Ramsdale7 Percutaneous coronary intervention: cardiogenic shock 22 John Ducas, Ever D Grech8 Interventional pharmacotherapy 25 Roger Philipp, Ever D Grech9 Non-coronary percutaneous intervention 29 Ever D Grech10 New developments in percutaneous coronary intervention 33 Julian Gunn, Ever D Grech, David Crossman, David Cumberland11 Percutaneous interventional electrophysiology 37 Gerry C Kaye12 Implantable devices for treating tachyarrhythmias 41 Timothy Houghton, Gerry C Kaye13 Interventional paediatric cardiology 45 Kevin P Walsh Index 49 v
  • 7. ContributorsDavid Crossman Timothy HoughtonProfessor of Clinical Cardiology, Cardiovascular Research Registrar in Cardiology, Hull and East Yorkshire Trust, CastleGroup, Clinical Sciences Centre, Northern General Hospital, Hill Hospital, HullSheffield Gerry C KayeDavid Cumberland Consultant Cardiologist, Hull and East Yorkshire Trust, CastleConsultant Cardiovascular Interventionist, Ampang Puteri Hill Hospital, HullSpecialist Hospital, Kuala Lumpur, Malaysia Laurence O’TooleJohn Ducas Consultant Cardiologist and Physician, Royal HallamshireConsultant Cardiologist, Health Sciences Centre and Hospital, SheffieldSt Boniface Hospital, Winnipeg, Manitoba and AssociateProfessor, University of Manitoba, Winnipeg, Canada Roger Philipp Fellow in Interventional Cardiology, Health Sciences CentreEver D Grech and St Boniface Hospital, Winnipeg, Manitoba, CanadaConsultant Cardiologist, South Yorkshire CardiothoracicCentre, Northern General Hospital, Sheffield, UK David R Ramsdale Consultant Cardiologist, Cardiothoracic Centre, LiverpoolJulian GunnSenior Lecturer and Honorary Consultant Cardiologist, Kevin P WalshCardiovascular Research Group, Clinical Sciences Centre, Consultant Paediatric Cardiologist, Our Lady’s Hospital forNorthern General Hospital, Sheffield Sick Children, Crumlin, Dublin, Republic of Irelandvi
  • 8. PrefaceIt is only 26 years since the first percutaneous transluminal coronary angioplasty (PTCA) was carried out by the pioneering Swissradiologist, Andreas Greuntzig, heralding the dawn of interventional cardiology. In this short time, interventional cardiology hasovercome many limitations and undergone major evolutionary changes—most notably the development of the coronary stent.Worldwide, many thousands of patients now safely undergo percutaneous coronary intervention every day, and the numberscontinue to grow. In many countries, the numbers are similar to, or exceed, bypass surgical procedures. Although, at first, PTCA was indicated only as treatment for chronic stable angina caused by a discrete lesion in a single vessel,this has now progressed to encompass multi-lesion and multi-vessel disease. Moreover, percutaneous intervention is now becomingwidely used in the management of unstable angina and acute myocardial infarction with definite benefits in terms of morbidity andmortality. The effectiveness and safety of these procedures has undoubtedly been enhanced by the adjunctive use of new anti-plateletand antithrombotic agents. As the indications increase and more patients are treated, so inevitably do the demands on healthcare budgets. Undoubtedly,percutaneous intervention is expensive. However, this burden must be weighed against bypass surgery, which is even more costly, andmulti-drug treatment—which would be required over many years. Although percutaneous coronary intervention has held centre stage in cardiology, major in-roads have also been made in non-coronary areas. Transcatheter valvuloplasty, ethanol septal ablation and closure devices have become effective and safe alternativesto surgery, as have paediatric interventional procedures. A greater understanding of cardiac electrophysiology has led to importantadvances in the treatment of arrhythmias, and implantable cardioverter defibrillators are benefiting ever larger numbers of patients. Where are we heading? This is perhaps the biggest question in the minds of many interventional cardiologists. New technologygenerated by industry and new techniques coupled with high levels of expertise are fuelling advances in almost all areas ofinterventional cardiology. As drug-eluting stents address the Achilles’ heel of angioplasty and stenting—restenosis—the hugeincrease in percutaneous coronary procedures seen over recent years is likely to increase even further, and will probably be doublethe rate of bypass surgery within a decade. In writing and editing this book, I have endeavoured to present broad (and sometimes complex) aspects of interventionalcardiology in a clear, concise and balanced manner. To this end, an easy-to-read style of text, avoiding jargon and exhaustive detail,has been used supplemented with many images and graphics. EVER D GRECH Sheffield, July 2003 vii
  • 9. AcknowledgementsI have many people to thank for helping me develop and produce this book. I am very grateful to my coauthors who have allwillingly contributed their time and expertise. I would also like to recognise the positive efforts and invaluable assistance of theBritish Medical Journal editors and illustrators. These include Trish Groves, Mary Banks, Eleanor Lines, Greg Cotton, and NaomiWilkinson. Finally, my enduring gratitude goes to my family for their unfailing encouragement, patience, and love.viii
  • 10. 1 Pathophysiology and investigation of coronaryartery diseaseEver D GrechIn affluent societies, coronary artery disease causes severedisability and more death than any other disease, including Foam Fatty Intermediate Atheroma Fibrous Complicated cells streak lesion plaque lesion or rupturecancer. It manifests as angina, silent ischaemia, unstable angina,myocardial infarction, arrhythmias, heart failure, and suddendeath.PathophysiologyCoronary artery disease is almost always due to atheromatousnarrowing and subsequent occlusion of the vessel. Early From first decade From third decade From fourth decadeatheroma (from the Greek athera (porridge) and oma (lump)) is Smoothpresent from young adulthood onwards. A mature plaque is Growth mainly by lipid accumulation Thrombosis, muscle haematomacomposed of two constituents, each associated with a particular and collagencell population. The lipid core is mainly released from necrotic“foam cells”—monocyte derived macrophages, which migrate Progression of atheromatous plaque from initial lesion to complex andinto the intima and ingest lipids. The connective tissue matrix is ruptured plaquederived from smooth muscle cells, which migrate from themedia into the intima, where they proliferate and change theirphenotype to form a fibrous capsule around the lipid core. When a plaque produces a > 50% diameter stenosis (or > 75% reduction in cross sectional area), reduced blood flow Normal coronary Lumen arterythrough the coronary artery during exertion may lead to Intima (endothelium and internal elastic lamina)angina. Acute coronary events usually arise when thrombusformation follows disruption of a plaque. Intimal injury causes Lumen Media (smooth muscle cellsdenudation of the thrombogenic matrix or lipid pool and and elastic tissue)triggers thrombus formation. In acute myocardial infarction,occlusion is more complete than in unstable angina, where Adventitia (fibroblasts andarterial occlusion is usually subtotal. Downstream embolism of connective tissue)thrombus may also produce microinfarcts. Monocyte Plasma low density lipoprotein LumenInvestigations Key Development Collagen of atheromaPatients presenting with chest pain may be identified as having Intimadefinite or possible angina from their history alone. In the Dividing smooth muscle cellformer group, risk factor assessment should be undertaken, Oxidised low Lumen Media density lipoproteinboth to guide diagnosis and because modification of some Monocyteassociated risk factors can reduce cardiovascular events andmortality. A blood count, biochemical screen, and thyroid Monocyte-derivedfunction tests may identify extra factors underlying the onset of Adventitia macrophages (foam cells)angina. Initial drug treatment should include aspirin, a blocker, and a nitrate. Antihypertensive and lipid lowering Schematic representation of normal coronary artery wall (top) anddrugs may also be given, in conjunction with advice on lifestyle development of atheroma (bottom)and risk factor modification. All patients should be referred to a cardiologist to clarify thediagnosis, optimise drug treatment, and assess the need andsuitability for revascularisation (which can improve bothsymptoms and prognosis). Patients should be advised to seek Cardiovascular risk factorsurgent medical help if their symptoms occur at rest or on Non-modifiable risk factorsminimal exertion and if they persist for more than 10 minutes x Positive family history x Age x Male sexafter sublingual nitrate has been taken, as these may herald the Modifiable risk factorsonset of an acute coronary syndrome. x Hypercholesterolaemia x Hypertension x Smoking x Left ventricular x Sedentary lifestyle x Diabetes hypertrophy x Excessive alcoholPriorities for cardiology referral x Overweight and obesity intakex Recent onset of symptoms x Severe symptoms (minimal Uncertain risk factorsx Rapidly progressive symptoms exertion or nocturnal angina) x Hypertriglyceridaemia x Lp(a) lipoprotein x Uric acidx Possible aortic stenosis x Angina refractory to medical x Microalbuminuria x Fibrinogen x Reninx Threatened employment treatment x Hyperhomocysteinaemia x C reactive protein 1
  • 11. ABC of Interventional CardiologyNon-invasive investigationsElectrocardiography Exercise stress testingAn abnormal electrocardiogram increases the suspicion of Indications Contraindicationssignificant coronary disease, but a normal result does not x Confirmation of suspected angina x Cardiac failureexclude it. x Evaluation of extent of myocardial x Any feverish illness ischaemia and prognosis x Left ventricular outflow tract x Risk stratification after myocardial obstruction or hypertrophicChest x ray infarction cardiomyopathyPatients with angina and no prior history of cardiac disease x Detection of exercise induced x Severe aortic or mitralusually have a normal chest x ray film. symptoms (such as arrhythmias or stenosis syncope) x Uncontrolled hypertension x Evaluation of outcome of x Pulmonary hypertensionExercise electrocardiography interventions (such as x Recent myocardial infarctionThis is the most widely used test in evaluating patients with percutaneous coronary x Severe tachyarrhythmiassuspected angina. It is generally safe (risk ratio of major adverse interventions or coronary artery x Dissecting aortic aneurysmevents 1 in 2500, and of mortality 1 in 10 000) and provides bypass surgery) x Left main stem stenosis ordiagnostic as well as prognostic information. The average x Assessment of cardiac transplant equivalent x Rehabilitation and patient x Complete heart block (insensitivity and specificity is 75%. The test is interpreted in terms motivation adults)of achieved workload, symptoms, and electrocardiographicresponse. A 1 mm depression in the horizontal ST segment isthe usual cut-off point for significant ischaemia. Poor exercisecapacity, an abnormal blood pressure response, and profound Restischaemic electrocardiographic changes are associated with apoor prognosis. I aVR V1 V4Main end points for exercise electrocardiographyx Target heart rate achieved ( > 85% of maximum predicted heart rate) II aVL V2 V5x ST segment depression > 1 mm (downsloping or planar depression of greater predictive value than upsloping depression)x Slow ST recovery to normal ( > 5 minutes) III aVF V3 V6x Decrease in systolic blood pressure > 20 mm Hgx Increase in diastolic blood pressure > 15 mm Hgx Progressive ST segment elevation or depression Peak exercisex ST segment depression > 3 mm without painx Arrhythmias (atrial fibrillation, ventricular tachycardia)Features indicative of a strongly positive exercise testx Exercise limited by angina to < 6 minutes of Bruce protocol I aVR V1 V4x Failure of systolic blood pressure to increase > 10 mm Hg, or fall with evidence of ischaemiax Widespread marked ST segment depression > 3 mmx Prolonged recovery time of ST changes ( > 6 minutes) II aVL V2 V5x Development of ventricular tachycardiax ST elevation in absence of prior myocardial infarction III aVF V3 V6Stress echocardiographyStress induced impairment of myocardial contraction is a Example of a strongly positive exercise test. After only 2 minutes and 24sensitive marker of ischaemia and precedes seconds of exercise (according to Bruce protocol), the patient developed chest pain and electrocardiography showed marked ischaemic changeselectrocardiographic changes and angina. Cross sectional (maximum 3 mm ST segment depression in lead V6)echocardiography can be used to evaluate regional and globalleft ventricular impairment during ischaemia, which can beinduced by exercise or an intravenous infusion of drugs thatincrease myocardial contraction and heart rate (such asdobutamine) or dilate coronary arterioles (such as dipyridamoleor adenosine). The test has a higher sensitivity and specificitythan exercise electrocardiography and is useful in patientswhose physical condition limits exercise.Radionuclide myocardial perfusion imagingThallium-201 or technetium-99m (99mTc-sestamibi,99m Tc-tetrofosmin) is injected intravenously at peak stress, and itsmyocardial distribution relates to coronary flow. Images areacquired with a gamma camera. This test can distinguishbetween reversible and irreversible ischaemia (the lattersignifying infarcted tissue). Although it is expensive andrequires specialised equipment, it is useful in patients whose 99m Tc-tetrofosmin perfusion scan showing reversible anterolateral wallexercise test is non-diagnostic or whose exercise ability is ischaemia, induced by intravenous dobutamine infusion (white arrows).limited. Normal rest images are shown by yellow arrows2
  • 12. Pathophysiology and investigation of coronary artery disease A multigated acquisition (MUGA) scan assesses leftventricular function and can reveal salvageable myocardium inpatients with chronic coronary artery disease. It can beperformed with either thallium scintigraphy at rest or metabolicimaging with fluorodeoxyglucose by means of either positronemission tomography (PET) or single photon emissioncomputed tomography (SPECT).Invasive investigationsCoronary angiographyThe only absolute way to evaluate coronary artery disease is byangiography. It is usually performed as part of cardiac Angiograms of normal coronary arteries (LAD=left anterior descendingcatheterisation, which includes left ventricular angiography and artery, DG=diagonal artery, LCx=left circumflex artery, OM=obtuse marginalhaemodynamic measurements, providing a more complete artery, SAN=sino-atrial node artery, RV=right ventricular branch artery,evaluation of an individual’s cardiac status. Cardiac LV=left ventricular branch artery, PDA=posterior descending artery)catheterisation is safely performed as a day case procedure. Patients must be fully informed of the purpose of theprocedure as well as its risks and limitations. Majorcomplications, though rare in experienced hands, include death(risk ratio 1 in 1400), stroke (1 in 1000), coronary artery Main indications for coronary angiographydissection (1 in 1000), and arterial access complications (1 in x Uncertain diagnosis of angina (coronary artery disease cannot be500). Risks depend on the individual patient, and predictors excluded by non-invasive testing)include age, coronary anatomy (such as severe left main stem x Assessment of feasibility and appropriateness of various forms ofdisease), impaired left ventricular function, valvar heart disease, treatment (percutaneous intervention, bypass surgery, medical)the clinical setting, and non-cardiac disease. The commonest x Class I or II stable angina with positive stress test or class III or IVcomplications are transient or minor and include arterial access angina without positive stress test x Unstable angina or non-Q wave myocardial infarction (mediumbleeding and haematoma, pseudoaneurysm, arrhythmias, and high risk patients)reactions to the contrast medium, and vagal reactions (during x Angina not controlled by drug treatmentsheath insertion or removal). x Acute myocardial infarction—especially cardiogenic shock, Before the procedure, patients usually fast and may be given ineligibility for thrombolytic treatment, failed thrombolytica sedative. Although a local anaesthetic is used, arterial access reperfusion, re-infarction, or positive stress test(femoral, brachial, or radial) may be mildly uncomfortable. x Life threatening ventricular arrhythmia x Angina after bypass surgery or percutaneous interventionPatients do not usually feel the catheters once they are inside x Before valve surgery or corrective heart surgery to assess occultthe arteries. Transient angina may occur during injection of coronary artery diseasecontrast medium, usually because of a severely diseased artery.Patients should be warned that, during left ventricularangiography, the large volume of contrast medium may cause atransient hot flush and a strange awareness of urinaryincontinence (and can be reassured that this does not actuallyhappen). Modern contrast agents rarely cause nausea andvomiting. Insertion of an arterial sheath with a haemostatic valveminimises blood loss and allows catheter exchange. Three typesof catheter, which come in a variety of shapes and diameters,are commonly used. Two have a single hole at the end and aredesigned to facilitate controlled engagement of the distal tipwithin the coronary artery ostium. Contrast medium is injectedthrough the lumen of the catheter, and moving x ray images areobtained and recorded. Other catheters may be used for graftangiography. The “pigtail” catheter has an end hole and severalside holes and is passed across the aortic valve into the leftventricle. It allows injection of 30-40 ml of contrast medium Left ventricular angiogram during diastole (top) and systole (bottom) after injection of contrast medium via a pigtail catheter, showing good contractility (LCA=left coronary artery) Commonly used diagnostic catheters (from left to right): right Judkins, left Judkins, multipurpose, left Amplatz, and pigtail 3
  • 13. ABC of Interventional Cardiologyover three to five seconds by a motorised pump, providing Ultrasoundvisualisation of left ventricular contraction over two to four scan plane Vesselcardiac cycles. Aortic and ventricular pressures are alsorecorded during the procedure. IVUS catheterIntravascular ultrasound (IVUS)In contrast to angiography, which gives a two dimensionalluminal silhouette with little information about the vessel wall,intravascular ultrasound provides a cross sectional, three Media and Stent strutsdimensional image of the full circumference of the artery. It adventitia borderallows precise measurement of plaque length and thickness and Fibro-fattyminimum lumen diameter, and it may also characterise the plaqueplaque’s composition. It is often used to clarify ambiguous angiographic findingsand to identify wall dissections or thrombus. It is most useful IVUS catheterduring percutaneous coronary intervention, when target lesions Lumencan be assessed before, during, and after the procedure and atfollow up. The procedure can also show that stents which seem The intravascular ultrasound (IVUS) catheter (above) and images showing ato be well deployed on angiography are, in fact, suboptimally stent within a diseased coronary artery (below)expanded. Its main limitations are the need for an operatorexperienced in its use and its expense; for these reasons it is notroutinely used in many centres.Doppler flow wire and pressure wireUnlike angiography or intravascular ultrasound, the Dopplerflow wire and pressure wire provide information on thephysiological importance of a diseased coronary artery. Theyare usually used when angiography shows a stenosis that is ofintermediate severity, or to determine the functional severity of Angina?a residual stenosis after percutaneous coronary intervention. Intracoronary adenosine is used to dilate the distal coronaryvessels in order to maximise coronary flow. The Doppler flow Definite or possible Unlikelywire has a transducer at its tip, which is positioned beyond thestenosis to measure peak flow velocity. The pressure wire has a Risk factor assessment, blood tests, electrocardiographytip micrometer, which records arterial pressures proximal anddistal to the stenosis. Drug treatment for symptoms and risk factor reductionThe figure showing progression of atheromatous plaque from initial lesionis adapted with permission from Pepine CJ, Am J Cardiol 1998;82(suppl Refer to cardiologist10A):23-7S.Competing interests: None declared. Stress testFurther reading Strongly positive Mildly positive Negativex Mark DB, Shaw L, Harrell FE Jr, Hlatky MA, Lee KL, Bengtson JR, et al. Prognostic value of a treadmill exercise score in outpatients Review diagnosis with suspected coronary artery disease. N Engl J Med 1991;325: 849-53x Marwick TH, Case C, Sawada S, Rimmerman C, Brenneman P, Angina Not angina Kovacs R, et al. Prediction of mortality using dobutamine echocardiography. J Am Coll Cardiol 2001;37:754-60x Scanlon PJ, Faxon DP, Audet AM, Carabello B, Dehmer GJ, Eagle Medical treatment KA, et al. ACC/AHA guidelines for coronary angiography. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Coronary Angiography). J Am Coll Cardiol 1999;33:1756-824 Angiography Poor control Good controlx Mintz GS, Nissen SE, Anderson WD, Bailey SR, Erbel R, Fitzgerald PJ, et al. American College of Cardiology clinical expert consensus Revascularisation (PCI or CABG) Continue medical treatment document on standards for acquisition, measurement and reporting of intravascular ultrasound studies (IVUS). J Am Coll Cardiol 2001;37:1478-92 Algorithm for management of suspected angina (PCI=percutaneous coronary intervention, CABG=coronary artery bypass grafting)4
  • 14. 2 Percutaneous coronary intervention.I: History and developmentEver D Grech Canadian Cardiovascular Society classification of anginaThe term “angina pectoris” was introduced by Heberden in1772 to describe a syndrome characterised by a sensation of Class I x No angina during ordinary physical activity such as walking or“strangling and anxiety” in the chest. Today, it is used for chest climbing stairsdiscomfort attributed to myocardial ischaemia arising from x Angina during strenuous, rapid, or prolonged exertionincreased myocardial oxygen consumption. This is often Class IIinduced by physical exertion, and the commonest aetiology is x Slight limitation of ordinary activityatheromatous coronary artery disease. The terms “chronic” and x Angina on walking or climbing stairs rapidly; walking uphill;“stable” refer to anginal symptoms that have been present for at walking or climbing stairs shortly after meals, in cold or wind, whenleast several weeks without major deterioration. However, under emotional stress, or only in the first few hours after wakingsymptom variation occurs for several reasons, such as mental x Angina on walking more than two blocks (100-200 m) on the levelstress, ambient temperature, consumption of alcohol or large or climbing more than one flight of stairs at normal pace and in normal conditionsmeals, and factors that may increase coronary tone such asdrugs and hormonal change. Class III x Marked limitation of ordinary physical activity x Angina on walking one or two blocks on the level or climbing one flight of stairs at normal pace and in normal conditionsClassification Class IVThe Canadian Cardiovascular Society has provided a graded x Inability to carry out any physical activity without discomfortclassification of angina which has become widely used. In x Includes angina at restclinical practice, it is important to describe accurately specificactivities associated with angina in each patient. This shouldinclude walking distance, frequency, and duration of episodes. Percutaneous transluminal coronary angioplasty (PTCA) 1977History of myocardial Development in PTCA equipment Mid (soft tipped guide catheters, steerable guidewires, lower profile balloon catheters) 1980srevascularisation MidIn the management of chronic stable angina, there are two Stents Athero-ablative devices 1990s (directional coronary atherectomy, rotablator, lasers)invasive techniques available for myocardial revascularisation: onwardscoronary artery bypass surgery and catheter attached devices.Although coronary artery bypass surgery was introduced in New stent designs Brachytherapy New balloon designs Adjunctive1968, the first percutaneous transluminal coronary angioplasty and "smart" stents • β radiation • Low profile pharmacotherapywas not performed until September 1977 by Andreas • Pre-mounted emission • High inflation • ADP antagonists • Increased flexibility • γ radiation • Short or long • Glycoprotein IIb/Gruentzig, a Swiss radiologist, in Zurich. The patient, 38 year and radial strength emission balloons IIIa inhibitorsold Adolph Bachman, underwent successful angioplasty to a left • Covered stents • Cutting balloonscoronary artery lesion and remains well to this day. After the • Coated stents • "Designer" drugssuccess of the operation, six patients were successfully treatedwith percutaneous transluminal coronary angioplasty in that • Biodegradable stents • Drug or gene deliveryyear. stents By today’s standards, the early procedures used • Radioactive stentscumbersome equipment: guide catheters were large and couldeasily traumatise the vessel, there were no guidewires, and Major milestones in percutaneous coronary interventionballoon catheters were large with low burst pressures. As aresult, the procedure was limited to patients with refractoryangina, good left ventricular function, and a discrete, proximal,concentric, and non-calcific lesion in a single major coronaryartery with no involvement of major side branches orangulations. Consequently, it was considered feasible in only10% of all patients needing revascularisation. Modern balloonDevelopments in percutaneous catheter: its low profile facilitatesintervention lesion crossing, the flexible shaft allowsDuring 1977-86 guide catheters, guidewires, and balloon tracking downcatheter technology were improved, with slimmer profiles and tortuous vessels, and the balloon can beincreased tolerance to high inflation pressures. As equipment inflated to highimproved and experience increased, so more complex lesions pressures withoutwere treated and in more acute situations. Consequently, distortion or rupture 5
  • 15. ABC of Interventional Cardiologypercutaneous transluminal coronary angioplasty can now beundertaken in about half of patients needing revascularisation(more in some countries), and it is also offered to high-riskpatients for whom coronary artery bypass surgery may beconsidered too dangerous. Although percutaneous transluminal coronary angioplastycauses plaque compression, the major change in lumengeometry is caused by fracturing and fissuring of the atheroma,extending into the vessel wall at variable depths and lengths.This injury accounts for the two major limitations ofpercutaneous transluminal coronary angioplasty{acute vesselclosure and restenosis. Micrographs showing arterial Acute vessel closure—This usually occurs within the first 24 barotrauma caused by coronaryhours of the procedure in about 3-5% of cases and follows angioplasty. Top left: coronary arterial dissection with large flap.vessel dissection, acute thrombus formation, or both. Important Top right: deep fissuring withinclinical consequences include myocardial infarction, emergency coronary artery wall atheroma.coronary artery bypass surgery, and death. Bottom: fragmented plaque tissue Restenosis occurring in the first six months after angioplasty (dark central calcific plaque surrounded by fibrin andis caused largely by smooth muscle cell proliferation and platelet-rich thrombus), which mayfibrointimal hyperplasia (often called neointimal proliferation), embolise in distal arterioles to causeas well as elastic recoil. It is usually defined as a greater than infarction50% reduction in luminal diameter and has an incidence of25-50% (higher after vein graft angioplasty). Furtherintervention may be indicated if angina and ischaemia recur.Drills, cutters, and lasersIn the 1980s, two main developments aimed at limiting theseproblems emerged. The first were devices to remove plaquematerial, such as by rotational atherectomy, directional coronaryatherectomy, transluminal extraction catheter, and excimerlaser. By avoiding the vessel wall trauma seen duringpercutaneous transluminal coronary angioplasty, it wasenvisaged that both acute vessel closure and restenosis rates Tools for coronary atherectomy. Top:would be reduced. the Simpson atherocath has a cutter in However, early studies showed that, although acute closure a hollow cylindrical housing. The cutter rotates at 2000 rpm, and excisedrates were reduced, there was no significant reduction in atheromatous tissue is pushed into therestenosis. Moreover, these devices are expensive, not distal nose cone. Left: the Rotablatorparticularly user friendly, and have limited accessibility to more burr is coated with 10 m diamonddistal stenoses. As a result, they have now become niche tools chips to create an abrasive surface. The burr, connected to a drive shaft and aused by relatively few interventionists. However, they may have turbine powered by compressed air,an emerging role in reducing restenosis rates when used as rotates at speeds up to 200 000 rpmadjunctive treatment before stenting (especially for largeplaques) and in treating diffuse restenosis within a stent.Intracoronary stentsThe second development was the introduction of intracoronarystents deployed at the site of an atheromatous lesion. Thesewere introduced in 1986 with the objective of tacking downdissection flaps and providing mechanical support. They alsoreduce elastic recoil and remodelling associated with restenosis. The first large randomised studies conclusively showed thesuperiority of stenting over coronary angioplasty alone, both inclinical and angiographic outcomes, including a significant 30%reduction in restenosis rates. Surprisingly, this was not due toinhibition of neointimal proliferation—in fact stents mayincrease this response. The superiority of stenting is that theinitial gain in luminal diameter is much greater than afterangioplasty alone, mostly because of a reduction in elasticrecoil. Although neointimal proliferation through the struts of thestent occurs, it is insufficient to cancel out the initial gain, Coronary stents. Top: Guidant Zeta stent. Middle: BiodivYsio AS stent coatedleading to a larger lumen size and hence reduced restenosis. with phosphorylcholine, a synthetic copy of the outer membrane of red blood cells, which improves haemocompatibility and reduces thrombosis.Maximising the vessel lumen is therefore a crucial mechanism Bottom: the Jomed JOSTENT coronary stent graft consists of a layer offor reducing restenosis. “Bigger is better” is the adage followed PTFE (polytetrafluoroethylene) sandwiched between two stents and is usefulin this case. in sealing perforations, aneurysms, and fistulae6
  • 16. Percutaneous coronary intervention. I: History and developmentEarly stent problemsAs a result of initial studies, stents were predominantly usedeither as “bail out” devices for acute vessel closure duringcoronary angioplasty (thus avoiding the need for immediatecoronary artery bypass surgery) or for restenosis afterangioplasty. Thrombosis within a stent causing myocardial infarctionand death was a major concern, and early aggressiveanticoagulation to prevent this led to frequent complicationsfrom arterial puncture wounds as well as major systemichaemorrhage. These problems have now been overcome by theintroduction of powerful antiplatelet drugs as a substitute forwarfarin. The risk of thrombosis within a stent diminishes whenthe stent is lined with a new endothelial layer, and antiplatelettreatment can be stopped after a month. The recognition thatsuboptimal stent expansion is an important contributor tothrombosis in stents has led to the use of intravascular Coronary angiogram showing three lesions (arrows) affectingultrasound to guide stent deployment and high pressure the left anterior descendinginflations to ensure complete stent expansion. artery (top left). The lesions are stented withoutCurrent practice pre{dilatation (top right), with good results (bottom)A greater understanding of the pathophysiology of stentdeployment, combined with the development of more flexiblestents (which are pre-mounted on low-profile catheterballoons), has resulted in a massive worldwide increase in stentuse, and they have become an essential component of coronaryintervention. Low profile stents have also allowed “direct”stenting—that is, implanting a stent without the customary 2500 Stents deployed (1000s/year)balloon dilatation—to become prevalent, with the advantages ofeconomy, shorter procedure time, and less radiation from 2000imaging. Most modern stents are expanded by balloon and 1500made from stainless steel alloys. Their construction and design,metal thickness, surface coverage, and radial strength vary 1000considerably. 500 Stents are now used in most coronary interventions and in awide variety of clinical settings. They substantially increase 0 1986 1994 1998 2001procedural safety and success, and reduce the need for Yearemergency coronary artery bypass surgery. Proceduresinvolving stent deployment are now often referred to aspercutaneous coronary interventions to distinguish them from Exponential increase in use of intracoronary stents since 1986. In 2001, 2.3 million stents were implanted (moreconventional balloon angioplasty (percutaneous transluminal than double the 1998 rate)coronary angioplasty). A major recent development has been the introduction ofdrug eluting stents (also referred to as “coated stents”), whichreduce restenosis to very low rates. Their high cost currentlylimits their use, but, with increasing competition amongmanufacturers, they will probably become more affordable. Unequivocal indications for use of coronary stents x Acute or threatened vessel closure during angioplastyCompeting interests: None declared. x Primary reduction in restenosis in de novo lesions in arteries > 3.0 mm in diameterThe micrographs showing deep fissuring within a coronary artery wall x Focal lesions in saphenous vein graftsatheroma and fragmented plaque tissue caused by coronary angioplasty x Recanalised total chronic occlusionswere supplied by Kelly MacDonald, consultant histopathologist at St x Primary treatment of acute coronary syndromesBoniface Hospital, Winnipeg, Canada.Further readingx Gruentzig AR. Transluminal dilatation of coronary artery stenosis. x Meyer BJ, Meier B. Percutaneous transluminal coronary angioplasty Lancet 1978;1:263 of single or multivessel disease and chronic total occlusions. In:x Smith SC Jr, Dove JT, Jacobs AK, Kennedy JW, Kereiakes D, Kern Grech ED, Ramsdale DR, eds. Practical interventional cardiology. MJ, et al. ACC/AHA guidelines of percutaneous coronary 2nd ed. London: Martin Dunitz, 2002:35-54 interventions (revision of the 1993 PTCA guidelines)—executive x Costa MA, Foley DP, Serruys PW. Restenosis: the problem and how summary. A report of the American College of Cardiology/ to deal with it. In: Grech ED, Ramsdale DR, eds. Practical American Heart Association Task Force on Practice Guidelines interventional cardiology. 2nd ed. London: Martin Dunitz, 2002: (committee to revise the 1993 guidelines for percutaneous 279-94 transluminal coronary angioplasty). J Am Coll Cardiol 2001;37: x Topol EJ, Serruys PW. Frontiers in interventional cardiology. 2215-39 Circulation 1998;98:1802-20 7
  • 17. 3 Percutaneous coronary intervention.II: The procedureEver D GrechA wide range of patients may be considered for percutaneouscoronary intervention. It is essential that the benefits and risks ofthe procedure, as well as coronary artery bypass graft surgery andmedical treatment, are discussed with patients (and their families)in detail. They must understand that, although the percutaneousprocedure is more attractive than bypass surgery, it has importantlimitations, including the likelihood of restenosis and potentialfor incomplete revascularisation compared with surgery. Thepotential benefits of antianginal drug treatment and the need forrisk factor reduction should also be carefully explained.Clinical risk assessmentRelief of anginal symptoms is the principal clinical indicationfor percutaneous intervention, but we do not know whether theprocedure has the same prognostic benefit as bypass surgery.Angiographic features determined during initial assessmentrequire careful evaluation to determine the likely success of the Percutaneous coronary intervention in progress. Above the patient’s chest isprocedure and the risk of serious complications. the x ray imaging camera. Fluoroscopic images, electrocardiogram, and Until recently, the American College of Cardiology and haemodynamic data are viewed at eye level screens. All catheterisation laboratory operators wear lead protection covering body, thyroid, and eyes,American Heart Association classified anginal lesions into types and there is lead shielding between the primary operator and patient(and subtypes) A, B, or C based on the severity of lesioncharacteristics. Because of the ability of stents to overcomemany of the complications of percutaneous intervention, this New classification system of stenotic lesions (Americanclassification has now been superseded by one reflecting low, College of Cardiology and American Heart Association)moderate, and high risk. Successful percutaneous intervention depends on adequate Low risk Moderate risk High riskvisualisation of the target stenosis and its adjacent arterial Discrete ( < 10 mm) Tubular (10-20 mm) Diffuse ( > 20 mm)branches. Vessels beyond the stenosis may also be important Concentric Eccentricbecause of the potential for collateral flow and myocardial Readily accessible Proximal segment Proximal segmentsupport if the target vessel were to occlude abruptly. Factors moderately tortuous excessively tortuousthat adversely affect outcome include increasing age, comorbid Segment not angular Segment moderately Segment extremelydisease, unstable angina, pre-existing heart or renal failure, ( < 45°) angular (45°- < 90°) angular (>90°)previous myocardial infarction, diabetes, a large area of Smooth contour Irregular contourmyocardium at risk, degree of collaterisation, and multivessel Little or no Moderate or heavy calcification calcificationdisease. Occlusion not total Total occlusion Total occlusion < 3 months old > 3 months or bridgingPreparation for intervention collateral vessels Non-ostial OstialPatients must be fully informed of the purpose of the procedure No major side Bifurcated lesions Inability to protectas well as its risks and limitations before they are asked for their branch affected requiring double major side branchesconsent. The procedure must always be carried out (or directly guidewiressupervised) by experienced, high volume operators ( > 75 No thrombus Some thrombus Degenerated vein graftsprocedures a year) and institutions ( > 400 a year). with friable lesions. A sedative is often given before the procedure, as well asaspirin, clopidogrel, and the patient’s usual antianginal drugs.In very high risk cases an intra-aortic balloon pump may be Clinical indications for percutaneousused. A prophylactic temporary transvenous pacemaker wire coronary interventionmay be inserted in some patients with pre-existing, high grade x Stable angina (and positive stress test)conduction abnormality or those at high risk of developing it. x Unstable angina x Acute myocardial infarction x After myocardial infarctionThe procedure x After coronary artery bypass surgery (percutaneous intervention to native vessels,For an uncomplicated, single lesion, a percutaneous procedure arterial or venous conduits)may take as little as 30 minutes. However, the duration of the x High risk bypass surgeryprocedure and radiation exposure will vary according to x Elderly patientthenumber and complexity of the treated stenoses and vessels.8
  • 18. Percutaneous coronary intervention. II: The procedure As with coronary angiography, arterial access (usuallyfemoral but also brachial or radial) under local anaesthesia isrequired. A guide catheter is introduced and gently engaged atthe origin of the coronary artery. The proximal end of thecatheter is attached to a Y connector. One arm of thisconnector allows continuous monitoring of arterial bloodpressure. Dampening or “ventricularisation” of this arterialtracing may indicate reduced coronary flow because ofover-engagement of the guide catheter, catheter tip spasm, or apreviously unrecognised ostial lesion. The other arm has anadjustable seal, through which the operator can introduce theguidewire and balloon or stent catheter once the patient hasbeen given heparin as an anticoagulant. A glycoprotein IIb/IIIainhibitor, which substantially reduces ischaemic events during Equipment commonly used in percutaneous coronary interventionspercutaneous coronary intervention, may also be given. Visualised by means of fluoroscopy and intracoronaryinjections of contrast medium, a soft tipped, steerable guidewire A(usually 0.014" (0.36 mm) diameter) is passed down thecoronary artery, across the stenosis, and into a distal branch. Aballoon or stent catheter is then passed over the guidewire andpositioned at the stenosis. The stenosis may then be stenteddirectly or dilated before stenting. Additional balloon dilatation Bmay be necessary after deployment of a stent to ensure its fullexpansion. Balloon inflation inevitably stops coronary blood flow,which may induce angina. Patients usually tolerate this quitewell, especially if they have been warned beforehand. If it Cbecomes severe or prolonged, however, an intravenous opiatemay be given. Ischaemic electrocardiographic changes are oftenseen at this time, although they are usually transient and returnto baseline once the balloon is deflated (usually after 30-60seconds). During the procedure, it is important to talk to thepatient (who may be understandably apprehensive) to let him Dor her know what is happening, as this encourages a goodrapport and cooperation.Recovery Deployment of a balloon-mounted stent across stenotic lesion. Once the guide catheter is satisfactorily engaged,After the procedure the patient is transferred to a ward where the lesion is crossed with a guidewire and the balloon-mounted stent positioned to cover the lesion (A).close monitoring for signs of ischaemia and haemodynamic It may be necessary to pre-dilate a severe lesion with ainstability is available. If a femoral arterial sheath was used, it balloon to provide adequate passageway for the balloonmay be removed when the heparin effect has declined to an and stent. The balloon is inflated to expand the stent (B).acceptable level (according to unit protocols). Arterial sealing The balloon is then deflated (C) and withdrawn leaving the guidewire (D), which is also removed once thedevices have some advantages over manual compression: they operator is satisfied that a good result has been obtainedpermit immediate sheath removal and haemostasis, are morecomfortable for patients, and allow early mobilisation anddischarge. However, they are not widely used as they add Fconsiderably to the cost of the procedure. 6 After a few hours, the patient should be encouraged togradually increase mobility, and in uncomplicated casesdischarge is scheduled for the same or the next day. Beforedischarge, the arterial access site should be examined and thepatient advised to seek immediate medical advice if bleeding orchest pain (particularly at rest) occurs. Outpatient follow up and Example of adrug regimens are provided, as well as advice on modification femoral artery closure device.of risk factors and lifestyle. The Angio-Seal device creates a mechanical sealComplications and sequelae by sandwiching the arteriotomyComplications are substantially lower in centres where large B between annumbers of procedures are carried out by adequately trained anchor placedand experienced operators. Major complications are Femoral against the inneruncommon and include death (0.2% but higher in high risk artery arterial wall (A) and collagencases), acute myocardial infarction (1%) which may require A sponge (B), whichemergency coronary artery bypass surgery, embolic stroke both dissolve(0.5%), cardiac tamponade (0.5%), and systemic bleeding (0.5%). within 60-90 days 9
  • 19. ABC of Interventional Cardiology Minor complications are more common and include allergyto the contrast medium and nephropathy and complications ofthe access site (bleeding, haematoma, and pseudoaneurysm).Restenosis within a stentAlthough stents prevent restenosis from vascular recoil andremodelling, restenosis within the stent (known as “in-stentrestenosis”) due to neointimal proliferation does occur and isthe most important late sequel of the procedure. In-stentrestenosis is the Achilles’ heel of percutaneous revascularisationand develops within six months of stenting. Angiographic restenosis rates ( > 50% diameter stenosis)depend on several factors and are higher in smaller vessels,long and complex stenoses, and where there are coexistingconditions such as diabetes. Approximate rates of angiographicrestenosis after percutaneous angioplasty arex Angioplasty to de novo lesion in native artery—35%x Angioplasty and stent to de novo lesion in native artery—25% Focal in-stent restenosis. A 2.0 mm stent had been deployed six months earlier. After recurrence of angina, angiography showedx Angioplasty and stent to restenotic lesion in native artery—20% focal in-stent restenosis (arrow, top left). This was confirmed withx Angioplasty and stent to successfully recanalised chronic intravascular ultrasound (top right), which also revealed that thetotal occlusion—30% stent was underexpanded. The stent was further expanded with ax Angioplasty to de novo lesion in vein graft—60% balloon catheter, with a good angiographic result (arrow, bottom left) and an increased lumen diameter to 2.7 mm (bottom right)x Angioplasty and stent to de novo lesion in vein graft—30%. It should be noted that angiographically apparentrestenoses do not always lead to recurrent angina (clinicalrestenosis). In some patients only mild anginal symptoms recur, A Band these may be well controlled with antianginal drugs,thereby avoiding the need for further intervention. Stented artery with area Balloon angioplasty catheter Using repeat percutaneous angioplasty alone to re-dilate of in-stent restenosis inside stented arteryin{stent restenosis results in a high recurrence of restenosis(60%). Various other methods, such as removing restenotic C Dtissue by means of atherectomy or a laser device or re-dilatingwith a cutting balloon, are being evaluated. Another method is Radiation source train placed at Artery after balloon angioplastybrachytherapy, which uses a special intracoronary catheter to treatment site for < 5 minutes and vascular brachytherapydeliver a source of or radiation. It significantly reducesfurther in-stent restenosis, but it has limitations, including late Diagrammatic representation of the Novoste Beta Cath system used for vascular brachytherapy. Pre-dilatation of the in-stent restenosis with athrombosis and new restenosis at the edges of the radiation balloon catheter is usual and is followed by positioning of the radiationtreated segments, giving rise to a “candy wrapper” appearance. source train, containing strontium-90, at the site for less than 5 minutesThe cutting balloon catheter. The longitudinal cutting blades are exposed Angiogram showing late “candyonly during balloon inflation (top left). In this case (top right) a severe wrapper” edge effect (arrows)ostial in-stent restenosis in the right coronary artery (arrow) was dilated because of new restenosis at thewith a short cutting balloon (bottom left), and a good angiographic result edges of a segment treated bywas obtained (arrow, bottom right) brachytherapy10
  • 20. Percutaneous coronary intervention. II: The procedureDrug eluting, coated stentsCoated stents contain drugs that inhibit new tissue growthwithin the sub-intima and are a promising new option forpreventing or treating in-stent restenosis. Sirolimus (animmunosuppressant used to prevent renal rejection whichinhibits smooth muscle proliferation and reduces intimalthickening after vascular injury), paclitaxel (the activecomponent of the anticancer drug taxol), everolimus, ABT-578,and tacrolimus are all being studied, as are other agents.Although long term data and cost benefit analyses are not yetavailable, it seems probable that coated stents will be commonlyused in the near future. Top left: four months after two stents (yellow lines) were deployedOccupation and driving in the proximal and middle right coronary artery, severe diffuse in-stent restenosis has occurredDoctors may be asked to advise on whether a patient is “fit for with recurrent angina. Top right:work” or “recovered from an event” after percutaneous two sirolimus coated Cypher stentscoronary intervention. “Fitness” depends on clinical factors (red lines) were deployed within(level of symptoms, extent and severity of coronary disease, left the original stents. Bottom: after six months there was noventricular function, stress test result) and the nature of the recurrence of restenosis, and theoccupation, as well as statutory and non-statutory fitness 51 year old patient remainedrequirements. Advisory medical standards are in place for asymptomaticcertain occupations, such as in the armed forces and police,railwaymen, and professional divers. Statutory requirementscover the road, marine, and aviation industries and somerecreational pursuits such as driving and flying. Patients often ask when they may resume driving afterpercutaneous coronary intervention. In Britain, the Driver andVehicle Licensing Agency recommends that group 1 (privatemotor car) licence holders should stop driving when anginalsymptoms occur at rest or at the wheel. After percutaneouscoronary intervention, they should not drive for a week. Driversholding a group 2 licence (lorries or buses) will be disqualifiedfrom driving once the diagnosis of angina has been made, andfor at least six weeks after percutaneous coronary intervention.Re-licensing may be permitted provided the exercise testrequirement (satisfactory completion of nine minutes of theBruce protocol while not taking blockers) can be met andthere is no other disqualifying condition.The diagram of the Angio-Seal device is used with permission of St JudeMedical, Minnetonka, Minnesota, USA. The angiogram showing the “candywrapper” effect is reproduced with permission of R Waksman, WashingtonHospital Center, and Martin Dunitz, London. The incidence of restenosis is particularly high with percutaneousCompeting interests: None declared. revascularisation of small vessels. A small diseased diagonal artery (arrows, top left) in a 58 year old patient with limiting angina was stented with a sirolimus coated Cypher stent (red line, top right). After six months, no restenosis was present (left), and the patient remained asymptomaticFurther readingx Smith SC Jr, Dove JT, Jacobs AK, Kennedy JW, Kereiakes D, Kern x Almond DG. Coronary stenting I: intracoronary stents—form, MJ, et al. ACC/AHA guidelines of percutaneous coronary function future. In: Grech ED, Ramsdale DR, eds. Practical interventions (revision of the 1993 PTCA guidelines)—executive interventional cardiology. 2nd ed. London: Martin Dunitz, 2002:63-76 summary. A report of the American College of Cardiology/ x Waksman R. Management of restenosis through radiation therapy. American Heart Association Task Force on Practice Guidelines In: Grech ED, Ramsdale DR, eds. Practical interventional cardiology. (committee to revise the 1993 guidelines for percutaneous 2nd ed. London: Martin Dunitz, 2002:295-305 transluminal coronary angioplasty). J Am Coll Cardiol 2001;37: x Kimmel SE, Berlin JA, Laskey WK. The relationship between 2215{39 coronary angioplasty procedure volume and major complications.x Morice MC, Serruys PW, Sousa JE, Fajadet J, Ban Hayashi E, Perin JAMA 1995;274:1137-42 M, et al. A randomized comparison of a sirolimus-eluting stent with x Rensing BJ, Vos J, Smits PC, Foley DP, van den Brand MJ, van der a standard stent for coronary revascularization. N Engl J Med Giessen WJ, et al. Coronary restenosis elimination with a sirolimus 2002;346:1773-80 eluting stent. Eur Heart J 2001;22:2125-30 11
  • 21. 4 Chronic stable angina: treatment optionsLaurence O’Toole, Ever D GrechIn patients with chronic stable angina, the factors influencingthe choice of coronary revascularisation therapy (percutaneous Major factors influencing risks and benefits of coronarycoronary intervention or coronary artery bypass surgery) are revascularisationvaried and complex. The severity of symptoms, lifestyle, extent x Advanced age x Multiple coronary vessels affected x Female x Coexisting valve diseaseof objective ischaemia, and underlying risks must be weighed x Severe angina x Impaired left ventricular functionagainst the benefits of revascularisation and the patient’s x Smoking x Impaired renal functionpreference, as well as local availability and expertise. Evidence x Diabetes x Cerebrovascular or peripheral vascular diseasefrom randomised trials and large revascularisation registers can x Obesity x Recent acute coronary syndromeguide these decisions, but the past decade has seen rapid x Hypertension x Chronic obstructive airways diseasechange in medical treatment, bypass surgery, and percutaneousintervention. Therefore, thought must be given to whether olderdata still apply to contemporary practice. Patients with chronic stable angina have an average annualmortality of 2-3%, only twice that of age matched controls, andthis relatively benign prognosis is an important considerationwhen determining the merits of revascularisation treatment. Left internal Saphenous mammary vein graftCertain patients, however, are at much higher risk. Predictors artery withinclude poor exercise capacity with easily inducible ischaemia pedicleor a poor haemodynamic response to exercise, angina of recentonset, previous myocardial infarction, impaired left ventricularfunction, and the number of coronary vessels with significantstenoses, especially when disease affects the left main stem orproximal left anterior descending artery. Although the potentialbenefits of revascularisation must be weighed against adversefactors, those most at risk may have the most to gain.Treatment strategiesMedical treatmentAnti-ischaemic drugs improve symptoms and quality of life, buthave not been shown to reduce mortality or myocardialinfarction. blockers may improve survival in hypertension, inheart failure, and after myocardial infarction, and so are Top: Diagrams of saphenous vein and left internal mammary artery grafts for coronary artery bypass surgery. Bottom: Three completed grafts—(1) leftconsidered by many to be first line treatment. Nicorandil has internal mammary artery (LIMA) to left anterior descending artery (LAD),recently been shown to reduce ischaemic events and need for and saphenous vein grafts (SVG) to (2) diagonal artery (DG) and (3) obtusehospital admission. marginal artery (OM) Trials comparing medical treatment with revascularisationpredate the widespread use of antiplatelet and cholesterollowering drugs. These drugs reduce risk, both in patients Risk score for assessing probable mortality from bypasstreated with drugs only and in those undergoing surgery in patients with chronic stable anginarevascularisation, and so may have altered the risk-benefit ratio Risk factor Weighted scorefor a particular revascularisation strategy in some patients. Age > 60 Score 1 for every 5 years over Female sex 1Coronary artery bypass graft surgery Chronic obstructive pulmonary disease 1Coronary artery bypass surgery involves the placement of grafts Extracardiac arteriopathy 2to bypass stenosed native coronary arteries, while maintaining Neurological dysfunction 2cerebral and peripheral circulation by cardiopulmonary bypass. Previous cardiac surgery 3The grafts are usually saphenous veins or arteries (principally Serum creatinine > 200 mol/l 2the left internal mammary artery). Reduced left ventricular ejection fraction 1 for 30-50% Operative mortality is generally 1-3% but may be much 3 for < 30% Myocardial infarction in past 90 days 2higher in certain subsets of patients. Scoring systems can Pulmonary artery systolic pressure > 60 mm Hg 2predict operative mortality based on clinical, investigational, and Major cardiac procedure as well as bypass surgery 2operative factors. Important developments that have occurred Emergency operation 2since trials of bypass surgery versus medical treatment were x Total score <2 predicts < 1% operative mortalityconducted include increased use of arterial grafts (which have x Total score of 3-5 predicts 3% operative mortalitymuch greater longevity than venous grafts), surgery without x Total score >6 predicts > 10% operative mortalityextracorporeal circulation (“off-pump” bypass), and minimal A more detailed assessment with logistic analysis is available at www.euroscore.org andaccess surgery. is recommended for assessing high risk patients12
  • 22. Chronic stable angina: treatment optionsPercutaneous coronary intervention Subgroup analysis of mortality benefit from coronary arteryThe main advantages of percutaneous intervention over bypass bypass surgery compared with medical treatment at 10 yearssurgery are the avoidance of the risks of general anaesthesia, after randomisation for patients with chronic stable anginauncomfortable sternotomy and saphenous wounds, andcomplications of major surgery (infections and pulmonary Subgroup Mean (1.96 SE) increased P value ofemboli). Only an overnight hospital stay is necessary (and many survival time (months) differenceprocedures can be performed as day cases), and the procedure Vessel disease:can be easily repeated. The mortality is low (0.2%), and the most 1 or 2 vessels 1.8 (3.0) 0.25serious late complication is restenosis. 3 vessels 5.7 (3.6) 0.001 Patient suitability is primarily determined by technical factors. Left main stem 19.3 (13.7) 0.005A focal stenosis on a straight artery without proximal vessel Left ventricular function:tortuousness or involvement of major side branches is ideal for Normal 2.3 (2.4) 0.06percutaneous intervention. Long, heavily calcified stenoses in Abnormal 10.6 (6.1) < 0.001tortuous vessels or at bifurcations and chronic total occlusions are Exercise test:less suitable. This must be borne in mind when interpreting data Normal 3.3 (4.4) 0.14from trials of percutaneous intervention and bypass surgery, as Abnormal 5.1 (3.3) 0.002only a minority of patients were suitable for both procedures. Severity of angina:Nowadays, more and more patients undergo percutaneous CCS class 0, I, II 3.3 (2.7) 0.02intervention, and referral rates for bypass surgery are falling. CCS class III, IV 7.3 (4.8) 0.002 CCS=Canadian Cardiovascular SocietyComparative studies ofrevascularisation strategiesCoronary artery bypass surgery versus medical treatmentIn a meta-analysis of seven trials comparing bypass surgery withmedical treatment, surgery conferred a survival advantage inpatients with severe left main stem coronary disease, threevessel disease, or two vessel disease with severely affectedproximal left anterior descending artery. The survival gain wasmore pronounced in patients with left ventricular dysfunctionor a strongly positive exercise test. However, only 10% of trialpatients received an internal mammary artery graft, only 25%received antiplatelet drugs, and the benefit of lipid loweringdrugs on long term graft patency was not appreciated whenthese studies were carried out. Furthermore, 40% of themedically treated patients underwent bypass surgery during 10years of follow up. Thus, these data may underestimate thebenefits of surgery compared with medical treatment alone. In lower risk patients bypass surgery is indicated only forsymptom relief and to improve quality of life when medicaltreatment has failed. Surgery does this effectively, with 95% ofpatients gaining immediate relief from angina and 75%remaining free from angina after five years. Unfortunately, Left: Angiogram of a 10 year old diseased venous graft to the obtusevenous grafts have a median life span of only seven years, and marginal artery showing proximal aneurysmal dilatation (A) and severeafter 15 years only 15% of patients are free from recurrent stenosis in middle segment (B). Right: Removal of this graft after repeat bypass surgery shows its gross appearance (graft longitudinally opened inangina or death or myocardial infarction. However, the right image), with atherosclerosis in a thin walled aneurysm and a smallincreased use of internal mammary artery grafts, which have residual lumenexcellent long term patency (85% at 10 years), has increasedpostoperative survival and reduced long term symptoms.Old saphenous vein grafts may contain large amounts of necrotic clotted debris, friable laminated thrombus, and ulcerated atheromatous plaque and areunattractive for percutaneous intervention because of the high risk of distal embolisation. However, distal embolisation protection devices such as theFilterWire EX (far right) reduce this risk by trapping any material released. Such a device (far left, B) is positioned in the distal segment of a subtotallyoccluded saphenous vein graft of the left anterior descending artery (A) before it is dilated and stented (inner left, C) to restore blood flow (inner right) 13
  • 23. ABC of Interventional CardiologyPercutaneous coronary intervention versus medicaltreatmentMost percutaneous procedures are undertaken to treat single Coronary angiogramvessel or two vessel disease, but few randomised controlled trials showing a severehave compared percutaneous intervention with medical focal stenosis (arrow)treatment. These showed that patients undergoing the in a large oblique marginal branch ofpercutaneous procedure derived greater angina relief and took the left circumflexless drugs but required more subsequent procedures and had artery (LCx), suitablemore complications (including non-fatal myocardial infarction), for percutaneouswith no mortality difference. Patients with few symptoms did coronary intervention. The leftnot derive benefit. Therefore, percutaneous intervention is anterior descendingsuitable for low risk patients with one or two vessel disease and artery (LAD) has nopoor symptom control with drugs, at a cost of a slightly higher important diseaserisk of non-fatal myocardial infarction. However, the proceduremay not be indicated if symptoms are well controlled.Percutaneous intervention versus bypass surgerySingle vessel diseaseIn a meta-analysis by Pocock et al percutaneous intervention inpatients with single vessel disease resulted in mortality similar tothat found with bypass surgery (3.7% v 3.1% respectively) but ahigher rate of non-fatal myocardial infarction (10.1% v 6.1%,P=0.04). Angina was well treated in both groups, but persistenceof symptoms was slightly higher with percutaneousintervention. Rates of repeat revascularisation were muchhigher with percutaneous intervention than bypass surgery.Multivessel disease Coronary angiograms of 70 yearSince comparative trials could recruit only those patients who old woman with limiting angina.were suitable for either revascularisation strategy, only 3-7% of There were severe stenosesscreened patients were included. These were predominantly (arrows) in the proximal and“low risk” patients with two vessel disease and preserved left middle left anterior descending artery (LAD, top) and in the distalventricular function—patients in whom bypass surgery has not right coronary artery (RCA, left).been shown to improve survival—and thus it is unlikely that a Because of the focal nature ofpositive effect in favour of percutaneous intervention would these lesions, percutaneoushave been detected. The generally benign prognosis of chronic coronary intervention was the preferred optionstable angina means that much larger trials would have beenrequired to show significant differences in mortality. A meta-analysis of data available to the end of 2000revealed similar rates of death and myocardial infarction withboth procedures, but repeat revascularisation rates were higherwith percutaneous intervention. The prevalence of appreciableangina was greater with percutaneous intervention at one year,but this difference disappeared at three years. The nature of percutaneous coronary intervention haschanged considerably over the past 10 years, with importantdevelopments including stenting and improved antiplateletdrugs. The integrated use of these treatments clearly improvesoutcomes, but almost all of the revascularisation trials predatethese developments. A more recent trial comparing percutaneous interventionand stenting with bypass surgery in multivessel diseaseconfirmed similar rates of death, myocardial infarction, andstroke at one year, with much lower rates of repeatrevascularisation after percutaneous intervention compared Coronary angiograms of awith earlier trials. There was also a cost benefit of nearly $3000 69 year old man with limiting angina and(£1875) per patient associated with percutaneous intervention exertional breathlessness.at 12 months. The recent introduction of drug eluting (coated) There was severe proximalstents, which seem to reduce substantially the problem of disease (arrows) of the leftrestenosis, is likely to extend the use of percutaneous anterior descending (LAD) and left circumflex arteriesintervention in multivessel disease over the next few years. (LCx) (top) and occlusion of the right coronary artery (RCA, left). The patient wasDiabetes referred for coronary arteryBypass surgery confers a survival advantage in symptomatic bypass surgery on prognosticdiabetic patients with multivessel disease The BARI trial and symptomatic grounds14
  • 24. Chronic stable angina: treatment optionsrevealed a significant difference in five year mortality (21% with Names of trialspercutaneous intervention v 6% with bypass surgery). Similartrends have been found in other large trials. However, the x BARI—Bypass angioplasty revascularisation investigation x SIRIUS—Sirolimus-coated velocity stent in treatment of patientsrecent RAVEL and SIRIUS studies, in which the sirolimus with de novo coronary artery lesions trialeluting Cypher stent was compared with the same stent x RAVEL—Randomised study with the sirolimus-eluting velocityuncoated, showed a remarkable reduction in restenosis rates balloon-expandable stent in the treatment of patients with de novowithin the stented segments in diabetic patients (0% v 42% and native coronary artery lesions18% v 51% respectively). Ongoing trials will investigate thisissue further. Emerging treatment options for refractory anginaOther study dataLarge registries of outcomes in patients undergoing x Drugs—Analgesics, statins, angiotensin converting enzyme inhibitors, antiplatelet drugsrevascularisation have the advantage of including all patients x Neurostimulation—Interruption or modification of afferentrather than the highly selected groups included in randomised nociceptive signals: transcutaneous electric nerve stimulationtrials. The registry data seem to agree with those from (TENS), spinal cord stimulation (SCS)randomised trials: patients with more extensive disease fare x Enhanced external counterpulsation—Non-invasive pneumatic legbetter with bypass surgery, whereas percutaneous intervention compression, improving coronary perfusion and decreasing leftis preferable in focal coronary artery disease. ventricular afterload x Laser revascularisation—Small myocardial channels created by laserAn unusual observation is that patients screened and beams: transmyocardial laser revascularisation (TMLR),considered suitable for inclusion in a trial fared slightly better if percutaneous transmyocardial laser revascularisation (PTMLR)they refused to participate than did those who enrolled. The x Therapeutic angiogenesis—Cytokines, vascular endothelial growthheterogeneous nature of coronary disease means that certain factor, and fibroblast growth factor injected into ischaemicpatient subsets will probably benefit more from one treatment myocardium, or adenoviral vector for gene transport to promotethan another. The better outcome in the patients who were neovascularisationsuitable but not randomised may indicate that cardiologists and x Percutaneous in situ coronary venous arterialisation (PICVA)—Flow redirection from diseased coronary artery into adjacent coronarysurgeons recognise which patients will benefit more from a vein, causing arterialisation of the vein and retroperfusion intoparticular strategy—subtleties that are lost in the randomisation ischaemic myocardiumprocess of controlled trials. x Percutaneous in situ coronary artery bypass (PICAB)—Flow redirection from diseased artery into adjacent coronary vein and then rerouted back into the artery after the lesionRefractory coronary artery disease x Heart transplantation—May be considered when all alternative treatments have failedIncreasing numbers of patients with coronary artery diseasehave angina that is unresponsive to both maximal drugtreatment and revascularisation techniques. Many will have Further readingalready undergone multiple percutaneous interventions or x Yusuf S, Zucker D, Peduzzi P, Fisher LD, Takaro T, Kennedy JW, et al.bypass surgery procedures, or have diffuse and distal coronary Effect of coronary artery bypass graft surgery on survival; overviewartery disease. In addition to functional limitations, their of 10-year results from randomised trials by the Coronary Arteryprognosis may be poor because of impaired ventricular Bypass Graft Surgery Trialists Collaboration. Lancet 1994; 344:function. Emerging treatments may provide alternative 563-70symptomatic improvement for some patients. There is also x Pocock SJ, Henderson RA, Rickards AF, Hampton JR, King SB 3rd,renewed interest in the potential anti-ischaemic effects of Hamm CW, et al. Meta-analysis of randomised trials comparingangiotensin converting enzyme inhibitors and the plaque coronary angioplasty with bypass surgery. Lancet 1995;345:1184-9 x Raco DL, Yusuf S. Overview of randomised trials of percutaneousstabilising properties of statins. coronary intervention: comparison with medical and surgical therapy for chronic coronary artery disease. In: Grech ED,The picture showing three completed coronary artery bypass grafts and Ramsdale DR, eds. Practical interventional cardiology. 2nd ed.the pictures of a 10 year old diseased venous graft to the obtuse marginal London: Martin Dunitz, 2002:263-77artery were provided by G Singh, consultant cardiothoracic surgeon, x Serruys PW, Unger F, Sousa JE, Jatene A, Bonnier HJ, SchonbergerHeath Sciences Centre, Winnipeg, E Pascoe, consultant cardiothoracic JP, et al for the Arterial Revascularisation Therapies Study (ARTS)surgeon, St Boniface Hospital, Winnipeg, and J Scatliff, consultant Group. Comparison of coronary-artery bypass surgery and stentinganaesthetist, St Boniface Hospital. The picture of the FilterWire EX distal for multivessel disease. N Engl J Med 2001;344:1117-24embolisation protection device was provided by Boston Scientific x Kim MC, Kini A, Sharma SK. Refractory angina pectoris.Corporation, Minneapolis, USA. Mechanisms and therapeutic options. J Am Coll Cardiol 2002;39:Competing interests: None declared. 923-34 x Morice M-C, Serruys PW, Sousa JE, Fajadet J, Ban Hayashi E, Perin M, et al. A randomized comparison of a sirolimus-eluting stent with a standard stent for coronary revascularization. N Engl J Med 2002;346:1773-80 x Scottish Intercollegiate Guidelines Network. Coronary revascularisation in the management of stable angina pectoris. Edinburgh: SIGN, 1998 (SIGN Publication No 32) 15
  • 25. 5 Acute coronary syndrome: unstable angina andnon-ST segment elevation myocardial infarctionEver D Grech, David R RamsdaleThe term acute coronary syndrome refers to a range of acutemyocardial ischaemic states. It encompasses unstable angina, Plaque disruption or erosionnon-ST segment elevation myocardial infarction (ST segmentelevation generally absent), and ST segment elevation infarction Thrombus formation with or without embolisation(persistent ST segment elevation usually present). This articlewill focus on the role of percutaneous coronary intervention in Acute cardiac ischaemiathe management of unstable angina and non-ST segmentelevation myocardial infarction; the next article will address therole of percutaneous intervention in ST segment elevation No ST segment elevation ST segment elevationinfarction. Although there is no universally accepted definition ofunstable angina, it has been described as a clinical syndrome Markers of myocardial Elevated markers of Elevated markers of necrosis not elevated myocardial necrosis myocardial necrosisbetween stable angina and acute myocardial infarction. Thisbroad definition encompasses many patients presenting withvarying histories and reflects the complex pathophysiological Non-ST segment elevation ST segment elevation Unstable myocardial infarction myocardial infarctionmechanisms operating at different times and with different angina (Q waves usually absent) (Q waves usually present)outcomes. Three main presentations have been described—angina at rest, new onset angina, and increasing angina. Acute coronary syndromes Spectrum of acute coronary syndromes according to electrocardiographicPathogenesis and biochemical markers of myocardial necrosis (troponin T, troponin I, and creatine kinase MB), in patients presenting with acute cardiac chest painThe process central to the initiation of an acute coronarysyndrome is disruption of an atheromatous plaque. Fissuring orrupture of these plaques—and consequent exposure of core Three main presentations of unstable anginaconstituents such as lipid, smooth muscle, and foam cells—leadsto the local generation of thrombin and deposition of fibrin. x Angina at rest—Also prolonged, usually > 20 minutes x Angina of new onset—At least CCS class III in severityThis in turn promotes platelet aggregation and adhesion and x Angina increasing—Previously diagnosed angina that has becomethe formation of intracoronary thrombus. more frequent, longer in duration, or lower in threshold (change in Unstable angina and non-ST segment elevation myocardial severity by >1 CCS class to at least CCS class III)infarction are generally associated with white, platelet-rich, and CCS=Canadian Cardiovascular Societyonly partially occlusive thrombus. Microthrombi can detach andembolise downstream, causing myocardial ischaemia andinfarction. In contrast, ST segment elevation (or Q wave)myocardial infarction has red, fibrin-rich, and more stable Platelet-rich thrombusocclusive thrombus. Activated platelets KeyEpidemiology Collagen Intima Dividing smoothUnstable angina and non-ST segment elevation myocardial muscle cellinfarction account for about 2.5 million hospital admissions Lumen Oxidised low Media density lipoproteinworldwide and are a major cause of mortality and morbidity in LysosomesWestern countries. The prognosis is substantially worse than forchronic stable angina. In-hospital death and re-infarction affect Adventitia5-10%. Despite optimal treatment with anti-ischaemic andantithrombotic drugs, death and recurrent myocardialinfarction occur in another 5-10% of patients in the month after Diagram of an unstable plaque with superimposed luminal thrombusan acute episode. Several studies indicate that these patientsmay have a higher long term risk of death and myocardialinfarction than do patients with ST segment elevation.Diagnosis Distal embolisation of a platelet-rich thrombus causingUnstable angina and non-ST segment elevation myocardial occlusion of intramyocardialinfarction are closely related conditions with clinical arteriole (arrow). Such an event may result inpresentations that may be indistinguishable. Their distinction micro-infarction and elevationdepends on whether the ischaemia is severe enough to cause of markers of myocardialmyocardial damage and the release of detectable quantities of necrosis16
  • 26. Acute coronary syndrome: unstable angina and non-ST segment elevation myocardial infarctionmarkers of myocyte necrosis. Cardiac troponin I and T are thepreferred markers as they are more specific and reliable than I aVR V1 V4creatine kinase or its isoenzyme creatine kinase MB. An electrocardiogram may be normal or show minornon{specific changes, ST segment depression, T wave inversion,bundle branch block, or transient ST segment elevation that II aVL V2 V5resolves spontaneously or after nitrate is given. Physicalexamination may exclude important differential diagnoses suchas pleuritis, pericarditis, or pneumothorax, as well as revealingevidence of ventricular failure and haemodynamic instability. III aVF V3 V6Management IIManagement has evolved considerably over the past decade. Asplatelet aggregation and thrombus formation play a key role inacute coronary syndrome, recent advances in treatment (such asthe glycoprotein IIb/IIIa inhibitors, low molecular weightheparin, and clopidogrel) and the safer and more widespreaduse of percutaneous coronary intervention have raisedquestions about optimal management. As patients with unstable angina or non-ST segmentelevation myocardial infarction represent a heterogeneousgroup with a wide spectrum of clinical outcomes, tailoringtreatment to match risk not only ensures that patients who willbenefit the most receive appropriate treatment, but also avoidspotentially hazardous treatment in those with a good prognosis.Therefore, an accurate diagnosis and estimation of the risk ofadverse outcome are prerequisites to selecting the most Electrocardiogram of a 48 year old woman with unstable angina (top). Noteappropriate treatment. This should begin in the emergency the acute ischaemic changes in leads V1 to V5 (arrows). Coronarydepartment and continue throughout the hospital admission. angiography revealed a severe mid-left anterior descending coronary artery stenosis (arrow, bottom left), which was successfully stented (bottom right)Ideally, all patients should be assessed by a cardiologist on theday of presentation.Medical treatmentMedical treatment includes bed rest, oxygen, opiate analgesicsto relieve pain, and anti-ischaemic and antithrombotic drugs.These should be started at once on admission and continued inthose with probable or confirmed unstable angina or non-STsegment elevation myocardial infarction. Anti-ischaemic drugsinclude intravenous, oral, or buccal nitroglycerin, blockers,and calcium antagonists. Antithrombotic drugs include aspirin,clopidogrel, intravenous unfractionated heparin or lowmolecular weight heparin, and glycoprotein IIb/IIIa inhibitors. Right coronary arteryConservative versus early invasive strategy angiogram in patient with non-ST segment elevation“Conservative” treatment involves intensive medical myocardial infarction (topmanagement, followed by risk stratification by non-invasive left), showing hazymeans (usually by stress testing) to identify patients who may appearance of intraluminalneed coronary angiography. This approach is based on the thrombus overlying a severe stenosis (arrow). Abciximabresults of two randomised trials (TIMI IIIB and VANQWISH), was given before directwhich showed no improvement in outcome when an “early stenting (top right), withinvasive” strategy was used routinely, compared with a selective good angiographic outcome (bottom)approach. These findings generated much controversy and have been Names of trialssuperseded by more recent randomised trials (FRISC II, x TIMI IIIB—Thrombolysis in myocardial infarction IIIBTACTICS-TIMI 18, and RITA 3), which have taken advantage of x VANQWISH—Veterans affairs non-Q-wave infarction strategies inthe benefits of glycoprotein IIb/IIIa inhibitors and stents. All hospitalthree studies showed that an early invasive strategy x GUSTO IV ACS—Global use of strategies to open occluded(percutaneous coronary intervention or coronary artery bypass arteries-IV in acute coronary syndromessurgery) produced a better outcome than non-invasive x RITA 3—Randomised intervention treatment of anginamanagement. TACTICS-TIMI 18 also showed that the benefit x FRISC II—Fast revascularisation during instability in coronary artery diseaseof early invasive treatment was greatest in higher risk patients x TACTICS-TIMI 18—Treat angina with Aggrastat and determine costwith raised plasma concentrations of troponin T, whereas the of therapy with an invasive or conservative strategy-thrombolysis inoutcomes for lower risk patients were similar with early invasive myocardial infarctionand non-invasive management. 17
  • 27. ABC of Interventional CardiologyIdentifying higher risk patients The seven variables for the TIMI risk scoreIdentifying patients at higher risk of death, myocardial infarction,and recurrent ischaemia allows aggressive antithrombotic x Age >65 years x >3 risk factors for coronary artery diseasetreatment and early coronary angiography to be targeted to those x >50% coronary stenosis on angiographywho will benefit. The initial diagnosis is made on the basis of a x ST segment change > 0.5 mmpatient’s history, electrocardiography, and the presence of x >2 anginal episodes in 24 hours before presentationelevated plasma concentrations of biochemical markers. The x Elevated serum concentration of cardiac markerssame information is used to assess the risk of an adverse x Use of aspirin in 7 days before presentationoutcome. It should be emphasised that risk assessment is acontinuous process. Low risk Higher risk 20 Death or myocardial infarction at 14 days (%)The TIMI risk scoreAttempts have been made to formulate clinical factors into a 15user friendly model. Notably, Antman and colleagues identifiedseven independent prognostic risk factors for early death and 10myocardial infarction. Assigning a value of 1 for each risk factorpresent provides a simple scoring system for estimating risk, the 5TIMI risk score. It has the advantage of being easy to calculate 0and has broad applicability in the early assessment of patients. 0 or 1 2 3 4 5 6 or 7 Applying this score to the results in the TACTICS-TIMI 18 No of TIMI risk factors presentstudy indicated that patients with a TIMI risk score of >3benefited significantly from an early invasive strategy, whereas Rates of death from all causes and non-fatal myocardial infarction at 14those with a score of <2 did not. Therefore, those with an initial days, by TIMI risk score. Note sharp rate increase when score >3TIMI score of >3 should be considered for early angiography(ideally within 24 hours), with a view to revascularisation by Unstable angina or non-ST segment elevation myocardial infarctionpercutaneous intervention or bypass surgery. In addition, anypatient with an elevated plasma concentration of troponin TIMI risk assessment on presentationmarker, ST segment changes, or haemodynamic instability (aspirin, clopidogrel, heparin, nitrates, β blockers)should also undergo early angiography. Low risk Higher riskConclusion (TIMI risk score 0-2, negative troponin test) (TIMI risk score >3, positive troponin test, dynamic ST changes,The diagnosis of unstable angina or non-ST segment elevation or haemodynamically unstable)myocardial infarction demands urgent hospital admission and Conservative managementcoronary monitoring. A clinical history and examination, 12 Invasive managementlead electrocardiography, and measurement of troponin Stress testconcentration are the essential diagnostic tools. Bed rest, Possible glycoprotein IIb/IIIa inhibitoraspirin, clopidogrel, heparin, antianginal drugs, and opiateanalgesics are the mainstay of initial treatment. Negative Positive Coronary angiography Early risk stratification will help identify high risk patients,who may require early treatment with glycoprotein IIb/IIIainhibitors, angiography, and coronary revascularisation. Those Discharge Percutaneous coronary Coronarydeemed suitable for percutaneous intervention should receive a Medical intervention plus artery bypass treatmentglycoprotein IIb/IIIa inhibitor and stenting as appropriate. glycoprotein IIb/IIIa inhibitor surgeryThere seems to be little merit in prolonged stabilisation ofpatients before percutaneous intervention, and an early invasive Simplified management pathway for patients with unstable angina orstrategy is generally preferable to a conservative one except for non-ST segment elevation myocardial infarctionpatients at low risk of further cardiac events. This approach willshorten hospital stays, improve acute and long term outcomes, Further readingand reduce the need for subsequent intervention. x Braunwald E, Antman EM, Beasley JW, Califf RM, Cheitlin MD, In the longer term, aggressive modification of risk factors is Hochman JS, et al. ACC/AHA 2002 guideline update for thewarranted. Smoking should be strongly discouraged, and statins management of patients with unstable angina and non-ST-segmentshould be used to lower blood lipid levels. Long term treatment elevation myocardial infarction: a report of the American Collegewith aspirin, clopidogrel (especially after stenting), blockers, of Cardiology/American Heart Association task force on practiceangiotensin converting enzyme inhibitors, and antihypertensive guidelines. J Am Coll Cardiol 2002;40:1366-74 x Bertrand ME, Simoons ML, Fox KA, Wallentin LC, Hamm CW,drugs should also be considered. Anti-ischaemic drugs may be McFadden E, et al. Management of acute coronary syndromes:stopped when ischaemia provocation tests are negative. acute coronary syndromes without persistent ST segment elevation. Recommendations of the Task Force of the European Society ofThe picture of a microthrombus occluding an intramyocardial arteriole Cardiology. Eur Heart J 2000;21:1406-32was provided by K MacDonald, consultant histopathologist, St Boniface x Antman EM, Cohen M, Bernink PJ, McCabe CH, Horacek T,Hospital, Winnipeg. Papuchis G, et al. The TIMI risk score for unstable angina/non-ST elevation MI: a method for prognostication and therapeuticCompeting interests: None declared. decision making. JAMA 2000;284:835-42 x Ramsdale DR, Grech ED. Percutaneous coronary intervention unstable angina and non-Q-wave myocardial infarction. In: Grech ED, Ramsdale DR, eds. Practical interventional cardiology. 2nd ed. London: Martin Dunitz, 2002:165-8718
  • 28. 6 Acute coronary syndrome: ST segment elevationmyocardial infarctionEver D Grech, David R RamsdaleAcute ST segment elevation myocardial infarction usuallyoccurs when thrombus forms on a ruptured atheromatousplaque and occludes an epicardial coronary artery. Patientsurvival depends on several factors, the most important beingrestoration of brisk antegrade coronary flow, the time taken toachieve this, and the sustained patency of the affected artery.RecanalisationThere are two main methods of re-opening an occluded artery: Histological appearance of aadministering a thrombolytic agent or primary percutaneous ruptured atheromatous plaquetransluminal coronary angioplasty. (bottom arrow) and occlusive Although thrombolysis is the commonest form of treatment thrombus (top arrow) resulting in acute myocardial infarctionfor acute myocardial infarction, it has important limitations: arate of recanalisation (restoring normal flow) in 90 minutes ofonly 55% with streptokinase or 60% with accelerated alteplase; Acute ST segment elevationa 5-15% risk of early or late reocclusion leading to acute myocardial infarctionmyocardial infarction, worsening ventricular function, or death;a 1-2% risk of intracranial haemorrhage, with 40% mortality;and 15-20% of patients with a contraindication to thrombolysis. Thrombolytic treatment Primary angioplasty Primary angioplasty (also called direct angioplasty)mechanically disrupts the occlusive thrombus and compressesthe underlying stenosis, rapidly restoring blood flow. It offers a Infarct artery recanalised, Infarct artery not recanalised but significant residual stenosissuperior alternative to thrombolysis in the immediate treatmentof ST segment elevation myocardial infarction. This differs from Rescue angioplasty Adjunctive angioplastysequential angioplasty, when angioplasty is performed after (1-2 hours after failed thrombolysis) Deferred angioplastythrombolysis. After early trials of thrombolytic drugs, there was Elective angioplasty (if continued ischaemia) (1-7 days after thrombolysis)much interest in “adjunctive” angioplasty (angioplasty used as asupplement to successful thrombolysis) as this was expected to Methods of recanalisation for acute myocardial infarctionreduce recurrent ischaemia and re-infarction. Later studies,however, not only failed to show any advantage, but foundhigher rates of major haemorrhage and emergency bypass Comparison of methods of recanalisationsurgery. In contrast, “rescue” (also known as “salvage”) Rescue Primaryangioplasty, which is performed if thrombolysis fails to restore Thrombolysis angioplasty angioplastypatency after one to two hours, may confer benefit. Time from admission 1-3 hours Time to start of 20-60 to recanalisation after start of thrombolysis minutes thrombolysis plus 2 hoursPros and cons of primary angioplasty Recanalisation with 55-60% 85% 95% brisk antegrade flowAdvantages Systemic fibrinolysis +++ +++ −Large randomised studies have shown that thrombolysis Staff and catheter − + +++significantly reduces mortality compared with placebo, and this laboratory “burden”effect is maintained long term. Primary angioplasty confers Cost of procedure + +++ +++ Mortality Cerebrovascular events Re-infarction 15 3 8 Incidence (%) P<0.0001 P<0.0001 P=0.0004 6 Effects of treatment with placebo, thrombolytic P=0.0002 10 2 drugs, or primary percutaneous coronary intervention (PCI) on mortality, incidence of P<0.0001 4 cerebrovascular events, and incidence of 5 1 non-fatal re-infarction after acute myocardial 2 infarction in randomised studies. Of the 1% incidence of cerebrovascular events in patients undergoing primary percutaneous intervention, 0 0 0 9 studies 23 studies 9 studies 23 studies 23 studies only 0.05% were haemorrhagic. In contrast (n=58 600)* (n=7437)✝ (n=58 600)* (n=6271)✝ (n=6497)✝ patients receiving thrombolytic drugs had a 1% * FTT Collaborative Group, Lancet 1994;343:311-22 Controls Thrombolytic PCI incidence of haemorrhagic cerebrovascular ✝ Keeley et al, Lancet 2003;361:13-20 events (P<0.0001) and an overall 2% incidence of cerebrovascular events (P=0.0004) 19
  • 29. ABC of Interventional Cardiologyextra benefits in terms of substantial reductions in rates ofdeath, cerebrovascular events, and re-infarction. The information provided by immediate coronary Severe distal left mainangiography is valuable in determining subsequent stem stenosis (arrow 1)management. Patients with severe three vessel disease, severe and partially occludedleft main coronary artery stenosis, or occluded vessels mid-left anteriorunsuitable for angioplasty can be referred for bypass surgery. descending artery due to thrombus (arrow 2). InConversely, patients whose arteries are found to have view of the severity of thespontaneously recanalised or who have an insignificant infarct lesion salvage angioplastyrelated artery may be selected for medical treatment, and thus was contraindicated. An intra-aortic balloonavoid unnecessary thrombolytic treatment. pump was used to augment blood pressureDisadvantages and coronary flow before successful bypass surgeryThe morbidity and mortality associated with primaryangioplasty is operator dependent, varying with the skill andexperience of the interventionist, and it should be consideredonly for patients presenting early ( < 12 hours after acutemyocardial infarction). Pros and cons of primary angioplasty* compared with Procedural complications are more common than with thrombolysiselective angioplasty for chronic angina, and, even though it is Advantagesusual to deal only with the occluded vessel, procedures may be x High patency rates ( > 90%) with brisk, antegrade flowprolonged. Ventricular arrhythmias are not unusual on x Lower mortalityrecanalisation, but these generally occur while the patient is still x Better residual left ventricular function x More rapid electrocardiographic normalisationin the catheterisation laboratory and can be promptly treated by x Less recurrent ischaemia (angina, reinfarction, exercise inducedintravenous drugs or electrical cardioversion. Right coronary ischaemia)artery procedures are often associated with sinus arrest, x No systemic fibrinolysis, therefore bleeding problems avoidedatrioventricular block, idioventricular rhythm, and severe x Improved risk stratification by angiography with identification ofhypotension. Up to 5% of patients initially referred for primary patients suitable for coronary artery bypass surgeryangioplasty require urgent coronary artery bypass surgery, so Disadvantagessurgical backup is essential if risks are to be minimised. x Higher procedural cost than streptokinase or alteplase (although There are logistical hurdles in delivering a full 24 hour long term costs lower)service. Primary angioplasty can be performed only when x Can be performed only when cardiac catheterisation facilities and experienced staff availableadequate facilities and experienced staff are available. The time x Recanalisation more rapid than thrombolysis only if 24 hourfrom admission to recanalisation should be less than 60 minutes, on-call team availablewhich may not be possible if staff are on call from home. x Risks and complications of cardiac catheterisation andHowever, recent evidence suggests that, even with longer delays, percutaneous interventionprimary angioplasty may still be superior to thrombolysis. x Reperfusion arrhythmias probably more common because of more A catheterisation laboratory requires large initial capital rapid recanalisation *With or without stentingexpenditure and has substantial running costs. However, in anexisting, fully supported laboratory operating at high volume,primary angioplasty is at least as cost effective as thrombolysis.Primary angioplasty and coronarystentsAlthough early randomised studies of primary angioplastyshowed its clinical effectiveness, outcomes were marred by highrates of recurrent ischaemia (10-15% of patients) and earlyreinfarction of the affected artery (up to 5%). Consequently,haemodynamic and arrhythmic complications arose, with theneed for repeat catheterisation and revascularisation, prolongedhospital stay, and increased costs. Furthermore, restenosis ratesin the first six months remained disappointingly high (25-45%),and a fifth of patients required revascularisation. Although stenting the lesion seemed an attractive answer, itwas initially thought that deploying a stent in the presence ofthrombus over a ruptured plaque would provoke furtherthrombosis. However, improvements in stent deployment andadvances in adjunctive pharmacotherapy have led to greatertechnical success. Recent studies comparing primary stenting Anterior myocardial infarction of 4 hours’ duration and severewith balloon angioplasty alone have shown that stented patients hypotension, caused by a totally occluded proximal left anteriorhave significantly less recurrent ischaemia, reinfarction, and descending artery (arrow, top left). After treatment with abciximab, a stent was positioned. Initial inflation showed “waisting” of the balloon (topsubsequent need for further angioplasty. Economic analysis has right), due to fibrous lesion resistance, which resolved on higher inflationshown that, as expected, the initial costs were higher but were (bottom left). Successful recanalisation resulted in brisk flow (bottom right),offset by lower follow up costs after a year. and the 15 minute procedure completely resolved the patient’s chest pain20
  • 30. Acute coronary syndrome: ST segment elevation myocardial infarction However, one study (Stent-PAMI) showed that stenting wasassociated with a small (but significant) decrease in normalcoronary flow and a trend towards increased six and 12 monthmortality. This led some to examine the use of adjunctiveglycoprotein IIb/IIIa inhibitors as a solution.Stenting and glycoprotein IIb/IIIa inhibitorsThe first study (CADILLAC) to examine the potential benefitsof glycoprotein IIb/IIIa inhibitors combined with stentingshowed that abciximab significantly reduced early recurrentischaemia and reocclusion due to thrombus formation. Therewas no additional effect on restenosis or late outcomescompared with stenting alone. The slightly reduced rate ofnormal coronary flow that had been seen in other studies wasagain confirmed, but did not translate into a significant effecton mortality. Another study (ADMIRAL) examined the potential benefitof abciximab when given before (rather than during) primarystenting. Both at 30 days’ and six months’ follow up, abciximabsignificantly reduced the composite rate of reinfarction, theneed for further revascularisation, and mortality. In addition,abciximab significantly improved coronary flow ratesimmediately after stenting, which persisted up to six monthswith a significant improvement in residual left ventricularfunction. Inferior myocardial infarction of 2.5 hours’ duration caused by a totally occluded middle right coronary artery (arrow, top left). A guide wire passed through the fresh thrombus produced slow distal filling (top right).Future of primary angioplasty Deployment of a stent (bottom left) resulted in brisk antegrade flow, a good angiographic result, and relief of chest pain (bottom right). A temporaryPrimary stenting is not only safe but, by reducing recurrent pacemaker electrode was used to counter a reperfusion junctionalischaemic events, also confers advantages over balloon bradycardia. Note resolution in ST segments compared with top angiogramsangioplasty alone. Abciximab treatment seems to furtherimprove flow characteristics, prevents distalthrombo{embolisation, and reduces the need for repeat Names of trialsangioplasty. A strategy of primary stenting in association with x CADILLAC—Controlled abciximab and deviceabciximab seems to be the current gold standard of care for investigation to lower late angioplastypatients with acute myocardial infarction. Future studies will complicationsexamine the potential benefit of other glycoprotein IIb/IIIa x ADMIRAL—Abciximab before direct angioplastyinhibitors. The question of whether on-site surgical cover is still and stenting in myocardial infarction regarding acute and long-term follow-upessential for infarct intervention continues to be debated. x Stent-PAMI—Stent primary angioplasty in myocardial infarctionFurther readingx Fibrinolytic Therapy Trialists’ (FTT) Collaborative Group. x Grines CL, Cox DA, Stone GW, Garcia E, Mattos LA, Indications for fibrinolytic therapy in suspected acute myocardial Giambartolomei A, et al, for the Stent Primary Angioplasty in infarction: collaborative overview of early mortality and major Myocardial Infarction Study Group. Coronary angioplasty with or morbidity results from all randomised trials of more than 1000 without stent implantation for acute myocardial infarction. N Engl J patients. Lancet 1994;343:311-22 Med 1999;341: 1949-56x Keeley EC, Boura JA, Grines CL. Primary angioplasty versus x Montalescot G, Barragan P, Wittenberg O, Ecollan P, Elhadad S, intravenous thrombolytic therapy for acute myocardial infarction: a Villain P, et al. Platelet glycoprotein IIb/IIIa inhibition with quantitative review of 23 randomised trials. Lancet 2003;361:13-20 coronary stenting for acute myocardial infarction. N Engl J Medx De Boer MJ, Zijlstra F. Coronary angioplasty in acute myocardial 2001;344:1895-903 infarction. In: Grech ED, Ramsdale DR, eds. Practical interventional x Stone GW, Grines CL, Cox DA, Garcia E, Tcheng JE, Griffin JJ, et al. cardiology. 2nd ed. London: Martin Dunitz, 2002:189-206 Comparison of angioplasty with stenting, with or withoutx Lieu TA, Gurley RJ, Lundstrom RJ, Ray GT, Fireman BH, Weinstein abciximab, in acute myocardial infarction. N Engl J Med MC, et al. Projected cost-effectiveness of primary angioplasty for 2002;346:957-66 acute myocardial infarction. J Am Coll Cardiol 1997;30:1741-50 21
  • 31. 7 Percutaneous coronary intervention:cardiogenic shockJohn Ducas, Ever D GrechCardiogenic shock is the commonest cause of death after acutemyocardial infarction. It occurs in 7% of patients with STsegment elevation myocardial infarction and 3% with non-STsegment elevation myocardial infarction. Cardiogenic shock is a progressive state of hypotension(systolic blood pressure < 90 mm Hg) lasting at least30 minutes, despite adequate preload and heart rate, whichleads to systemic hypoperfusion. It is usually caused by leftventricular systolic dysfunction. A patient requiring drug ormechanical support to maintain a systolic blood pressure over90 mm Hg can also be considered as manifesting cardiogenicshock. As cardiac output and blood pressure fall, there is anincrease in sympathetic tone, with subsequent cardiac and A 65 year old man with asystemic effects—such as altered mental state, cold extremities, 3-4 hour history of acute anterior myocardialperipheral cyanosis, and urine output < 30 ml/hour. infarction had cardiogenic shock and acute pulmonary oedema,Effects of cardiogenic shock requiring mechanical ventilation and inotropicCardiac effects support. He underwentIn an attempt to maintain cardiac output, the remaining emergency angiography (top), which showed anon{ischaemic myocardium becomes hypercontractile, and its totally occluded proximaloxygen consumption increases. The effectiveness of this left anterior descendingresponse depends on the extent of current and previous left artery (arrow). A softventricular damage, the severity of coexisting coronary artery tipped guidewire was passed across thedisease, and the presence of other cardiac pathology such as occlusive thromboticvalve disease. lesion, which was Three possible outcomes may occur: successfully stentedx Compensation—which restores normal blood pressure and (middle). Restoration of brisk antegrade flow downmyocardial perfusion pressure this artery (bottom)x Partial compensation—which results in a pre-shock state with followed by insertion ofmildly depressed cardiac output and blood pressure, as well as an intra-aortic balloon pump markedly improvedan elevated heart rate and left ventricular filling pressure blood pressure and organx Shock—which develops rapidly and leads to profound perfusion. The next dayhypotension and worsening global myocardial ischaemia. he was extubated andWithout immediate reperfusion, patients in this group have weaned off all inotropic drugs, and the intra-aorticlittle potential for myocardial salvage or survival. balloon pump was removedSystemic effectsThe falling blood pressure increases catecholamine levels,leading to systemic arterial and venous constriction. In time, Fall in cardiac outputactivation of the renin-aldosterone-angiotensin axis causesfurther vasoconstriction, with subsequent sodium and water Increased sympathetic toneretention. These responses have the effect of increasing leftventricular filling pressure and volume. Although this partlycompensates for the decline in left ventricular function, a high Non-ischaemic zone hypercontractility Increased myocardial oxygen demandleft ventricular filling pressure leads to pulmonary oedema,which impairs gas exchange. The ensuing respiratory acidosis Extent of:exacerbates cardiac ischaemia, left ventricular dysfunction, and • Left ventricular damage?intravascular thrombosis. • Associated coronary artery disease? • Other cardiac disease?Time course of cardiogenic shockThe onset of cardiogenic shock is variable. In the GUSTO-Istudy, of patients with acute myocardial infarction, 7% Compensation Pre-shock Shock (Restoration of normal (Increased heart rate, (Impaired left ventriculardeveloped cardiogenic shock—11% on admission and 89% in perfusion pressure) increased left ventricular perfusion, worseningthe subsequent two weeks. Almost all of those who developed end diastolic pressure) left ventricular function)cardiogenic shock did so by 48 hours after the onset ofsymptoms, and their overall 30 day mortality was 57%, Cardiac compensatory response to falling cardiac output after acutecompared with an overall study group mortality of just 7%. myocardial infarction.22
  • 32. Percutaneous coronary intervention: cardiogenic shockDifferential diagnosis Hallmarks of right ventricular infarctionHypotension can complicate acute myocardial infarction in x Rising jugular venous pressure, Kassmaul sign, pulsus paradoxus x Low output with little pulmonary congestionother settings. x Right atrial pressure > 10 mm Hg and > 80% of pulmonaryRight coronary artery occlusion capillary wedge pressure x Right atrial prominent Y descentAn occluded right coronary artery (which usually supplies a x Right ventricle shows dip and plateau pattern of pressuresmaller proportion of the left ventricular muscle than the left x Profound hypoxia with right to left shunt through a patent foramencoronary artery) may lead to hypotension in various ways: ovalecardiac output can fall due to vagally mediated reflex x ST segment elevation in lead V4Rvenodilatation and bradycardia, and right ventricular dilationmay displace the intraventricular septum towards the left Main indications and contraindications for intra-aorticventricular cavity, preventing proper filling. balloon pump counterpulsation In addition, the right coronary artery occasionally supplies asizeable portion of left ventricular myocardium. In this case Indications x Cardiogenic shock x Enhancement of coronary flowright ventricular myocardial infarction produces a unique set of x Unstable and refractory angina after succesful recanalisation byphysical findings, haemodynamic characteristics, and ST x Cardiac support for high risk percutaneous interventionsegment elevation in lead V4R. When this occurs aggressive percutaneous intervention x Ventricular septal defect andtreatment is indicated as the mortality exceeds 30%. x Hypoperfusion after coronary papillary muscle rupture after artery bypass graft surgery myocardial infarctionVentricular septal defect, mitral regurgitation, or myocardial x Septic shock x Intractable ischaemicrupture ventricular tachycardiaIn 10% of patients with cardiogenic shock, hypotension arises Contraindicationsfrom a ventricular septal defect induced by myocardial x Severe aortic regurgitation x Severe aorto-iliac disease or x Abdominal or aortic aneurysm peripheral vascular diseaseinfarction or severe mitral regurgitation after papillary musclerupture. Such a condition should be suspected if a patientdevelops a new systolic murmur, and is readily confirmed byechocardiography—which should be urgently requested. Such Catheter tippatients have high mortality, and urgent referral for surgery Central lumenmay be needed. Even with surgery, the survival rate can be low. Myocardial rupture of the free wall may cause low cardiac Balloon membraneoutput as a result of cardiac compression due to tamponade. Itis more difficult to diagnose clinically (raised venous pressure,pulsus paradoxus), but the presence of haemopericardium canbe readily confirmed by echocardiography. Pericardial Catheteraspiration often leads to rapid increase in cardiac output, andsurgery may be necessary. Sheath seal Suture padsManagementThe left ventricular filling volume should be optimised, and in Y fittingthe absence of pulmonary congestion a saline fluid challenge of Stylet wireat least 250 ml should be administered over 10 minutes.Adequate oxygenation is crucial, and intubation or ventilationshould be used early if gas exchange abnormalities are present. One way valveOngoing hypotension induces respiratory muscle failure, andthis is prevented with mechanical ventilation. Antithrombotictreatment (aspirin and intravenous heparin) is appropriate. Diagram of intra-aortic balloon pump (left) and its position in the aorta (right)Supporting systemic blood pressure Systole: deflation Diastole: inflationBlood pressure support maintains perfusion of vital organs and Decreased afterload Augmentation of diastolic pressure • Decreases cardiac work • Increases coronary perfusionslows or reverses the metabolic effects of organ hypoperfusion. • Decreases myocardial oxygen consumptionInotropes stimulate myocardial function and increase vascular • Increases cardiac outputtone, allowing perfusion pressures to increase. Intra-aorticballoon pump counterpulsation often has a dramatic effect onsystemic blood pressure. Inflation occurs in early diastole,greatly increasing aortic diastolic pressure to levels above aorticsystolic pressure. In addition, balloon deflation during the startof systole reduces the aortic pressure, thereby decreasingmyocardial oxygen demand and forward resistance (afterload).ReperfusionAlthough inotropic drugs and mechanical support increasesystemic blood pressure, these measures are temporary andhave no effect on long term survival unless they are combinedwith coronary artery recanalisation and myocardial reperfusion. Effects of intra-aortic balloon pump during systole and diastole 23
  • 33. ABC of Interventional Cardiology Thrombolysis is currently the commonest form of treatmentfor myocardial infarction. However, successful fibrinolysis Rprobably depends on drug delivery to the clot, and as blood P Electrocardiogrampressure falls, so reperfusion becomes less likely. One study T(GISSI) showed that, in patients with cardiogenic shock, Q A B Sstreptokinase conferred no benefit compared with placebo. The GUSTO-I investigators examined data on 2200 patientswho either presented with cardiogenic shock or who developed Cit after enrolment and survived for at least an hour after itsonset. Thirty day mortality was considerably less in those Arterial D pressureundergoing early angiography (38%) than in patients with lateor no angiography (62%). Further analysis suggested that early A = Unassisted systolic pressure C = Unassisted aortic end diastolic pressureangiography was independently associated with a 43% B = Diastolic augmentation D = Reduced aortic end diastolic pressurereduction in 30 day mortality. Diagram of electrocardiogram and aortic pressure wave showing In the SHOCK trial, patients with cardiogenic shock were timing of intra-aortic balloon pump and its effects of diastolictreated aggressively with inotropic drugs, intra-aortic balloon augmentation (D) and reduced aortic end diastolic pressurepump counterpulsation, and thrombolytic drugs. Patients werealso randomised to either coronary angiography pluspercutaneous intervention or bypass surgery within six hours,or medical stabilisation (with revascularisation only permittedafter 54 hours). Although the 30 day primary end point did notachieve statistical significance, the death rates progressivelydiverged, and by 12 months the early revascularisation groupshowed a significant mortality benefit (55%) compared with themedical stabilisation group (70%). The greatest benefit was seenin those aged < 75 years and those treated early ( < 6 hours).Given an absolute risk reduction of 15% at 12 months, one lifewould be saved for only seven patients treated by aggressive,early revascularisation.Support and reperfusion: impact on survival Aortic pressure wave recording before (left) and during (right) intra-aorticOver the past 10 years, specific measures to improve blood balloon pump counterpulsation in a patient with cardiogenic shock afterpressure and restore arterial perfusion have been instituted. myocardial infarction. Note marked augmentation in diastolic pressure (arrowMortality data collected since the 1970s show a significant fall A) and reduction in end diastolic pressures (arrow B). (AO=aortic pressure)in mortality in the 1990s corresponding with increased use ofcombinations of thrombolytic drugs, the intra-aortic balloon Mortality (%) Shock present Shock absentpump, and coronary angiography with revascularisation by 80either percutaneous intervention or bypass surgery. Before 60these measures, death rates of 80% were consistently observed. Cardiogenic shock is the commonest cause of death in acute 40myocardial infarction. Although thrombolysis can be attemptedwith inotropic support or augmentation of blood pressure with 20the intra-aortic balloon pump, the greatest mortality benefit is 0seen after urgent coronary angiography and revascularisation. 1975 1978 1981 1984 1986 1988 1990 1991 1993 1995 1997 YearCardiogenic shock is a catheter laboratory emergency. Mortality after myocardial infarction with or without cardiogenic shock (1975 toThe diagram of patient mortality after myocardial infarction is adapted with 1997). Mortality of patients in shock fell from roughly 80% to 60% in the 1990spermission from Goldberg RJ et al, N Engl J Med 1999;340:1162-8. Names of trialsCompeting interests: None declared. x GISSI—Gruppo Italiano per lo studio della sopravvivenza nell’infarto miocardico x GUSTO—global utilization of streptokinase and tissue plasminogen activator for occluded coronary arteries x SHOCK—should we emergently revascularize occluded coronaries for cardiogenic shockFurther readingx Hochman JS, Sleeper LA, Webb JG, Sanborn TA, White HD, Talley x Golberg RJ, Samad NA, Yarzebski J, Gurwitz J, Bigelow C, Gore JM. JD, et al. Early revascularization in acute myocardial infarction Temporal trends in cardiogenic shock complicating acute complicated by cardiogenic shock. N Engl J Med 1999;341:625-34 myocardial infarction. N Engl J Med 1999;340:1162-8x Berger PB, Holmes DR Jr, Stebbins AL, Bates ER, Califf RM, Topol x Hasdai D, Topol EJ, Califf RM, Berger PB, Holmes DR. EJ. Impact of an aggressive invasive catheterization and Cardiogenic shock complicating acute coronary syndromes. Lancet revascularization strategy on mortality in patients with cardiogenic 2000;356:749-56 shock in the global utilization of streptokinase and tissue x White HD. Cardiogenic shock: a more aggressive approach is now plasminogen activator for occluded coronary arteries (GUSTO-I) warranted. Eur Heart J 2000;21:1897-901 trial. Circulation 1997;96:122-724
  • 34. 8 Interventional pharmacotherapyRoger Philipp, Ever D GrechThe dramatic increase in the use of percutaneous coronaryintervention has been possible because of advances in Thrombin inhibitors Clopidogreladjunctive pharmacotherapy, which have greatly improved Adhesion Ticlopidinesafety. Percutaneous intervention inevitably causes vessel Shear Thrombin stress Adenosinetrauma, with disruption of the endothelium and atheromatous diphosphate Aspirinplaque. This activates prothrombotic factors, leading to localised Adrenalinethrombosis; this may impair blood flow, precipitate vessel Thromboxane A2occlusion, or cause distal embolisation. Coronary stents Activationexacerbate this problem as they are thrombogenic. For these Plateletreasons, drug inhibition of thrombus formation duringpercutaneous coronary intervention is mandatory, although this Serotoninmust be balanced against the risk of bleeding, both systemic and Collagen Glycoproteinat the access site. IIb/IIIa Glycoprotein inhibitors IIb/IIIa Aggregation FibrinogenCoronary artery thrombosis PlateletPlatelets are central to thrombus formation. Vessel traumaduring percutaneous intervention exposes subendothelialcollagen and von Willebrand factor, which activate platelet Action of antiplatelet and antithrombotic agents in inhibiting arterialsurface receptors and induce the initial steps of platelet thrombosisactivation. Further platelet activation ultimately results inactivation of platelet glycoprotein IIb/IIIa receptor—the finalcommon pathway for platelet aggregation. Adjunctive pharmacology during percutaneous coronary Vascular injury and membrane damage also trigger interventioncoagulation by exposure of tissue factors. The resulting Aspirin—For all clinical settingsthrombin formation further activates platelets and converts Clopidogrel—For stenting; unstable angina or non-ST segmentfibrinogen to fibrin. The final event is the binding of fibrinogen elevation myocardial infarctionto activated glycoprotein IIb/IIIa receptors to form a platelet Unfractionated heparin—For all clinical settingsaggregate. Glycoprotein IIb/IIIa receptor inhibitors Understanding of these mechanisms has led to the Abciximab—For elective percutaneous intervention for chronic stabledevelopment of potent anticoagulants and antiplatelet angina; unstable angina or non-ST segment elevation myocardialinhibitors that can be used for percutaneous coronary infarction (before and during percutaneous intervention); STintervention. Since the early days of percutaneous transluminal segment elevation myocardial infarction (before and duringcoronary angioplasty, heparin and aspirin have remained a primary percutaneous intervention) Eptifibatide—For elective percutaneous intervention for chronic stablefundamental part of percutaneous coronary intervention angina; unstable angina or non-ST segment elevation myocardialtreatment. Following the introduction of stents, ticlopidine and infarction (before and during percutaneous intervention)more recently clopidogrel have allowed a very low rate of stent Tirofiban—For unstable angina or non-ST segment elevationthrombosis. More recently, glycoprotein IIb/IIIa receptor myocardial infarction (before and during percutaneousantagonists have reduced procedural complications still further intervention)and improved the protection of the distal microcirculation,especially in thrombus-containing lesions prevalent in acutecoronary syndromes. Comparison of unfractionated heparin and low molecular weight heparin Unfractionated heparin Low molecular weight heparinAntithrombotic therapy Molecular weight—3000-30 000 Da Molecular weight—4000-6000 Da Mechanism of action—Binds Mechanism of action—BindsUnfractionated heparin and low molecular weight heparin antithrombin and inactivates antithrombin and inactivatesUnfractionated heparin is a heterogeneous factor Xa and thrombin equally factor Xa more than thrombinmucopolysaccharide that binds antithrombin, which greatly (1:1) (2-4:1)potentiates the inhibition of thrombin and factor Xa. Pharmacokinetics—Variable Pharmacokinetics—Minimal An important limitation of unfractionated heparin is its binding to plasma proteins, plasma protein binding and no endothelial cells, and binding to endothelial cells andunpredictable anticoagulant effect due to variable, non-specific macrophages, giving macrophages, giving predictablebinding to plasma proteins. Side effects include haemorrhage at unpredictable anticoagulant anticoagulant effectsthe access site and heparin induced thrombocytopenia. About effects Longer half life10-20% of patients may develop type I thrombocytopenia, Short half life Partially reversible withwhich is usually mild and self limiting. However, 0.3-3.0% of Reversible with protamine protaminepatients exposed to heparin for longer than five days develop Laboratory monitoring—Activated Laboratory monitoring—Not required clotting time Cost—10-20 times more expensivethe more serious immune mediated, type II thrombocytopenia, Cost—Inexpensive than unfractionated heparinwhich paradoxically promotes thrombosis by platelet activation. 25
  • 35. ABC of Interventional Cardiology Despite these disadvantages, unfractionated heparin is Unfractionated heparincheap, relatively reliable, and reversible, with a brief duration ofanticoagulant effect that can be rapidly reversed by protamine.It remains the antithrombotic treatment of choice during +percutaneous coronary intervention. For patients already taking a low molecular weight heparinwho require urgent revascularisation, a switch to unfractionatedheparin is generally recommended. Low molecular weightheparin is longer acting and only partially reversible with Factor Xa Thrombinprotamine. The use of low molecular weight heparin during 1:1percutaneous intervention is undergoing evaluation.Direct thrombin inhibitorsThese include hirudin, bivalirudin, lepirudin, and argatroban.They directly bind thrombin and act independently ofantithrombin III. They bind less to plasma proteins and have amore predictable dose response than unfractionated heparin.At present, these drugs are used in patients with immunemediated heparin induced thrombocytopenia, but their Antithrombin III-factor Xa and antithrombin III-thrombin complexes neutralisedpotential for routine use during percutaneous intervention isbeing evaluated, in particular bivalirudin. Low molecular weight heparin KeyAntiplatelet drugs Antithrombin III +Aspirin Unfractionated heparinAspirin irreversibly inhibits cyclo-oxygenase, preventing thesynthesis of prothrombotic thromboxane-A2 during platelet Factor Xaactivation. Aspirin given before percutaneous interventionreduces the risk of abrupt arterial closure by 50-75%. It is well Thrombin Factor Xatolerated, with a low incidence of serious adverse effects. Thestandard dose results in full effect within hours, and in patients Low molecular weight heparinwith established coronary artery disease it is given indefinitely.However, aspirin is only a mild antiplatelet agent and has noapparent effect in 10% of patients. These drawbacks have led tothe development of another class of antiplatelet drugs, thethienopyridines.ThienopyridinesTiclopidine and clopidogrel irreversibly inhibit binding of Antithrombin III-factor Xa complex neutralisedadenosine diphosphate (ADP) during platelet activation. Thecombination of aspirin plus clopidogrel or ticlopidine has Mechanisms of catalytic inhibitory action of unfractionated heparin and lowbecome standard antiplatelet treatment during stenting in order molecular weight heparin. Unfractionated heparin interacts with antithrombinto prevent thrombosis within the stent. As clopidogrel has fewer III, accelerating binding and neutralisation of thrombin and factor Xa (in 1:1serious side effects, a more rapid onset, and longer duration of ratio). Dissociated heparin is then free to re-bind with antithrombin III. Lowaction, it has largely replaced ticlopidine. The loading dose is molecular weight heparin is less able to bind thrombin because of its shorter length. This results in selective inactivation of factor Xa relative to thrombin.300 mg at the time of stenting or 75 mg daily for three days Irreversibly bound antithrombin III and factor Xa complex is neutralised, andbeforehand. It is continued for about four weeks, until new dissociated low molecular weight heparin is free to re-bind with antithrombinendothelium covers the inside of the stent. However, the recent IIICREDO study supports the much longer term (1 year) use ofclopidogrel and aspirin after percutaneous coronary Glycoprotein IIb/IIIa inhibitors currently in useintervention, having found a significant (27%) reduction in Abciximab Eptifibatide Tirofibancombined risk of death, myocardial infarction, or stroke. Source Chimeric Peptide Non-peptide monoclonal mouse antibodyGlycoprotein IIb/IIIa receptor inhibitors Time for platelet 24-48 4-6 4-8These are potent inhibitors of platelet aggregation. The three inhibition to returndrugs in clinical use are abciximab, eptifibatide, and tirofiban. In to normal (hours)combination with aspirin, clopidogrel (if a stent is to be Approximate cost per $1031, €1023, $263, €260, $404, €401,deployed), and unfractionated heparin, they further decrease percutaneous £657 (12 hour £167 £257ischaemic complications in percutaneous coronary procedures. coronary intervention infusion) (18 hour (18 hour Glycoprotein IIb/IIIa receptor inhibition may be beneficial infusion) infusion) Severe 1.0% (higher if Similar to Similar toin elective percutaneous intervention for chronic stable angina; thrombocytopenia readministered) placebo placebofor unstable angina or non-ST segment elevation myocardial Reversible with Yes No Noinfarction, for acute myocardial infarction with ST segment platelet transfusion?elevation.26
  • 36. Interventional pharmacotherapyElective percutaneous intervention for chronic stable angina ADP, thrombin, plasmin GlycoproteinLarge trials have established the benefit of abciximab and adrenaline, serotonin, IIb/IIIa receptoreptifibatide during stenting for elective and urgent thromboxane A2, collagen, platelet activating factorpercutaneous procedures. As well as reducing risk of myocardialinfarction during the procedure and the need for urgent repeat Resting Activatedpercutaneous intervention by 35-50%, these drugs seem to platelet plateletreduce mortality at one year (from 2.4% to 1% in EPISTENTand from 2% to 1.4% in ESPRIT). In diabetic patients Fibrinogen Glycoproteinundergoing stenting, the risk of complications was reduced to IIb/IIIathat of non-diabetic patients. receptor antagonist Although most trials showing the benefits of glycoproteinIIb/IIIa inhibitors during percutaneous coronary intervention Aggregated plateletsrelate to abciximab, many operators use the less expensive Inhibition of platelet caused by formation of fibrinogen bridgeseptifibatide and tirofiban. However, abciximab seems to be aggregation occupying glycoproteinsuperior to tirofiban, with lower 30 day mortality and rates of IIb/IIIa receptorsnon-fatal myocardial infarction and urgent repeat percutaneous Mechanisms of activated platelet aggregation by fibrin cross linking and itscoronary intervention or coronary artery bypass graft surgery blockade with glycoprotein IIb/IIIa inhibitorsin a wide variety of circumstances (TARGET study). In theESPRIT trial eptifibatide was primarily beneficial in stenting forelective percutaneous intervention, significantly reducing thecombined end point of death, myocardial infarction, and urgentrepeat percutaneous procedure or bypass surgery at 48 hoursfrom 9.4% to 6.0%. These benefits were maintained at follow up. As complication rates are already low during electivepercutaneous intervention and glycoprotein IIb/IIIa inhibitors Riskare expensive, many interventionists reserve these drugs for Glycoprotein Trial No of Risk ratio (95% CI) Placebo IIb/IIIahigher risk lesions or when complications occur. However, this patients (%) inhibitor (%)may be misguided; ESPRIT showed that eptifibatide started at PRISM 3232 7.1 5.8the time of percutaneous intervention was superior to a PRISM Plus 1915 11.9 10.2glycoprotein IIb/IIIa inhibitor started only when complications PARAGON A 2282 11.7 11.3occurred. PURSUIT 9461 15.7 14.2 PARAGON B 5165 11.4 10.5Unstable angina and non-ST segment elevation myocardial infarction GUSTO-IV ACS 7800 8.0 8.7 0.92 (0.86 to 0.995)The current role of glycoprotein IIb/IIIa inhibitors has been Total 29 855 P=0.037 11.5 10.7defined by results from several randomised trials. In one group 0.5 1.0 1.5of studies 29 885 patients (largely treated without percutaneous P=0.339 Breslow-Day Inhibitor better Placebo better homogeneityintervention) were randomised to receive a glycoproteinIIb/IIIa inhibitor or placebo. The end point of “30 day death or Composite 30 day end point of death and myocardial infarction for sixnon-fatal myocardial infarction” showed an overall significant medical treatment trials of glycoprotein IIb/IIIa inhibitors in unstable angina and non{ST segment elevation myocardial infarctionbenefit of the glycoprotein IIb/IIIa inhibitor over placebo.Surprisingly, the largest trial (GUSTO IV ACS) showed nobenefit with abciximab, which may be partly due to inclusion oflower risk patients. The use of glycoprotein IIb/IIIa inhibitors inall patients with unstable angina and non-ST segment elevationmyocardial infarction remains debatable, although theconsistent benefit seen with these drugs has led to therecommendation that they be given to high risk patients Riskscheduled for percutaneous coronary intervention. Glycoprotein Another study (CURE) showed that the use of clopidogrel Trial No of Risk ratio (95% CI) Placebo IIb/IIIa patients (%) inhibitor (%)rather than a glycoprotein IIb/IIIa inhibitor significantly EPIC 2099 9.6 6.6reduced the combined end point of cardiovascular death, IMPACT-II 4010 8.5 7.0non{fatal myocardial infarction, or stroke (from 11.4% to 9.3%). EPILOG 2792 9.1 4.0Similar benefits were seen in the subset of patients who CAPTURE 1265 9.0 4.8underwent percutaneous coronary intervention. The impact RESTORE 2141 6.3 5.1this study will have on the use of glycoprotein IIb/IIIa inhibitors EPISTENT 2399 10.2 5.2in this clinical situation remains unclear. ESPRIT 2064 10.2 6.3 In another group of studies (n=16 770), patients were given 0.62 (0.55 to 0.70) Total 16 770 8.8 5.6a glycoprotein IIb/IIIa inhibitor or placebo immediately before P<0.001 0 1.0 2.0or during planned percutaneous intervention. All showed Inhibitor better Placebo better P=0.014 Breslow-Dayunequivocal benefit with the active drug. Despite their efficacy, homogeneityhowever, some interventionists are reluctant to use glycoprotein Composite 30 day end point of death and myocardial infarction for sevenIIb/IIIa inhibitors in all patients because of their high costs and trials of glycoprotein IIb/IIIa inhibitors given before or during plannedreserve their use for high risk lesions or when complications percutaneous coronary intervention for unstable angina and non-SToccur. segment elevation myocardial infarction 27
  • 37. ABC of Interventional CardiologyAcute ST segment elevation myocardial infarction Names of trialsIn many centres primary percutaneous intervention is thepreferred method of revascularisation for acute myocardial x CAPTURE—C7E3 antiplatelet therapy in unstable refractory anginainfarction. To date, randomised studies have shown that x CREDO—Clopidogrel for the reduction of events duringabciximab is the only drug to demonstrate benefit in this observationsetting. The development of low cost alternatives and the x CURE—Clopidogrel in unstable angina to prevent recurrentpotential for combination with other inhibitors of the eventscoagulation cascade may increase the use of glycoprotein x EPIC—Evaluation of C7E3 for prevention of ischemicIIb/IIIa inhibitors. complications x EPILOG—Evaluation in PTCA to improve long-term outcome with abciximab glycoprotein IIb/IIIa blockadeRestenosis x EPISTENT—Evaluation of IIb/IIIa platelet inhibitor for stenting x ESPRIT—Enhanced suppression of the platelet glycoproteinAlthough coronary stents reduce restenosis rates compared IIb/IIIa receptor using integrilin therapy x GUSTO IV-ACS—Global use of strategies to open occludedwith balloon angioplasty alone, restenosis within stents remains arteries IV in acute coronary syndromea problem. Nearly all systemic drugs aimed at reducing x IMPACT II—Integrilin to minimize platelet aggregation andrestenosis have failed, and drug eluting (coated) stents may coronary thrombosisultimately provide the solution to this problem. x PARAGON—Platelet IIb/IIIa antagonism for the reduction of acute coronary syndrome events in the global organization networkThe future x PRISM—Platelet receptor inhibition in ischemic syndrome managementImprovements in adjunctive pharmacotherapy, in combination x PRISM-PLUS—Platelet receptor inhibition in ischemic syndromewith changes in device technology, will allow percutaneous management in patients limited by unstable signs and symptomscoronary intervention to be performed with increased x PURSUIT—Platelet glycoprotein IIb/IIIa in unstable angina: receptor suppression using integrilin therapylikelihood of acute and long term success and with lower x RESTORE—Randomized efficacy study of tirofiban for outcomesprocedural risks in a wider variety of clinical situations. Further and restenosisrefinements in antiplatelet treatment may soon occur withrapidly available bedside assays of platelet aggregation.Competing interests: None declared.Further readingx Lincoff AM, Califf RM, Moliterno DJ, Ellis SG, Ducas J, Kramer JH, x ESPRIT Investigators. Novel dosing regimen of eptifibatide in et al. Complementary clinical benefits of coronary-artery stenting planned coronary stent implantation (ESPRIT): a randomized, and blockade and blockade of platelet glycoprotein IIb/IIIa placebo-controlled trial. Lancet 2000;356:2037-44 receptors. N Engl J Med 1999;341:319-27 x Boersma E, Harrington RA, Moliterno DJ, White H, Theroux P,x PURSUIT Trial Investigators. Inhibition of platelet glycoprotein Van de Werf F, et al. Platelet glycoprotein IIb/IIIa inhibitors in IIb/IIIa with eptifibatide in patients with acute coronary syndromes. acute coronary syndromes: a meta-analysis of all major Platelet glycoprotein IIb/IIIa in unstable angina: receptor randomized clinical trials. Lancet 2002;359:189-98 suppression using integrilin therapy. N Engl J Med 1998;339:436-43 x Chew DP, Lincoff AM. Adjunctive pharmacotherapy andx PRISM-PLUS Study Investigators. Inhibition of the platelet coronary intervention. In: Grech ED, Ramsdale DR, eds. Practical glycoprotein IIb/IIIa receptor with tirofiban in unstable angina and interventional cardiology. 2nd ed. London: Martin Dunitz, non-Q wave myocardial infarction. Platelet receptor inhibition in 2002:207{24 ischemic syndrome management in patients limited by unstable x Steinhubl SR, Berger PB, Mann JT 3rd, Fry ET, DeLago A, Wilmer signs and symptoms. N Engl J Med 1998;338:1488-97 C, et al. Early and sustained dual oral antiplatelet therapy following percutaneous coronary intervention. A randomized controlled trial. JAMA 2002;288:2411-2028
  • 38. 9 Non-coronary percutaneous interventionEver D GrechAlthough most percutaneous interventional procedures involvethe coronary arteries, major developments in non-coronarytranscatheter cardiac procedures have occurred in the past 20years. In adults the commonest procedures are balloon mitralvalvuloplasty, ethanol septal ablation, and septal defect closure.These problems were once treatable only by surgery, butselected patients may now be offered less invasive alternatives.Carrying out such transcatheter procedures requiressupplementary training to that for coronary intervention.Balloon mitral valvuloplastyAcquired mitral stenosis is a consequence of rheumatic feverand is commonest in developing countries. Commissural fusion,thickening, and calcification of the mitral valve leaflets typicallyoccur, as well as thickening and shortening of the chordaetendinae. The mitral valve stenosis leads to left atrialenlargement, which predisposes patients to atrial fibrillation Stenotic mitral valve showing distorted, fused, and calcified valve leaflets.and the formation of left atrial thrombus. (AMVL=anterior mitral valve leaflet, PMVL=posterior mitral valve leaflet, LC=lateral commissure, MC=medial commissure) In the 1980s percutaneous balloon valvuloplasty techniqueswere developed that could open the fused mitral commissuresin a similar fashion to surgical commissurotomy. The resultingfall in pressure gradient and increase in mitral valve area led tosymptomatic improvement. Today, this procedure is most oftenperformed with the hourglass shaped Inoue balloon. This isintroduced into the right atrium from the femoral vein, passedacross the atrial septum by way of a septal puncture, and thenpositioned across the stenosed mitral valve before inflation. Left atriumPatient selectionIn general, patients with moderate or severe mitral stenosis Right(valve area < 1.5 cm2) with symptomatic disease despite optimal atrium Leftmedical treatment can be considered for this procedure. ventricleFurther patient selection relies heavily on transthoracic andtransoesophageal echocardiographic findings, which provide Right ventriclestructural information about the mitral valve and subvalvarapparatus. A scoring system for predicting outcomes is commonly usedto screen potential candidates. Four characteristics (valve Inferior vena cavamobility, leaflet thickening, subvalvar thickening, andcalcification) are each graded 1 to 4. Patients with a score of <8are more likely to have to have a good result than those withscores of > 8. Thus, patients with pliable, non-calcified valvesand minimal fusion of the subvalvar apparatus achieve the bestimmediate and long term results. Relative contraindications are the presence of pre-existingsignificant mitral regurgitation and left atrial thrombus.Successful balloon valvuloplasty increases valve area to > 1.5 cm2 without a substantial increase in mitral regurgitation,resulting in significant symptomatic improvement. Complications—The major procedural complications aredeath (1%), haemopericardium (usually during transseptalcatheterisation) (1%), cerebrovascular embolisation (1%), severemitral regurgitation (due to a torn valve cusp) (2%), and atrialseptal defect (although this closes or decreases in size in mostpatients) (10%). Immediate and long term results are similar tothose with surgical valvotomy, and balloon valvuloplasty can be Top: Diagram of the Inoue balloon catheter positionedrepeated if commissural restenosis (a gradual process with an across a stenosed mitral valve. Bottom: Fluoroscopicincidence of 30-40% at 6-8 years) occurs. image of the inflated Inoue balloon across the valve 29
  • 39. ABC of Interventional Cardiology In patients with suitable valvar anatomy, balloonvalvuloplasty has become the treatment of choice for mitralstenosis, delaying the need for surgical intervention. It may alsobe of particular use in those patients who are at high risk ofsurgical intervention (because of pregnancy, age, or coexisting Postmortem appearance of a heart with hypertrophicpulmonary or renal disease). cardiomyopathy showing In contrast, balloon valvuloplasty for adult aortic stenosis is massive ventricular andassociated with high complication rates and poor outcomes and septal hypertrophy causingis only rarely performed. obstruction of the left ventricular outflow tract (LVOT). This isEthanol septal ablation compounded by the anterior mitral valve leaflet (AMVL), which pressesHypertrophic cardiomyopathy against the ventricularHypertrophic cardiomyopathy is a disease of the myocytes septum (VS). Note thecaused by mutations in any one of 10 genes encoding various coincidental right atrialcomponents of the sarcomeres. It is the commonest genetic (RAE) and right ventricular (RVE) pacing electrodescardiovascular disease, being inherited as an autosomaldominant trait and affecting about 1 in 500 of the population. Ithas highly variable clinical and pathological presentations. Characteristics of hypertrophic cardiomyopathy It is usually diagnosed by echocardiography and is Anatomical—Ventricular hypertrophy of unknown cause, usually withcharacterised by the presence of unexplained hypertrophy in a disproportionate involvement of the interventricular septumnon-dilated left ventricle. In a quarter of cases septal Physiological—Well preserved systolic ventricular function, impaired diastolic relaxationenlargement may result in substantial obstruction of the left Pathological—Extensive disarray and disorganisation of cardiacventricular outflow tract. This is compounded by Venturi myocytes and increased interstitial collagensuction movement of the anterior mitral valve leaflet duringventricular systole, bringing it into contact with thehypertrophied septum. The systolic anterior motion of theanterior mitral valve leaflet also causes mitral regurgitation.TreatmentAlthough hypertrophic cardiomyopathy is often asymptomatic,common symptoms are dyspnoea, angina, and exertionalsyncope, which may be related to the gradient in the leftventricular outflow tract. The aim of treatment of symptomaticpatients is to improve functional disability, reduce the extent ofobstruction of the left ventricular outflow tract, and improvediastolic filling. Treatments include negatively inotropic drugssuch as blockers, verapamil, and disopyramide. However, 10%of symptomatic patients fail to respond to drugs, and surgery— Echocardiogram showing anterior mitral valveventricular myectomy (which usually involves removal of a small leaflet (AMVL) and septal contact (***) duringamount of septal muscle) or ethanol septal ablation—can be ventricular systole. Note marked left ventricular (LV)considered. free wall and ventricular septal (VS) hypertrophy. The objective of ethanol septal ablation is to induce a Injection of an echocontrast agent down the septal artery results in an area of septal echo-brightnesslocalised septal myocardial infarction at the site of obstruction (dotted line). (LA=left atrium, AoV=aortic valve)of the left ventricular outflow tract. The procedure involvesthreading a small balloon catheter into the septal arterysupplying the culprit area of septum. Echocardiography withinjection of an echocontrast agent down the septal artery allowsthe appropriate septal artery to be identified and reduces thenumber of unnecessary ethanol injections. Once the appropriate artery is identified, the catheterballoon is inflated to completely occlude the vessel, and a smallamount of dehydrated ethanol is injected through the centrallumen of the catheter into the distal septal artery. This causesimmediate vessel occlusion and localised myocardial infarction.The infarct reduces septal motion and thickness, enlarges theleft ventricular outflow tract, and may decrease mitral valvesystolic anterior motion, with consequent reduction in thegradient of the left ventricular outflow tract. Over the next few Angiograms showing ethanol septal ablation. The first septal artery (S1,months the infarcted septum undergoes fibrosis and shrinkage, top left) is occluded with a balloonwhich may result in further symptomatic improvement. catheter (top right) before ethanol The procedure is performed under local anaesthesia with injection. This results in permanentsedation as required. Patients inevitably experience chest septal artery occlusion (bottom) and a localised septal myocardialdiscomfort during ethanol injection, and treatment with infarction. (LAD=left anteriorintravenous opiate analgesics is essential. Patients are usually descending artery, TPW=temporarydischarged after four or five days. pacemaker wire)30
  • 40. Non-coronary percutaneous interventionComplicationsHeart block is a frequent acute complication, so a temporarypacing electrode is inserted via the femoral vein beforehandand is usually left in situ for 24 hours after the procedure,during which time the patient is monitored. The main procedural complications are persistent heartblock requiring a permanent pacemaker (10%), coronary arterydissection and infarction requiring immediate coronary arterybypass grafting (2%), and death (1-2%). The proceduralmortality and morbidity is similar to that for surgical myectomy,as is the reduction in left ventricular outflow tract gradient.Surgery and ethanol septal ablation have not as yet been Micrograph of hypertrophied myocytes in haphazard alignments characteristic of hypertrophicdirectly compared in randomised studies. cardiomyopathy. Interstitial collagen is also increasedSimultaneous aortic and left ventricular pressure waves before (left) and after (right) successful ethanol septal ablation. Note the differencebetween left ventricular peak pressure and aortic peak pressure, which represents the left ventricular outflow tract gradient, has beenreduced from 80 mm Hg to 9 mm HgSeptal defect closure Indications and contraindications for percutaneous closure of atrial septal defectsAtrial septal defectsAtrial septal defects are congenital abnormalities characterised Indications Clinicalby a structural deficiency of the atrial septum and account for x If defect causes symptoms x Pulmonary:systemic flow ratioabout 10% of all congenital cardiac disease. The commonest x Associated cerebrovascular > 1.5 and reversible pulmonaryatrial septal defects affect the ostium secundum (in the fossa embolic event hypertensionovalis), and most are suitable for transcatheter closure. Although x Divers with neurological x Right-to-left atrial shunt andatrial septal defects may be closed in childhood, they are the decompression sickness hypoxaemiacommonest form of congenital heart disease to become Anatomicalapparent in adulthood. x Defects within fossa ovalis x Presence of > 4 mm rim of tissue Diagnosis is usually confirmed by echocardiography, (or patent foramen ovale) surrounding defectallowing visualisation of the anatomy of the defect and Doppler x Defects with stretchedestimation of the shunt size. The physiological importance of diameter < 38 mmthe defect depends on the duration and size of the shunt, as well Contraindicationsas the response of the pulmonary vascular bed. Patients with x Sinus venosus defects x Ostium secundum defects with other x Ostium primum defects important congenital heart defectssignificant shunts (defined as a ratio of pulmonary blood flow to requiring surgical correctionsystemic blood flow > 1.5) should be considered for closurewhen the diagnosis is made in later life because the defectreduces survival in adults who develop progressive pulmonaryhypertension. They may also develop atrial tachyarrhythmias,which commonly precipitate heart failure. Patients within certain parameters can be selected fortranscatheter closure with a septal occluder. In those who areunsuitable for the procedure, surgical closure may be considered.Patent foramen ovaleA patent foramen ovale is a persistent flap-like openingbetween the atrial septum primum and secundum which occursin roughly 25% of adults. With microbubbles injected into aperipheral vein during echocardiography, a patent foramen Deployment sequence of the Amplatzer septal occluder for closing an atrialovale can be demonstrated by the patient performing and septal defect 31
  • 41. ABC of Interventional Cardiologyreleasing a prolonged Valsalva manoeuvre. Visualisation ofmicrobubbles crossing into the left atrium reveals a right-to-leftshunt mediated by transient reversal of the interatrial pressuregradient. Although a patent foramen ovale (or an atrial septalaneurysm) has no clinical importance in otherwise healthyadults, it may cause paradoxical embolism in patients withcryptogenic transient ischaemic attack or stroke (up to half ofwhom have a patent foramen ovale), decompression illness indivers, and right-to-left shunting in patients with rightventricular infarction or severe pulmonary hypertension.Patients with patent foramen ovale and paradoxical embolism Amplatzer occluder devices for patent foramen ovale (left) and muscular ventricular septal defects (right)have an approximate 3.5% yearly risk of recurrentcerebrovascular events. Secondary preventive strategies are drug treatment (aspirin,clopidogrel, or warfarin), surgery, or percutaneous closure using Further readinga dedicated occluding device. A lack of randomised clinical x Inoue K, Lau K-W, Hung J-S. Percutaneous transvenous mitraltrials directly comparing these options means optimal commissurotomy. In: Grech ED, Ramsdale DR, eds. Practical interventional cardiology. 2nd ed. London: Martin Dunitz, 2002:treatment remains uncertain. However, percutaneous closure 373{87offers a less invasive alternative to traditional surgery and allows x Bonow RO, Carabello B, de Leon AC, Edmunds LH Jr, Fedderlypatients to avoid potential side effects associated with BJ, Freed MD, et al. ACC/AHA guidelines for the management ofanticoagulants and interactions with other drugs. In addition, patients with valvular heart disease: A report of the Americandivers taking anticoagulants may experience haemorrhage in College of Cardiology/American Heart Association Task Force onthe ear, sinus, or lung from barotrauma. Practice Guidelines (Committee on Management of Patients with Valvular Heart Disease). J Am Coll Cardiol 1998;32:1486-582 x Wilkins GT, Weyman AE, Abascal VM, Bloch PC, Palacios IF.Congenital ventricular septal defects Percutaneous balloon dilatation of the mitral valve: an analysis ofUntreated congenital ventricular septal defects that require echocardiographic variables related to outcome and theintervention are rare in adults. Recently, there has been interest mechanism of dilatation. Br Heart J 1998;60:299-308in percutaneous device closure of ventricular septal defects x Wigle ED, Rakowski H, Kimball BP, Williams WG. Hypertrophicacquired as a complication of acute myocardial infarction. cardiomyopathy: clinical spectrum and treatment. Circulation 1995;However, more experience is necessary to assess the role of this 92:1680-92 x Nagueh SF, Ommen SR, Lakkis NM, Killip D, Zoghbi WA, Schaffprocedure as a primary closure technique or as a bridge to HV, et al. Comparison of ethanol septal reduction therapy withsubsequent surgery. surgical myectomy for the treatment of hypertrophic obstructive cardiomyopathy. J Am Coll Cardiol 2001;38:1701-6 x Braun MU, Fassbender D, Schoen SP, Haass M, Schraeder R, Scholtz W, et al. Transcatheter closure of patent foramen ovale inThe picture of a stenotic mitral valve and micrograph of myocytes showing patients with cerebral ischaemia. J Am Coll Cardiol 2002;39:hypertrophic cardiomyopathy were provided by C Littman, consultant 2019-25histopathologist at the Health Sciences Centre, Winnipeg, Manitoba, x Waight DJ, Cao Q-L, Hijazi ZM. Interventional cardiacCanada. The postmortem picture of a heart with hypertrophic catheterisation in adults with congenital heart disease. In: Grechcardiomyopathy was provided by T Balachandra, chief medical examiner for ED, Ramsdale DR, eds. Practical interventional cardiology. 2nd ed.the Province of Manitoba, Winnipeg. The pictures of Amplatzer occluder London: Martin Dunitz, 2002:390-406devices were provided by AGA Medical Corporation, Minnesota, USA.32
  • 42. 10 New developments in percutaneous coronaryinterventionJulian Gunn, Ever D Grech, David Crossman, David CumberlandPercutaneous coronary intervention has become a morecommon procedure than coronary artery bypass surgery inmany countries, and the number of procedures continues torise. In one day an interventionist may treat four to six patientswith complex, multivessel disease or acute coronary syndromes.Various balloons, stents, and other devices are delivered bymeans of a 2 mm diameter catheter introduced via a peripheralartery. The success rate is over 95%, and the risk of seriouscomplications is low. After a few hours patients can bemobilised, and they are usually discharged the same or the nextday. Even the spectre of restenosis is now fading.Refinements of existing techniquesThe present success of percutaneous procedures is largelybecause of refinement of our “basic tools” (intracoronaryguidewires and low profile balloons), which have greatlycontributed to the safety and effectiveness of procedures. Triple vessel disease is no longer a surgical preserve, and particularlyHowever, the greatest technological advance has been in the good results are expected with drug eluting stents. In this case, lesions indevelopment of stents. These are usually cut by laser from the left anterior descending (LAD), circumflex (Cx), and right coronarystainless steel tubes into a variety of designs, each with different arteries (RCA) (top row) are treated easily and rapidly by stent (S) implantation (bottom row)radial strength and flexibility. They are chemically etched orelectropolished to a fine finish and sometimes coated. Digital angiography is a great advance over cine-basedsystems, and relatively benign contrast media have replaced thetoxic media used in early angioplasty. Although magneticresonance and computed tomographic imaging may become Performance of percutaneous coronary interventionuseful in the non-invasive diagnosis of coronary artery disease, General statisticsangiography will remain indispensable to guide percutaneous x Success rate of procedure > 95%interventions for the foreseeable future. x Symptoms improved after procedure 90% x Complications* 2% x Restenosis 15% (range 5-50%)Interventional devices and their uses x Duration of procedure 15 minutes-3 hoursDevice Use (% of cases) Types of lesion x Access point: Femoral artery 95%Balloon catheter 100% Multiple types Radial or brachial artery 5%Stent 70-90% Most types x Time in hospital after procedure:Drug eluting stent 0-50% High risk of restenosis (possibly all) Overnight 60%Cutting balloon 1-5% In-stent restenosis, ostial Day case 20% lesions Longer 20%Rotablator 1-3% Calcified, ostial, undilatable x Intravenous contrast load 100-800 ml lesions x X ray dose to patient 75 Gy/cm2†Brachytherapy 1-3% In-stent restenosis Special conditionsAtherectomy < 1% Bulky, eccentric, ostial lesions x Success of direct procedure for acute myocardial infarction > 95%Stent graft < 1% Aneurysm, arteriovenous x Success for chronic ( > 3 month) occluded vessel 50-75% malformation, perforation x Mortality for procedure in severe cardiogenic shock 50%Thrombectomy < 1% Visible thrombus x Restenosis:Laser < 1% Occlusions, in-stent restenosis Vessels < 2.5 mm in diameter, > 40 mm length 60%Distal protection < 1% Degenerate vein graft Vessels > 3.5 mm diameter, < 10 mm length 5% x Lesion recurrence later than 6 months after procedure < 5% x Re-restenosis: After repeat balloon dilatation 30-50%New device technology After brachytherapy < 15%Pre-eminent among new devices is the drug eluting (coated) *Death, myocardial infarction, coronary artery bypass surgery, cerebrovascular accidentstent, which acts as a drug delivery device to reduce restenosis. †Equivalent to 1-2 computed tomography scansThe first of these was the sirolimus coated Cypher stent. 33
  • 43. ABC of Interventional CardiologySirolimus is one of several agents that have powerful antimitoticeffects and inhibit new tissue growth inside the artery and stent. Names of trialsIn a randomised controlled trial (RAVEL) this stent gave a six x ASPECT—Asian paclitaxel-eluting stent clinical trialmonth restenosis rate of 0% compared with 27% for an x RAVEL—Randomized study with the sirolimus eluting velocityuncoated stent of the same design. A later randomised study balloon expandable stent in the treatment of patients with de novo native coronary artery lesions(SIRIUS) of more complex stenoses (which are more prone to x SIRIUS—Sirolimus-coated velocity stent in treatment of patientsrecur) still produced a low rate of restenosis within stented with de novo coronary artery lesions trialsegments (9% v 36% with uncoated stents), even in patients with x TAXUS II—Study of the safety and superior performance of thediabetes (18% v 51% respectively). Other randomised studies TAXUS drug-eluting stent versus the uncoated stent on de novosuch as ASPECT and TAXUS II have also shown that coated lesionsstents (with the cytotoxic agent paclitaxel) have significantlylower six month restenosis rates than identical uncoated stents(14% v 39% and 6% v 20% respectively). By reducing theincidence of restenosis (and therefore recurrent symptoms),drug eluting stents will probably alter the balance of treatingcoronary artery disease in favour of percutaneous interventionrather than coronary artery bypass surgery. However, coatedstents will not make any difference to the potential forpercutaneous coronary intervention to achieve acute success inany given lesion; nor do they seem to have any impact on acuteand subacute safety. Although coated stents may, paradoxically, be too effective ataltering the cellular response and thus delay the desirableprocess of re-endothelialisation, there is no evidence that this isa clinical problem. However, this problem has been observed Angiograms showing severe, diffuse, in-stent restenosis in the left anteriorwith brachytherapy (catheter delivered radiotherapy over a descending artery and its diagonal branch (L and D, left). This was treatedshort distance to kill dividing cells), a procedure that is generally with balloon dilatation and brachytherapy with irradiation (Novoste) fromreserved for cases of in-stent restenosis. This may lead to late a catheter (Br, centre), with an excellent final result (right)thrombosis as platelets readily adhere to the “raw” surface thatresults from an impaired healing response. This risk isminimised by prolonged treatment with antiplatelet drugs andavoiding implanting any fresh stents at the time ofbrachytherapy. Other energy sources may also prove useful. Sonotherapy(ultrasound) may have potential, less as a treatment in its ownright than as a facilitator for gene delivery, and is “benign” in itseffect on healthy tissue. Photodynamic therapy (the interactionof photosensitising drug, light, and tissue oxygen) is also beinginvestigated but is still in early development. Laser energy, whendelivered via a fine intracoronary wire, is used in a few centresto recanalise blocked arteries.New work practices Angiogram of an aortocoronary vein graft with anTwenty years ago, a typical angioplasty treated one proximally aneurysm and stenoses (A and S, top). Treatment bylocated lesion in a single vessel in a patient with good left implantation of a membrane-covered stent excluded the aneurysm and restored a tubular lumen (bottom)ventricular function. Now, it commonly treats two or three vesseldisease, perhaps with multiple lesions (some of which may becomplex), in patients with impaired left ventricular function,advanced age, and comorbidity. Patients may have undergone Unprotected left main stem stenoses (LMS, top) may, with careful selection, be treated by stent implantation (S, bottom). Best results (similar to coronary artery bypass surgery) are achieved in stable patients with good left ventricular function and no other disease. Close follow up to detect restenosis is important. (LAD=left anterior Bifurcation lesions, such as of the left anterior descending descending artery, Cx= artery and its diagonal branch (L and D, left), are technically circumflex coronary challenging to treat but can be well dilated by balloon artery) dilatation and selective stenting (S, right)34
  • 44. New developments in percutaneous coronary interventioncoronary artery bypass surgery and be unsuitable for furtherheart surgery. Isolated left main stem and ostial right coronaryartery lesions, though requiring more experience andvariations on traditional techniques, are also no longer asurgical preserve.Role of percutaneous coronary interventionThe role of percutaneous intervention has extended to thepoint where up to 70% of patients treated have acute coronarysyndromes. Trial data now support the use of a combination ofa glycoprotein IIb/IIIa inhibitor and early percutaneousintervention to give high risk patients the best long term results.The same applies to acute myocardial infarction, where An acute coronary syndrome was found to be due to stenoses and anpercutaneous procedures achieve a much higher rate of arterial ulcerated plaque in the right coronary artery (S and U, left). This waspatency than thrombolytic treatment. Even cardiogenic shock, treated with a glycoprotein IIb/IIIa inhibitor followed by stent implantationthe most lethal of conditions, may be treated by an aggressive (right). This is an increasingly common presentation of coronary artery disease to catheterisation laboratoriescombination of intra-aortic balloon pumping and percutaneousintervention. The potential for percutaneous procedures to treat a widerange of lesions successfully with low rates of restenosis raisesthe question of the relative roles of percutaneous interventionand bypass surgery in everyday practice. It takes time toaccumulate sufficient trial data to make long termgeneralisations possible. Early trials comparing balloon angioplasty with bypasssurgery rarely included stents and few patients with three vesseldisease (as such disease carried higher risk and percutaneousintervention was not as widely practised as now). The long termresults favoured bypass surgery, but theses trials are nowoutdated. In the second generation of studies, stents were usedin percutaneous intervention, improving the results. As in the Right coronary artery containing large,early studies, surgery and intervention had similarly low lobulated thrombus (T, left) on a substantialcomplications and mortality. The intervention patients still had stenosis. After treatment with glycoproteinmore need for repeat procedures because of restenosis than the IIb/IIIa inhibitor, the lesion was stentedbypass surgery patients, but the differences were less. successfully (St, right) The major drawback of all these studies was an exclusionrate approaching 95%, making the general clinical application General roles of percutaneous coronary intervention (PCI)of the findings questionable. This was because it was unusual at and coronary artery bypass surgery (CABG)that time to find patients with multivessel disease who were PCItechnically suitable for both methods and thus eligible for Condition 1993 2003 CABGinclusion in the trials. Now that drug eluting stents are available, Acute presentationmore trials are under way: the balance will now probably tip in Acute coronary syndrome ++ +++ ++favour of percutaneous coronary intervention. Meanwhile, the Cardiogenic shock +/ − + +/ −decision of which treatment is better for a patient at a given Acute full thickness myocardial infarction + +++ −time is based on several factors, including the feasibility of Bailout after failed thrombolysis + ++ −percutaneous intervention (which is generally considered as the Chronic presentationfirst option), completeness of revascularisation, comorbidity, Impaired left ventricle with left main stem −− − +++age, and the patient’s own preferences. stenosis and blocked right coronary artery Impaired left ventricle and 3 vessel disease + ++ +++Implications for health services Impaired left ventricle and 3 vessel disease − + +++ with >1 occlusionThese issues are likely to pose major problems for health Diabetes and 3 vessel disease + ++ +++services. Modern percutaneous techniques can be used both to Good left ventricle and 3 vessel disease + ++ +++shorten patients’ stay in hospital and to make their treatment 2 occluded vessels − − ++minimally hazardous and more comfortable. They can also be Good left ventricle and 2 vessel disease + +++ ++used in the first and the last (after coronary artery bypass Repeat revascularisation after PCI ++ +++ ++surgery) stages of a patient’s “ischaemic career.” Good left ventricle and 1 vessel disease +++ +++ + On the other hand, for the role of percutaneous coronary 2-3 vessel diffuse or distal disease + ++ +intervention in acute infarction to be realised, universal Repeat revascularisation after CABG + ++ +emergency access to this service will be needed. However, most Palliative partial revascularisation + ++ −health systems cannot afford this—the main limiting factor Revascularisation of frail patient or with + ++ −being the number of interventionists and supporting staff severe comorbidityrequired to allow a 24 hour rota compatible with legal working +++ highly effective role, ++ useful role, + limited role, − treatment not preferred, − −hours and the survival of routine elective work. treatment usually strongly advised against 35
  • 45. ABC of Interventional CardiologyThe future for percutaneous coronary Further readingintervention x Morice M-C, Serruys PW, Sousa JE, Fajadet J, Ban Hayashi E, Perin M, et al. A randomized comparison of a sirolimus-eluting stent withWill percutaneous coronary intervention exist in 20 years time, a standard stent for coronary revascularization. N Engl J Medor, at least, be recognisable as a logical development of today’s 2002;346:1773-80procedures? Will balloons and stents still be in use? It is likely x Park SJ, Shim WH, Ho DS, Raizner AE, Park SW, Hong MK, et al. A paclitaxel-eluting stent for the prevention of coronary restenosis.that percutaneous procedures will expand further, although N Engl J Med 2003;348:1537-45some form of biodegradable stent is a possibility. A more x Raco DL, Yusuf S. Overview of randomised trials of percutaneous“biological” stent might also be able to act as an effective drug coronary intervention: comparison with medical and surgicalor gene reservoir, which may extend local drug delivery into therapy for chronic coronary artery disease. In: Grech ED,new areas of coronary artery disease. We may find ourselves Ramsdale DR, eds. Practical interventional cardiology. 2nd ed.detecting inflamed (“hot”) plaques with thermography catheters London: Martin Dunitz, 2002:263-77 x Teirstein PS, Kuntz RE. New frontiers in interventional cardiology:and treating these before they rupture. We may even be able to intravascular radiation to prevent restenosis. Circulation 2001;104:modify the natural course of coronary artery disease by 2620-6releasing agents “remotely” (possibly using an external x Tsuji T, Tamai H, Igaki K, Kyo E, Kosuga K, Hata T, et al.ultrasound trigger) or by injecting an agent that activates the Biodegradable stents as a platform to drug loading. Int J Cardiovascmolecular cargo in a stent. Intervent 2003;5:13-6 A persistent challenge still limiting the use of percutaneous x Hariawala MD, Sellke FW. Angiogenesis and the heart: therapeuticcoronary intervention is that of chronic total occlusions, which implications. J R Soc Med 1997;90:307-11 x Serruys PW, Unger F, Sousa JE, Jatene A, Bonnier HJ, Schonbergercan be too tough to allow passage of an angioplasty guidewire. JP, et al, for the Arterial Revascularization Therapies Study Group.An intriguing technique is percutaneous in situ coronary artery Comparison of coronary-artery bypass surgery and stenting for thebypass. With skill and ingenuity, a few enthusiasts have treatment of multivessel disease. N Engl J Med 2001;344:1117-24anastomosed the stump of a blocked coronary artery to the x SoS Investigators. Coronary artery bypass surgery versusadjacent cardiac vein under intracoronary ultrasound guidance, percutaneous coronary intervention with stent implantation inthereby using the vein as an endogenous conduit (with reversed patients with multivessel coronary artery disease (the stent or surgery trial): a randomised controlled trial. Lancet 2002;360:flow). This technique may assist only a minority of patients. 965-70More practical, we believe, is the concept of drilling throughocclusions with some form of external guidance, perhapsmagnetic fields. “Direct” myocardial revascularisation (punching an array ofholes into ischaemic myocardium) has had a mixed press overthe past decade. Some attribute its effect to new vesselformation, others cite a placebo effect. Although the channelsdo not stay open, they seem to stimulate new microvessels togrow. Injection of growth factors (vascular endothelial growthfactor and fibroblast growth factor) to induce new blood vesselgrowth also has this effect, and percutaneous injection of theseagents into scarred or ischaemic myocardium is achievable. The coronary artery imaging was provided by John Bowles, clinicalHowever, we need a more thorough understanding of specialist radiographer, and Nancy Alford, clinical photographer, Sheffield Teaching Hospitals NHS Trust, Sheffield.biological control mechanisms before we can be confident ofthe benefits of this technology. Competing interests: None declared.Challenges to mechanical revascularisationDeaths from coronary artery disease are being steadily reducedin the Western world. However, with increasing longevity, it isunlikely that we will see a reduction in the prevalence of itschronic symptoms. More effective primary and secondaryprevention; antismoking and healthy lifestyle campaigns; andthe widespread use of antiplatelet drugs, blockers, statins, andrenin-angiotensin system inhibitors may help prevent, or atleast delay, the presentation of symptomatic coronary arterydisease. In patients undergoing revascularisation, they areessential components of the treatment “package.” More effectiveanti-atherogenic treatments will no doubt emerge in the nearfuture to complement and challenge the dramatic progressbeing made in percutaneous coronary intervention.36
  • 46. 11 Percutaneous interventional electrophysiologyGerry C KayeBefore the 1980s, cardiac electrophysiology was primarily usedto confirm mechanisms of arrhythmia, with management Tachyarrhythmiasmainly by pharmacological means. However, recognisedshortcomings in antiarrhythmic drugs spurred the development Supraventricular tachycardias Ventricular tachycardiasof non-pharmacological treatments, particularly radiofrequencyablation and implantable defibrillators. The two major mechanisms by which arrhythmias occur are Ischaemic Non-ischaemicautomaticity and re-entrant excitation. Most arrhythmias are ofthe re-entrant type and require two or more pathways that areanatomically or functionally distinct but in electrical contact. Atrial Atrial Atrial Atrioventricular Junctional flutter fibrillation ectopy re-entry tachycardia re-entry tachycardiaThe conduction in one pathway must also be slowed to asufficient degree to allow recovery of the other so that anelectrical impulse may then re-enter the area of slowed Focal Multifocal Type A Type Bconduction. Concealed Overt accessory pathways (such as accessory pathways Wolff-Parkinson-White syndrome) B A B A B A Classification of arrhythmias Area of slow conduction Indications for electrophysiological studies Investigation of symptoms x History of persistent palpitations Normal Initiation by premature Tachycardia x Recurrent syncope sinus extrasystole (or due x Presyncope with impaired left ventricular function rhythm extrastimulus) causing to re-entry unidirectional block due continues Interventions to longer refractory x Radiofrequency ablation—Accessory pathways, junctional period down one arm tachycardias, atrial flutter, atrial fibrillation x Investigation of arrhythmias (narrow and broad complex) with orMechanism of a re-entry circuit. An excitation wave is propagated at a without radiofrequency ablationnormal rate down path A, but slowly down path B. An excitation wave from x Assessment or ablation of ventricular arrhythmiasan extrasystole now encounters the slow pathway (B), which is still Contraindicationsrefractory, creating unidirectional block. There is now retrograde x Severe aortic stenosis, unstable coronary disease, left main stemconduction from path A, which coincides with the end of the refractory stenosis, substantial electrolyte disturbanceperiod in path B. This gives rise to a persistent circus movementIntracardiac electrophysiologicalstudiesIntracardiac electrophysiological studies give valuableinformation about normal and abnormal electrophysiology of Tricuspidintracardiac structures. They are used to confirm the valvemechanism of an arrhythmia, to delineate its anatomical Mitral valvesubstrate, and to ablate it. The electrical stability of the ventricles Coronary HRAcan also be assessed, as can the effects of an antiarrhythmic HRA sinus HBE HBE ostiumregimen. CSE CSEAtrioventricular conductionElectrodes positioned at various sites in the heart can give only Tricuspid valvelimited data about intracardiac conduction during sinus rhythm RVA RVAat rest. “Stressing” the system allows more information to begenerated, particularly concerning atrioventricular nodal Diagrams showing position of pacing or recording electrodes in the heart inconduction and the presence of accessory pathways. the right anterior oblique and left anterior oblique views (views from the By convention, the atria are paced at 100 beats/min for right and left sides of the chest respectively). HRA=high right atrial electrode, usually on the lateral wall or appendage; HBE=His bundleeight beats. The ninth beat is premature (extrastimulus), and the electrode, on the medial aspect of the tricuspid valve; RVA=right ventricularAH interval (the time between the atrial signal (A) and the His apex; CSE=coronary sinus electrode, which records electrical deflectionssignal (H), which represents atrioventricular node conduction from the left side of the heart between the atrium and ventricle 37
  • 47. ABC of Interventional Cardiologytime) is measured. This sequence is repeated with the ninth beatmade increasingly premature. In normal atrioventricular nodalconduction, the AH interval gradually increases as the V5extrastimulus becomes more premature and is graphically Arepresented as the atrioventricular nodal curve. The gradual HBE1-2prolongation of the AH interval (decremental conduction) is afeature that rarely occurs in accessory pathway conduction. CS1-2 V A CS3-4 700 H1H2 (msec) V A 600 CS5-6 V A 500 A normal CS7-8 400 atrioventricular nodal V A “hockey stick” curve 300 CS9-10 during antegrade conduction of atrial V A 200 extrastimuli. As the HRA3-4 atrial extrastimulus 100 VP (A1-A2) becomes more 0 premature, the AH 0 100 200 300 400 500 600 700 interval (H1-H2) shortens A1A2 (msec) until the atrioventricular node becomes VP V5 functionally refractory HBE1-2Retrograde ventriculoatrial conduction V ARetrograde conduction through the atrioventricular node is CS1-2assessed by pacing the ventricle and observing conduction back V Ainto the atria. The coronary sinus electrode is critically CS3-4important for this. It lies between the left ventricle and atrium V Aand provides information about signals passing over the left CS5-6side of the heart. The sequence of signals that pass from the V Aventricle to the atria is called the retrograde activation CS7-8sequence. V A If an accessory pathway is present, this sequence changes: CS9-10with left sided pathways, there is an apparent “short circuit” inthe coronary sinus with a shorter ventriculoatrial conduction V Atime. This is termed a concealed pathway, as its effect cannot be HRA3-4seen on a surface electrocardiogram. It conducts retrogradely VPonly, unlike in Wolff-Parkinson-White syndrome, where thepathway is bidirectional. Often intracardiac electrophysiological Coronary sinus electrode signals, with poles CS9-10 placed proximally nearstudies are the only way to diagnose concealed accessory the origin of the coronary sinus and poles 1-2 placed distally reflectingpathways, which form the basis for many tachycardias with changes in the left ventricular-left atrial free wall. Top: normal retrogradenarrow QRS complexes. activation sequence with depolarisation passing from the ventricle back through the atrioventricular node to the right atrium and simultaneously across the coronary sinus to the left atrium. Bottom: retrograde activationSupraventricular tachycardia sequence in the presence of an accessory pathway in the free wall of the left ventricle showing a shorter ventriculoatrial (VA) time than would be expected in the distal coronary sinus electrodes (CS1-2). Such a pathwaySupraventricular tachycardias have narrow QRS complexes would not be discernible from a surface electrocardiogramwith rates between 150-250 beats/min. The two commonmechanisms involve re-entry due to either an accessorypathway (overt as in Wolff-Parkinson-White syndrome orconcealed) or junctional re-entry tachycardia.Accessory pathwaysThese lie between the atria and ventricles in the atrioventricularring, and most are left sided. Arrhythmias are usually initiatedby an extrasystole or, during intracardiac electrophysiologicalstudies, by an extrastimulus, either atrial or ventricular. Theextrasystole produces delay within the atrioventricular node,allowing the signal, which has passed to the ventricle, to re-enterthe atria via the accessory pathway. This may reach theatrioventricular node before the next sinus beat arrives butwhen the atrioventricular node is no longer refractory, thusallowing the impulse to pass down the His bundle and back upto the atrium through the pathway. As ventriculardepolarisation is normal, QRS complexes are narrow. This Mechanisms for orthodromic (left) and antedromic (right)circuit accounts for over 90% of supraventricular tachycardias in atrioventricular re-entrant tachycardia38
  • 48. Percutaneous interventional electrophysiologyWolff-Parkinson-White syndrome. Rarely, the circuit is reversed,and the QRS complexes are broad as the ventricles are fully V1 1pre-excited. This rhythm is often misdiagnosed as ventricular inorigin. CS DIST 1 Treatment—Pathway ablation effects a complete cure by A V A Vdestroying the arrhythmia substrate. Steerable ablation CS PROX 1catheters allow most areas within the heart to be reached. Theleft atrium can be accessed either retrogradely via the aorticvalve, by flexing the catheter tip through the mitral valve, or ABL CATH 2.5transeptally across the atrial septum. Radiofrequency energy isdelivered to the atrial insertion of a pathway and usually results V5 1in either a rapid disappearance of pre-excitation on the surfaceelectrocardiogram or, in the case of concealed pathways, Surface electrocardiogram leads V1 and V5 and signals from the distalnormalisation of the retrograde activation sequence. Accessory coronary sinus electrodes (CS dist), proximal electrodes (CS prox), and thepathway ablation is 95% successful. Failure occurs from an tip of the ablation catheter (ABL CATH) during pathway ablation to treatinability to accurately map pathways or difficulty in delivering Wolff-Parkinson-White syndrome. The onset of radiofrequency energy (thinenough energy, usually because of positional instability of the arrow) produces loss of pre-excitation after two beats with a narrow complex QRS seen at the fourth beat (broad arrow). Prolongation of the AVcatheter. Complications are rare ( < 0.5%) and are related to signal in the coronary sinus occurs when pre-excitation is lostvascular access—femoral artery aneurysms or, with left sidedpathways, embolic cerebrovascular accidents.Junctional re-entry tachycardiaThis is the commonest cause of paroxysmal supraventriculartachycardia. The atrioventricular nodal curve shows a sudden H1H2 (msec)unexpected prolongation of the AH interval known as a “jump” 700in the interval. The tachycardia is initiated at or shortly after the 600jump. The jump occurs because of the presence of two 500pathways—one slowly conducting but with relatively rapid 400recovery (the slow pathway), the other rapidly conducting but 300with relatively slow recovery (the fast pathway)—called duality ofatrioventricular nodal conduction. This disparity between 200conduction speed and recovery allows re-entrance to occur. On 100a surface electrocardiogram the QRS complexes are narrow, 0 0 100 200 300 400 500 600 700 0 100 200 300 400 500 600 700and the P waves are often absent or distort the terminal portion A1A2 (msec) A1A2 (msec)of the QRS complex. These arrhythmias can often beterminated by critically timed atrial or ventricular extrastimuli. Atrioventricular nodal curves. In a patient with slow-fast junctional In the common type of junctional re-entry tachycardia (type re-entrant tachycardia (left) there is a “jump” in atrioventricular nodalA) the circuit comprises antegrade depolarisation of the slow conduction when conduction changes from the fast to the slow pathway. In apathway and retrograde depolarisation of the fast pathway. patient with accessory pathways conducting antegradely (such asRarely ( < 5% of junctional re-entry tachycardias) the circuit is Wolff-Parkinson-White syndrome) there is no slowing of conduction as seen in the normal atrioventricular node, and the curve reflects conductionreversed (type B). The slow and fast pathways are anatomically exclusively over the pathway (right)separate, with both inputting to an area called the compactatrioventricular node. The arrhythmia can be cured by mappingand ablating either the slow or fast pathway, and overall successoccurs in 98% of cases. Irreversible complete heart blockrequiring a permanent pacemaker occurs in 1-2% of cases, withthe risk being higher for fast pathway ablation. Therefore, slowpathway ablation is the more usual approach. Atrial beat prematureAtrial flutter and atrial fibrillationAtrial flutter is a macro re-entrant circuit within the rightatrium. The critical area of slow conduction lies at the base of Slow Fast Slow Circus Fast pathway pathway pathway pathwaythe right atrium in the region of the slow atrioventricular nodal motionpathway. Producing a discrete line of ablation between thetricuspid annulus and the inferior vena cava gives a line ofelectrical block and is associated with a high success rate interminating flutter. Flutter responds poorly to standardantiarrhythmic drugs, and ablation carries a sufficientlyimpressive success rate to make it a standard treatment. Atrial fibrillation is caused by micro re-entrant waveletscirculating around the great venous structures, or it may berelated to a focus of atrial ectopy arising within the pulmonaryveins at their junction with the left atrium. The first indicationthat atrial fibrillation was electrically treatable came from the Mechanism of slow-fast junctional re-entrant tachycardia. A premature atrialMaze operation (1990). Electrical dissociation of the atria from impulse finds the fast pathway refractory, allowing retrograde conductionthe great veins was carried out by surgical excision of the veins back up to the atria 39
  • 49. ABC of Interventional Cardiologyfrom their insertion sites and then suturing them back. Thescarred areas acted as insulation, preventing atrial wave-frontsfrom circulating within the atria. Similar lines of block can beachieved by catheter ablation within the right and left atria. Theresults look promising, although this is a difficult, prolongedprocedure with a high relapse rate. Of more interest is asub-group of patients with runs of atrial ectopy, whichdegenerate to paroxysms of atrial fibrillation. Theseextrasystoles usually originate from the pulmonary veins, andtheir ablation substantially reduces the frequency ofsymptomatic atrial fibrillation. With better understanding of theunderlying mechanisms and improved techniques, atrialfibrillation may soon become a completely ablatablearrhythmia.Ventricular tachycardiaVentricular tachycardia carries a serious adverse prognosis,particularly in the presence of coronary artery disease andimpaired ventricular function. Treatment options include drugs, Diagram of basket-shaped mapping catheter with severaloccasional surgical intervention (bypass or arrhythmia surgery), recording electrodes (red dots). The basket retracts into aand implantable defibrillators, either alone or in combination. catheter for placement in either the atria or ventricles. Once it is in position, retraction of the catheter allows theVentricular tachycardia can be broadly divided into two groups, basket to expandischaemic and non-ischaemic. The latter includes arrhythmiasarising from the right ventricular outflow tract and thoseassociated with cardiomyopathies. Since the radiofrequency energy of an ablation catheter isdestructive only at the site of the catheter tip, this approachlends itself more to arrhythmias where a discrete abnormality Further readingcan be described, such as non-ischaemic ventricular tachycardia. x Olgin JE, Zipes DP. Specific arrhythmias: diagnosis and treatment.In ischaemic ventricular tachycardia, where the abnormal In: Braunwald E, Zipes DP, Libby P, eds. Heart disease. 6th ed. Philadelphia: Saunders, 2001:1877-85substrate often occurs over a wide area, the success rate is lower. x McGuire MA, Janse MJ. New insights on the anatomical location of Ideally, the arrhythmia should be haemodynamically stable, components of the reentrant circuit and ablation therapy forreliably initiated with ventricular pacing, and mapped to a atrioventricular reentrant tachycardia. Curr Opin Cardiol 1995;localised area within the ventricle. In many cases, however, this 10:3-8is not possible. The arrhythmia may be unstable after initiation x Jackman WM, Beckman KJ, McClelland JH, Wang X, Friday KJ,and therefore cannot be mapped accurately. The circuit may Roman CA, et al. Treatment of supraventricular tachycardia due toalso lie deep within the ventricular wall and cannot be fully atrioventricular nodal re-entry by radiofrequency catheter ablation of the slow-pathway conduction. N Engl J Med 1992;327:313-8ablated. However, detailed intracardiac maps can be made with x Calkins H, Leon AR, Deam AG, Kalbfleisch SJ, Langberg JJ,multipolar catheters. A newer approach is the use of a Morady F. Catheter ablation of atrial flutter using radiofrequencynon{contact mapping catheter, which floats freely within the energy. Am J Cardiol 1994;73:353-6ventricles but senses myocardial electrical circuits. x Schilling RJ, Peter NS, Davies DW. Feasibility of a non-contact Although the overall, long term, success rate for catheter for endocardial mapping of human ventricularradiofrequency ablation of ischaemic ventricular tachycardia is tachycardia. Circulation 1999;99:2543-52only about 65%, this may increase.ConclusionThe electrophysiological approach to treating arrhythmias has Competing interests: None declared.been revolutionised by radiofrequency ablation. Better The diagrams showing the mechanisms of orthodromic and antedromiccomputerised mapping, improved catheters, and more efficient atrioventricular re-entrant tachycardia and of slow-fast atrioventricularenergy delivery has enabled many arrhythmias to be treated nodal re{entrant tachycardia are reproduced from ABC of Clinicaland cured. The ability to ablate some forms of atrial fibrillation Electrocardiography, edited by Francis Morris, 2002.and improvement in ablation of ventricular tachycardia isheralding a new age of electrophysiology. Ten years ago it couldhave been said that electrophysiologists were a relatively benignbreed of cardiologists who did little harm but little good either.That has emphatically changed, and it can now be attested thatelectrophysiologists exact the only true cure in cardiology.40
  • 50. 12 Implantable devices for treating tachyarrhythmiasTimothy Houghton, Gerry C KayePacing treatment for tachycardia control has achieved success,notably in supraventricular tachycardia. Pacing termination forventricular tachycardia has been more challenging, but anunderstanding of arrhythmia mechanisms, combined withincreasingly sophisticated pacemakers and the ability to deliverintracardiac pacing and shocks, have led to success withimplantable cardioverter defibrillators.Mechanisms of pacing terminationThere are two methods of pace termination. Underdrive pacing was used by early pacemakers to treatsupraventricular and ventricular tachycardias. Extrastimuli areintroduced at a constant interval, but at a slower rate than thetachycardia, until one arrives during a critical period,terminating the tachycardia. Because of the lack of sensing ofthe underlying tachycardia, there is a risk of a paced beat fallingon the T wave, producing ventricular fibrillation or ventricular Changes in implantable cardioverter defibrillators over 10 yearstachycardia, or degenerating supraventricular tachycardias to (1992-2002). Apart from the marked reduction in size, the implant techniqueatrial fibrillation. It is also not particularly successful at and required hardware have also dramatically improved—from theterminating supraventricular tachycardia or ventricular sternotomy approach with four leads and abdominal implantation to the present two-lead transvenous endocardial approach that is no more invasivetachycardia and is no longer used routinely. than a pacemaker implant Overdrive pacing is more effective for terminating bothsupraventricular and ventricular tachycardias. It is painless,quick, effective, and associated with low battery drain of the Mechanisms of arrhythmiaspacemaker. Implantation of devices for terminating Unicellular Multicellularsupraventricular tachycardias is now rarely required because of x Enhanced automaticity x Re-entrythe high success rate of radiofrequency ablative procedures (see x Triggered activity—early or x Electrotonic interactionprevious article). Overdrive pacing for ventricular tachycardia is delayed after depolarisations x Mechanico-electrical couplingoften successful but may cause acceleration or induceventricular fibrillation. Therefore, any device capable of pacetermination of ventricular tachycardia must also havedefibrillatory capability. Arrhythmias associated with re-entry x Atrial flutter x Sinus node re-entry tachycardiaImplantable cardioverter defibrillators x Junctional re-entry tachycardia x Atrioventricular reciprocating tachycardias (suchInitially, cardioverter defibrillator implantation was a major as Wolff-Parkinson-White syndrome)operation requiring thoracotomy and was associated with 3-5% x Ventricular tachycardiamortality. The defibrillation electrodes were patches sewn on tothe myocardium, and leads were tunnelled subcutaneously tothe device, which was implanted in a subcutaneous abdominalpocket. Early devices were large and often shocked patientsinappropriately, mainly because these relatively unsophisticatedunits could not distinguish ventricular tachycardia fromsupraventricular tachycardia.Current implantation proceduresModern implantable cardioverter defibrillators are transvenoussystems, so no thoracotomy is required and implantationmortality is about 0.5%. The device is implanted eithersubcutaneously, as for a pacemaker, in the left or rightdeltopectoral area, or subpectorally in thin patients to preventthe device eroding the skin. The ventricular lead tip is positioned in the right ventricularapex, and a second lead can be positioned in the right atrialappendage to allow dual chamber pacing if required anddiscrimination between atrial and ventricular tachycardias. Theventricular defibrillator lead has either one or two shocking Chest radiograph of a dual chamber implantablecoils. For two-coil leads, one is proximal (usually within the cardioverter defibrillator with a dual coil ventricularsuperior vena cava), and one is distal (right ventricular apex). lead (black arrow) and right atrial lead (white arrow) 41
  • 51. ABC of Interventional CardiologyDuring implantation the unit is tested under conscioussedation. Satisfactory sensing during sinus rhythm, ventriculartachycardia, and ventricular fibrillation is established, as well aspacing and defibrillatory thresholds. Defibrillatory thresholdsshould be at least 10 joules less then the maximum output ofthe defibrillator (about 30 joules).New developmentsAn important development is the implantable cardioverterdefibrillator’s ability to record intracardiac electrograms. Thisallows monitoring of each episode of anti-tachycardia pacing ordefibrillation. If treatment has been inappropriate, thenprogramming changes can be made with a programming unitplaced over the defibrillator site. Current devices use anti-tachycardia pacing, with low andhigh energy shocks also available—known as tiered therapy.Anti-tachycardia pacing can take the form of adaptive burstpacing, with cycle length usually about 80-90% of that of the Posteroanterior and lateral chest radiographs of transvenous implantable cardioverter defibrillator showing the proximal and distal lead coils (arrows)ventricular tachycardia. Pacing bursts can be fixed (constantcycle length) or autodecremental, when the pacing burstaccelerates (each cycle length becomes shorter as the pacingtrain progresses). Should anti-tachycardia pacing fail, lowenergy shocks are given first to try to terminate ventriculartachycardia with the minimum of pain (as some patients remainconscious despite rapid ventricular tachycardia) and reducebattery drain, thereby increasing device longevity. With the advent of dual chamber systems and improveddiagnostic algorithms, shocking is mostly avoided duringsupraventricular tachycardia. Even in single lead systems the AF AF AS AS AS AS AS AS (AS) (AS) AF AF AFalgorithms are now sufficiently sophisticated to differentiate 165 225 380 420 420 390 380 AS 388 AS 353 AF 350 AF 200 AF 165 178 AF AF [AS] [AS] [AS] [AS] [AS] 353 505 238 208 188 350 170between supraventricular tachycardia and ventricular 98 VS VS VS VT VT VT VP VP-M VS 435 418VS 420 VS 383 VT 383 VT 373 VS 523 VP-MT 500tachycardia. There is a rate stability function, which assesses 410 418 410 385 375 703 500cycle length variability and helps to exclude atrial fibrillation. Intracardiac electrograms from an implantable cardioverter defibrillator. Device recognition of tachyarrhythmias is based mainly on Upper recording is intra-atrial electrogram, which shows atrial fibrillation.the tachycardia cycle length, which can initiate anti-tachycardia Middle and lower tracings are intracardiac electrograms from ventriclepacing or low energy or high energy shocks. With rapidtachycardias, the device can be programmed to give a highenergy shock as first line treatment.ComplicationsThese include infection; perforation, displacement, fracture, or V V V V V V V V V V VC V V C V V V Vinsulation breakdown of the leads; oversensing or undersensing S S S S S S S S S S SE R S D S S S Sof the arrhythmia; and inappropriate shocks for sinus tachycardiaor supraventricular tachycardia. Psychological problems arecommon, and counselling plays an important role. Regular followup is required. If antiarrhythmic drugs are taken the potential use T T T T T T T T T T T V V V V V V V V V V V V C V V C V V V Vof an implantable cardioverter defibrillator is reduced. S S D P P PP PPPP S S S S S S S S S S S S E R S D S S S S Precautions—after patient death the device must be switchedoff before removal otherwise a severe electric shock can bedelivered to the person removing the device. The implantingcentre or local hospital should be informed that the patient hasdied and arrangements can usually be made to turn the ICDoff. The device must be removed before cremation. T T T T T T T T T T T T T T T T T V F TDriving and implantable cardioverter defibrillators S S S S S S S D P P P P P P P P P S S SThe UK Driver and Vehicle Licensing Agency recommends thatgroup 1 (private motor car) licence holders are prohibited fromdriving for six months after implantation of a defibrillator whenthere have been preceding symptoms of an arrhythmia. If ashock is delivered within this period, driving is withheld for a T T T T T T T T T T T T T T T T T V V Vfurther six months. S S S S S S S S D P P P P P P P P S S S Any change in device programming or antiarrhythmic Intracardiac electrograms from implantable cardioverter defibrillators. Top:drugs means a month of abstinence from driving, and all Ventricular tachycardia terminated with a single high energy shock. Second down: Ventricular tachycardia acceleration after unsuccessful ramp pacing,patients must remain under regular review. There is a five year which was then terminated with a shock. Third down: Unsuccessful fixedprohibition on driving if treatment or the arrhythmia is burst pacing. Bottom: Successful ramp pacing termination of ventricularassociated with incapacity. tachycardia42
  • 52. Implantable devices for treating tachyarrhythmias Drivers holding a group 2 licence (lorries or buses) are Guidelines for implanting cardioverter defibrillatorspermanently disqualified from driving. For “primary prevention” x Non-sustained ventricular tachycardia on Holter monitoring (24Indications for defibrillator use hour electrocardiography) x Inducible ventricular tachycardia on electrophysiological testingPrimary prevention x Left ventricular dysfunction with an ejection fraction < 35% and noPrimary prevention is considered in those who have had a worse than class 3 of the NYHA functional classification of heart failuremyocardial infarction, depressed left ventricular systolicfunction, non-sustained ventricular tachycardia, and inducible For “secondary prevention” x Cardiac arrest due to ventricular tachycardia or ventricularsustained ventricular tachycardia at electrophysiological studies. fibrillation The major primary prevention trials, MADIT and MUSTT, x Spontaneous sustained ventricular tachycardia causing syncope orshowed that patients with implanted defibrillators had > 50% substantial haemodynamic compromiseimprovement in survival compared with control patients, x Sustained ventricular tachycardia without syncope or cardiac arrestdespite 75% of MADIT control patients being treated with the in patients who have an associated reduction in ejection fractionantiarrhythmic drug amiodarone. A recent trial (MADIT-II) ( < 35%) but are no worse than class 3 of NYHA functional classification of heart failurerandomised 1232 patients with any history of myocardial NYHA = New York Heart Associationinfarction and left ventricular dysfunction (ejection fraction < 30%) to receive a defibrillator or to continue medicaltreatment and showed that patients with the device had a 31%reduction in risk of death. Although these results are good news Names of trialsclinically, they raise difficult questions about the potentially x MADIT—Multicenter automatic defibrillator implantation trialcrippling economic impact of this added healthcare cost. x MUSTT—Multicenter unsustained tachycardia trial Implantation is also appropriate for cardiac conditions with x COMPANION—Comparison of medical therapy, pacing, anda high risk of sudden death—long QT syndrome, hypertrophic defibrillation in chronic heart failurecardiomyopathy, Brugada syndrome, arrhythmogenic rightventricular dysplasia, and after repair of tetralogy of Fallot.Secondary preventionSecondary prevention is suitable for patients who have survivedcardiac arrest outside hospital or who have symptomatic,sustained ventricular tachycardia. A meta-analysis of studies ofimplanted defibrillators for secondary prevention showed thatthey reduced the relative risk of death by 28%, almost entirelydue to a 50% reduction in risk of sudden death. When left ventricular function is impaired and heart failureis highly symptomatic, addition of a third pacing lead in thecoronary sinus allows left ventricular pacing andresynchronisation of ventricular contraction. Indications forthese new “biventricular” pacemakers include a broad QRScomplex ( > 115-130 ms), left ventricular dilatation, and severedyspnoea (New York Heart Association class 3). Biventricularpacing improves symptoms and, when combined with animplantable cardioverter defibrillator, confers a significant(40%) mortality benefit (COMPANION study). Chest radiograph showing biventricular pacemaker with leads in the right ventricle, right atrium, and coronary sinus (arrows)Atrial flutter and fibrillationPacing to prevent atrial tachycardias, including atrial fibrillation,is presently under intense scrutiny as early results have beenfavourable. Atrial fibrillation is often initiated by atrialextrasystoles, and attention has focused on pacing to suppressatrial extrasystole, thereby preventing paroxysmal and sustainedatrial fibrillation.Atrial flutterTermination of atrial flutter is most reliable with burst pacingfrom the coronary sinus or right atrium and usually requireslonger periods of pacing (5-30 s). The shorter the paced cyclelength, the sooner the rhythm converts to sinus. Directconversion to sinus rhythm is achievable with sustainedoverdrive pacing. However, the success of radiofrequencyablation means these techniques are rarely used.Atrial fibrillation Prevention with pacing—Retrospective studies have shown that Continuous electrocardiogram showing sinus rhythm with frequent atrialatrial based pacing results in a reduced burden of atrial extrasystoles (top) arising from the pulmonary veins degenerating into atrialfibrillation compared with ventricular based pacing. Pacing the fibrillation (bottom) 43
  • 53. ABC of Interventional Cardiologyatria at high rates may prevent the conditions required forre{entry and thus prevent atrial fibrillation. Current research is Further readingbased on triggered atrial pacing, and specific preventive and x O’Keefe DB. Implantable electrical devices for the treatment of tachyarrhythmias. In: Camm AJ, Ward DE, eds. Clinical aspects ofanti-tachycardia pacing systems are now available for patients cardiac arrhythmias. London: Kluwer Academic Publishers,with symptomatic paroxysmal atrial tachycardias that are not 1988:337-57controlled by drugs. Such devices continually scan the sinus rate x Cooper RAS, Ideker RE. The electrophysiological basis for theand monitor atrial extrasystoles. Right atrial overdrive pacing at prevention of tachyarrhythmias. In: Daubert JC, Prystowsky EN,10-29 beats per minute faster than the sinus rate suppresses the Ripart A, eds. Prevention of tachyarrhythmias with cardiac pacing.frequency of extrasystoles. The pacing rate then slows to allow Armonk, NY: Futura Publishing, 1997:3-24 x Josephson ME. Supraventricular tachycardias. In: Bussy K, ed.sinus activity to take over, provided no further extrasystoles are Clinical cardiac electrophysiology. Philadelphia: Lea and Febiger,sensed. In some patients atrial fibrillation is initiated during 1993:181-274sleep, when the sinus rate is vagally slowed. Resynchronisation x Connolly SJ, Hallstrom AP, Cappato R, Schron EB, Kuck KH,(simultaneous pacing at two different atrial sites) in patients Zipes DP, et al. Meta-analysis of the implantable cardioverterwith intra-atrial conduction delay may be beneficial. Clinical defibrillator secondary prevention trials. Eur Heart J 2000;21:trials will help answer the question of which form of pacing best 2071-8prevents atrial fibrillation. x Mirowski M, Mower MM, Staewen WS, Denniston RH, Mendeloff AI. The development of the transvenous automatic defibrillator. Cardioversion with implantable atrial defibrillators—These are Ann Intern Med 1973;129:773-9useful in some patients with paroxysmal atrial fibrillation. It isknown that rapid restoration of sinus rhythm reduces the risk ofprotracted or permanent atrial fibrillation. Cardioversion issynchronised to the R wave, and shocks are given between the Competing interests: TH has been reimbursed by Guidant for attending acoronary sinus and right ventricular leads. The problem is that conference in 2001.shocks of > 1 joule are uncomfortable, and the mean The figure of implantable cardioverter defibrillators from 1992 and 2002 isdefibrillation threshold is 3 joules. Thus, sedation is required supplied by C M Finlay, CRT coordinator, Guidant Canada Corporation,before each shock. Toronto.Future developmentsWith the development of anti-atrial fibrillation pacing, focalablation to the pulmonary veins, and flutter ablation,implantable cardioverter defibrillators will be used less often inyears to come. The future of device therapy for atrial fibrillationand atrial flutter probably lies in the perfection ofradiofrequency ablation and atrial pacing, although there willstill be a place for atrioventricular nodal ablation andpermanent ventricular pacing in selected patients.44
  • 54. 13 Interventional paediatric cardiologyKevin P WalshInterventional paediatric cardiology mainly involves dilatationof stenotic vessels or valves and occlusion of abnormalcommunications. Many transcatheter techniques—such asballoon dilatation, stent implantation, and coil occlusion—havebeen adapted from adult practice. Devices to occlude septaldefects, developed primarily for children, have also foundapplication in adults.Basic techniquesInterventional procedures follow a common method. Generalanaesthesia or sedation is required, and most procedures startwith percutaneous femoral access. Haemodynamicmeasurements and angiograms may further delineate theanatomy or lesion severity. A catheter is passed across thestenosis or abnormal communication. A guidewire is thenpassed through the catheter to provide a track over which Balloon atrial septostomy.therapeutic devices are delivered. Balloon catheters are Under echocardiographicthreaded directly, whereas stents and occlusion devices are control in a neonate with transposition of the greatprotected or constrained within long plastic sheaths. arteries, a balloon septostomy catheter has been passed via the umbilical vein, ductusDilatations venosus, inferior vena cava, and right atrium and throughSeptostomy the patent foramen ovale intoBalloon atrial septostomy, introduced by Rashkind 35 years ago, the left atrium. The balloon isimproves mixing of oxygenated and deoxygenated blood in inflated in the left atrium (top) and jerked back across thepatients with transposition physiology or in those requiring atrial septum into the rightventing of an atrium with restricted outflow. Atrial septostomy atrium (middle). Thisoutside the neonatal period, when the atrial septum is much manoeuvre tears the atrialtougher, is done by first cutting the atrial septum with a blade. septum to produce an atrial septal defect (arrow, bottom) with improved mixing and arterial saturationsBalloon valvuloplastyPulmonary valve stenosisBalloon valvuloplasty has become the treatment of choice forpulmonary valve stenosis in all age groups. It relieves thestenosis by tearing the valve, and the resultant pulmonaryregurgitation is mild and well tolerated. Surgery is used only fordysplastic valves in patients with Noonan’s syndrome, who havesmall valve rings and require a patch to enlarge the annulus. Valvuloplasty is especially useful in neonates with criticalpulmonary stenosis, where traditional surgery carried a highmortality. In neonates with the more extreme form ofpulmonary atresia with an intact ventricular septum,valvuloplasty can still be done by first perforating thepulmonary valve with a hot wire. Pulmonary valvuloplasty canalso alleviate cyanotic spells in patients with tetralogy of Fallot Balloon pulmonary valvuloplasty. A largewhose pulmonary arteries are not yet large enough to undergo valvuloplasty balloon isprimary repair safely. inflated across a stenotic pulmonary valve, which produces a waist-like balloonAortic valve stenosis indentation (A, top). FurtherUnlike in adults, aortic valve stenosis in children (which is inflation of the balloonnon{calcific) is usually treated by balloon dilatation. A balloon abolishes the waist (bottom). This patient had previouslysize close to the annulus diameter is chosen, as overdilatation undergone closure of a(routinely done in pulmonary stenosis) can result in substantial mid{muscular ventricularaortic regurgitation. The balloon is usually introduced septal defect with a drumretrogradely via the femoral artery and passed across the aortic shaped Amplatzer ventricular septal defect occluder (B, top).valve. Injection of adenosine, producing brief cardiac standstill A transoesophagealduring balloon inflation, avoids balloon ejection by powerful left echocardiogram probe is alsoventricular contraction. visible 45
  • 55. ABC of Interventional Cardiology In neonates with critical aortic stenosis and poor leftventricular function the balloon can be introduced in anantegrade fashion, via the femoral vein and across theinteratrial septum through the patent foramen ovale. Thisreduces the risk of femoral artery thrombosis and perforationof the soft neonatal aortic valve leaflets by guidewires. The longterm result of aortic valve dilatation in neonates depends onboth effective balloon dilatation of the valve and the degree ofassociated left heart hypoplasia. Pulmonary artery stenting. A child with previously repairedAngioplasty tetralogy of Fallot had severeBalloon dilatation for coarctation of the aorta is used for both stenoses at the junction of rightnative and postsurgical coarctation and is the treatment of and left branch pulmonarychoice for re-coarctation. Its efficacy in native coarctation arteries with main pulmonary artery (top left). Two stents weredepends on the patient’s age and whether there is appreciable inflated simultaneously acrossunderdevelopment of the aortic arch. Neonates in whom the the stenoses in criss-crossductal tissue forms a sling around the arch have a good initial arrangement (top right).response to dilatation but a high restenosis rate, probably Angiography shows complete relief of the stenoses (left)because of later contraction of ductal tissue. Older patients havea good response to balloon dilatation. However, overdilatationmay result in formation of an aneurysm.StentsThe problems of vessel recoil or dissection have been addressedby the introduction of endovascular stents. This developmenthas been particularly important for patients with pulmonaryartery stenoses, especially those who have undergone correctivesurgery, for whom repeat surgery can be disappointing. Moststents are balloon expandable and can be further expandedafter initial deployment with a larger balloon to keep up with achild’s growth. Results from stent implantation for pulmonary arterystenosis have been good, with sustained increases in vesseldiameter, distal perfusion, and gradient reduction.Complications consist of stent misplacement and embolisation,in situ thrombosis, and vessel rupture. Stents are increasingly used to treat native coarctation inpatients over 8 years old. Graded dilatation of a severely stenoticsegment over two operations may be required to avoid Stenting of coarctation of the aorta. An aortogram in an adolescent boy shows a long segment coarctation (arrows, left). A cineframe shows theoverdistension and possible formation of an aneurysm. In stent being inflated into place (middle). Repeat aortagraphy showspatients with pulmonary atresia without true central pulmonary complete relief of the coarctation (right)arteries, stenotic collateral arteries can be enlarged by stentimplantation (often preceded by cutting balloon dilation) toproduce a useful increase in oxygen saturation. An exciting new advance has been percutaneous valvereplacement. A bovine jugular vein valve is sutured to the inneraspect of a large stent, which is crimped on to a balloon deliverysystem and then expanded into a valveless outflow conduit thathas been surgically placed in the right ventricle. Several patientshave been treated successfully with this system, although followup is short.OcclusionsTranscatheter occlusion of intracardiac and extracardiaccommunications has been revolutionised by the development ofthe Amplatzer devices. These are made from a cylindricalNitinol wire mesh and formed by heat treatment into differentshapes. A sleeve with a female thread on the proximal end ofthe device allows attachment of a delivery cable with a malescrew. The attached device can then be pulled and pushed into Transcatheter closure of a perimembranous ventricular septal defect. Leftthe loader and delivery sheath respectively. A family of devices ventriculogram shows substantial shunting of dye (in direction of arrow) through a defect in the high perimembranous ventricular septum (left).has been produced to occlude ostium secundum atrial septal After placement of an eccentric Amplatzer membranous ventricular septaldefects, patent foramen ovale, patent ductus arteriosus, and defect device, a repeat left ventriculogram shows complete absence ofventricular septal defects. shunting (right)46
  • 56. Interventional paediatric cardiologyAtrial septal defectsThe Amplatzer atrial septal defect occluder has the shape oftwo saucers connected by a central stent-like cylinder that variesin diameter from 4 mm to 40 mm to allow closure of both smalland large atrial septal defects. Very large secundum atrial septaldefects with incomplete margins (other than at the aortic end ofthe defect) may require a surgically placed patch. Cineframe showing the three An atrial septal defect is sized with catheter balloons of components of the Amplatzerprogressively increasing diameter. An occluder of the correct atrial septal defect occluder—asize is then introduced into the left atrium via a long left atrial disk, central stent (arrows), and a right atrialtransvenous sheath. The left atrial disk of the occluder is disk. The device has just beenextruded and pulled against the defect. The sheath is then unscrewed from the deliverypulled back to deploy the rest of the device (central waist and wire, and the male screw onright atrial disk) and released after its placement is assessed by the delivery wire can be seen (arrowhead)transoesophageal echocardiography. The defect is closed by theinduction of thrombosis on three polyester patches sewn intothe device and is covered by neocardia within two months.Aspirin is usually for given for six months and clopidrogrel for6-12 weeks. Worldwide, several thousand patients have had their atrialseptal defects closed with Amplatzer devices, with highocclusion rates. Complications are unusual and consist of devicemigration ( < 1%), transient arrhythmias (1-2%), and, rarely,thrombus formation with cerebral thromboembolism or aorticerosion with tamponade. Transcatheter occlusion is now thetreatment of choice for patients with suitable atrial septaldefects. Other devices are available, but none has the same Atrial septal defect occlusion. Transoesophageal echocardiograms of anapplicability or ease of use. atrial septal defect before (left) and after (right) occlusion with an Amplatzer atrial septal defect device. The three components of the device are easilyPatent foramen ovale seen. (LA=left atrium, RA=right atrium)The Amplatzer atrial septal defect occluder can also be used totreat adults with paradoxical thromboembolism via a patentforamen ovale. The Amplatzer patent foramen ovale occluderhas no central stent and is designed to close the flap-valve ofthe patent foramen ovale. Randomised trials are under way to Patent foramen ovale closure.compare device closure with medical treatment for preventing A cine frame of an implanted Amplatzer patent foramenrecurrent thromboembolism. ovale device shows that it differs from the atrial septalPatent ductus arteriosus defect device in not having aAlthough premature babies and small infants with a large central stent. Its right atrial disk is larger than the leftpatent ductus arteriosus are still treated surgically, most patients atrial disk and faces in awith a patent ductus arteriosus are treated by transcatheter coil concave direction towards theocclusion. This technique has been highly successful at closing atrial septumsmall defects, but when the minimum diameter is > 3 mmmultiple and larger diameter coils are required, which prolongsthe procedure and increases the risk of left pulmonary arteryencroachment. The Amplatzer patent ductus arteriosus plug,which has a mushroom shaped Nitinol frame stuffed withpolyester, is used for occluding larger defects. The occlusionrates are close to 100%, higher than published results forsurgical ligation. Transcatheter plugging of a large patent ductus arteriosus. An aortogram shows a large tubular patent ductus arteriosus with a large shunt of dye from the aorta to the pulmonary artery (top left). An Amplatzer plug is deployed in the defect, still attached to itsCoil occlusion of a patent ductus arteriosus. An aortogram performed via delivery wire (top right). A repeatthe transvenous approach shows dye shunting through the small conical aortogram after release of thepatent ductus arteriosus into the pulmonary artery (left). After placement of device shows no significant residualmultiple coils, a repeat aortogram shows no residual shunting (right) shunting (left) 47
  • 57. ABC of Interventional CardiologyVentricular septal defectsOcclusion devices are especially useful for multiple congenitalmuscular ventricular septal defects, which can be difficult tocorrect surgically. The Amplatzer occluder device has adrum{like shape and is deployed through long sheaths withrelatively small diameter. Such devices have also been used to occludeperimembranous defects, although in this location they caninterfere with aortic valve function. A device with eccentricdisks, which should avoid interference with adjacent valves, hasrecently been introduced. The Amplatzer membranous devicehas two discs connected by a short cylindrical waist. The device Transcatheter closure of a mid-muscular ventricular septal defect. A leftis eccentric, with the left ventricular disc having no margin ventriculogram shows substantial shunting of dye through a defect in thesuperiorly, where it could come near the aortic valve, and a mid-muscular ventricular septum (left). After placement of an Amplatzer muscular ventricular septal defect device, a repeat left ventriculogram showslonger margin inferiorly to hold it on the left ventricular side of only a small amount of shunting through the device (right), which ceasedthe defect. The end screw of the device has a flat portion, which after three monthsallows it to be aligned with a precurved pusher catheter. Thispusher catheter then extrudes the eccentric left ventricular diskfrom the specially curved sheath with its longer marginorientated inferiorly in the left ventricle. Initial results are The Amplatzer perimembranouspromising, particularly for larger infants with ventricular septal defect device. Thehaemodynamically important ventricular septal defects. two disks are offset from each Transcatheter occlusion has also been used to treat other to minimise the chance of the left ventricular disk impinging onventricular septal defects in adults who have had a myocardial the aortic valve. The central stent isinfarction, and a specific occluder has been introduced. It differs much narrower than in thefrom the infant device in having a 10 mm long central stent to muscular ventricular septal defectaccommodate the thicker adult interventricular septum. Its role device as the membranous septum is much thinner than the muscularin treatment is uncertain, but it offers an alternative for patients septumwho have significant contraindications to surgical closure.Coil occlusion of unwanted blood vesselsCoil occlusion of unwanted blood vessels (aortopulmonarycollateral arteries, coronary artery fistulae, arteriovenousmalformations, venous collaterals) is increasingly effectivebecause of improvements in catheter and coil design.Percutaneous intervention versussurgeryThe growth of interventional cardiology has meant that thesimpler defects are now dealt with in catheterisationlaboratories, and cardiac surgeons are increasingly operating onmore complex lesions such as hypoplastic left heart syndrome.More importantly, interventional cardiology can complementthe management of these complex patients, resulting in a better Coil occlusion of a coronary fistula. A selective left coronary arteriogramoutcome for children with congenital heart disease. shows a fistula arising from the left anterior descending coronary artery (arrow, left) draining to the right ventricle (RV). Multiple interlocking Complications such as device embolisation, vessel or detachable coils are placed to completely occlude the fistula (arrow, right)chamber perforation, thrombosis, and radiation exposure canbe reduced by careful selection of patients and devices,meticulous technique, low dose pulsed fluoroscopy, and, most Further readingimportantly, operator experience. Further developments in x Kan JS, White RI Jr, Mitchell SE, Gardner TJ. Percutaneous ballooncatheter and device design will improve and widen treatment valvuloplasty: a new method for treating congenital pulmonary valve stenosis. N Engl J Med 1982;307:540-2applications. x Waight DJ, Cao Q-L, Hijazi ZM. Interventional cardiac catheterisation in adults with congenital heart disease. In: GrechCompeting interests: None declared. ED, Ramsdale DR, eds. Practical interventional cardiology. 2nd ed. London: Martin Dunitz, 2002:390-406 x Morrison WL, Walsh KP. Transcatheter closure of ventricular septal defect post myocardial infarction. In: Grech ED, Ramsdale DR, eds. Practical interventional cardiology. 2nd ed. London: Martin Dunitz, 2002:362-4 x Masura J, Walsh KP, Thanopoulous B, Chan C, Bass J, Goussous Y, et al. Catheter closure of moderate- to large-sized patent ductus arteriosus using the new Amplatzer duct occluder: immediate and short-term results. J Am Coll Cardiol 1998;31:878-82 x Walsh KP, Maadi IM. The Amplatzer septal occluder. Cardiol Young 2000;10:493-5048
  • 58. IndexPage numbers in bold type refer to figures; those in italics refer to tables.abciximab 21, 25, 26, 26, 27, 28 balloon pump, intra–aortic 8, 20ablation 30-1, 39–40 balloon septostomy 45, 45accessory pathways 37–8, 37, 38, 39–40 balloon valvuloplasty 29–30, 45–6, 45, 46acute coronary events 1 barotrauma, arterial 6acute coronary syndromes 16–18, 16, 19–21 blood vessels, coil occlusion 48, 48 diagnosis 16–17 brachytherapy 5, 10, 10, 34 management 35, 35 bypass surgery 12, 35adjunctive pharmacotherapy see pharmacotherapy, chronic stable angina 12, 12, 13, 13, 14–15, 14 interventional emergency 9, 24, 27AH interval 37–8 percutaneous in situ 36Amplatz catheter 3, 3Amplatzer septal defect occluders 31–2, 31, 32, 47, “candy wrapper” lesions 10, 10 47, 48 cardiac biochemical markers 16, 17, 18angina 1–4, 5, 15 cardiac tamponade 9, 23, 47 see also chronic stable angina; unstable angina cardiac troponin I/T 17, 18angiography 3, 3, 3, 17, 17, 24, 33 cardiogenic shock 22–4, 22angioplasty 5, 5, 6, 6, 19–20 cardiology referral, priorities for 1, 1 paediatric 46 cardiomyopathy, hypertrophic 30–1, 30, 30, 31anterior descending arteries 14, 20, 22, 33, 34 cardiovascular disease 1, 1anticoagulent therapy see aspirin; heparin genetic 30antiplatelet drugs 5, 7, 25, 26–8 see also coronary artery disease see also abciximab; clopidogrel; glycoprotein IIb/IIIa cardioverter defibrillators 41–4, 43 inhibitors cathetersantithrombotic therapy 25–8, 25 balloon 5, 5, 9, 9, 10, 10, 29aortic valve stenosis 30, 45–6 diagnostic 3–4, 3arrhythmias 37–40, 37, 41 guide 5, 9, 9 driving and 42 intravascular ultrasound (IVUS) 4 implantable devices 41–4 non-contact mapping 40, 40 reperfusion 20, 20, 21 cerebrovascular events 19, 20, 29arterial grafts 12, 13 chest pain 1arteries chronic stable angina 12–15 access 9, 9 circumflex coronary arteries 14, 33, 34 occlusion 6, 16, 19–21 clinical trials, refusal to participate in 15 restenosis 6 clopidogrel 8, 17, 25, 25, 26, 27 stenosis 1, 1, 4, 4, 8, 8, 45–6 coarctation of the aorta 46, 46aspirin 8, 17, 25, 25, 26 coil occlusion, transcatheter 47, 47, 48, 48athero-ablation/atherectomy 5, 6, 6, 10, 10 congenital abnormalities 31–2, 45–8atheroma 1, 1 contrast medium 3, 9, 10, 33atheromatous plaques 1, 1, 4 coronary arteries, normal 3 rupture 16, 16, 19–21 coronary artery, right, occlusion 11, 14, 17, 21, 23, 33, 35 ulcerated 35, 36 coronary artery bypass graft surgery see bypass surgeryatrial extrasystoles 43, 44 coronary artery disease 1–4, 15, 35atrial fibrillation 37, 39–40, 44 coronary sinus electrode signals 38, 38atrial flutter 37, 39–40 coronary stents see stentsatrial septal defects 29, 31, 31, 31, 47, 47 cutting devices 6, 6, 10, 10atrial septostomy 45, 45atrial tachycardias 43–4, 43 defibrillators 40, 41–4, 43atrioventricular conduction 37–8, 38 diabetes chronic stable angina and 14–15balloon angioplasty 20, 20 stents and 10, 27, 34balloon catheters 5, 5, 9, 9, 10, 10, 29 direct angioplasty see primary angioplastyballoon dilatation, paediatric 46 Doppler flow wire and pressure wire 4 49
  • 59. Indexdrills, plaque removal 6, 6 pacemakers 31, 39, 41driving fitness 11, 42 biventricular 43, 43 temporary 8, 21electrocardiography 2, 2, 17, 17 pacing termination 41 intracardiac 42, 42 paclitaxel coated stents 11, 34electrophysiology, percutaneous interventional 37–40 paediatric interventional cardiology 45–8endothelial layer, in stents 7, 34 paradoxical embolism 32, 47eptifibatide 25, 26, 26, 27 patent ductus arteriosus 47, 47ethanol septal ablation 30–1 patent foramen ovale 31–2, 32, 47, 47exercise tests 2, 2, 13, 13 patients high risk 17, 18, 18fitness for work 11 refusal to participate in trials 15fluoroscopy 9 percutaneous coronary interventions adjunctive pharmacotherapy 5, 25, 25, 27glycoprotein IIb/IIIa receptor inhibitors 9, 17, 21, 25, 25, developments 5–7, 33–6 26–8, 26 devices 33 see also abciximab; eptifibatide; tirofiban indications for 8, 13, 14guide catheters 5, 9, 9 procedure 8–11guidewires 5, 9, 9 risk assessment 8 roles of 35heart block, ablation-induced 31 statistics 33heparin 9, 17 percutaneous interventional electrophysiology low molecular weight 25, 26 37–40 unfractionated 25–6, 25 percutaneous interventions, non-coronary 29–32“hockey stick” curve 38 pharmacotherapy, interventional 25–8hypertrophic cardiomyopathy 30–1, 30, 30, 31 photodynamic therapy 34hypotension, in myocardial infarction 22, 23, 24 “pigtail” catheter 3–4, 3 platelets 16, 16, 25implantable devices 40, 41–4, 43 see also antiplatelet drugsinternal mammary artery graft 12, 12, 13 primary angioplasty 19–20intra-aortic balloon pump 22, 23, 23, 23, 24 pulmonary artery stenosis 46intravascular ultrasound (IVUS) 4, 4 pulmonary hypertension 31, 32ischaemia 1–4, 2, 2, 16–17 pulmonary oedema 22, 22 in percutaneous procedures 9 pulmonary valve stenosis 45, 45 pulsus paradoxus 23, 23junctional re-entry tachycardia 37, 39, 39laser recanalisation 6, 10, 34 radiofrequency ablation 39, 40left main stem coronary disease 13 radionuclide myocardial perfusion imaging 2–3, 2left ventricular angiography 3, 3 recanalisation methods 19, 19left ventricular dysfunction 13, 13, 22, 43 re-endothelialisation, in stents 7, 34left ventricular function, assessment 3, 3 re-entrant arrhythmia 37, 37, 38, 39, 41left ventricular hypertrophy 30–1, 30 refractory coronary artery disease 15 reperfusion 23–4mitral regurgitation 23, 29, 30 reperfusion arrhythmias 20, 20, 21mitral valve stenosis 29–30, 29 restenosis see arteries; stentsmortality rates retrograde ventriculoatrial conduction 38 cardiogenic shock 22 revascularisation 35–6 chronic stable angina 13 right coronary artery occlusion 11, 14, 17, 21, 23, 33, 35 glycoprotein IIb/IIIa inhibitors and 27, 27 right ventricular infarction 23, 23 myocardial infarction 24multigated acquisition scan (MUGA) 3 saphenous vein graft 12, 12, 13, 13multivessel disease 13, 13, 14, 33, 34, 34 septal ablation, ethanol 30–1myocardial infarction 1–4, 35, 43 septal artery 30 non-ST segment elevation 16–18 septal defect closure 31–2, 31, 32, 47, 47, 48 percutaneous procedures and 9, 27, 27 septal enlargement 30, 30 septal defects caused by 32 septostomy, balloon atrial 45, 45 ST segment elevation 19–21 sirolimus coated stents 11, 11, 33myocardial revascularisation 5, 36 smoking 1, 18, 36myocardial rupture 23, 23 sonotherapy 34 stents 5, 6–7, 6, 7, 7, 9, 9, 22non-contact mapping catheters 40, 40 adjunctive pharmacotherapy 25, 27non-ST segment elevation myocardial infarction 16–18, 27 developments 33–4, 35–6, 35 drug eluting 6, 7, 11, 11, 28, 33–4, 35occlusions, paediatric 46–8 paediatric 46, 46overdrive pacing 41 primary angioplasty and 20–1, 21oxygen need 17, 23, 23 PTFE coated 650
  • 60. Index re-endothelialisation 7, 34 see also antithrombotic therapy restenosis 10–11, 10, 11, 28, 34 ticlopidene 25, 26stress echocardiography 2, 2, 2 TIMI risk score 18, 18ST segment elevation myocardial infarction 19–21, 23, 23, 28 tirofiban 25, 26, 26, 27supraventricular tachycardia 37, 38–9, 41–2systolic murmur, cardiogenic shock 23, 23 ultrasonography 4, 4 underdrive pacing 41tachyarrhythmias, implantable devices 41–4 unstable angina 16–18, 16, 27tachycardias 37, 38–9, 40, 43–4, 43tetralogy of Fallot 45, 46 valves see aortic valve; mitral valve; pulmonary valvethienopyridines (antiplatelet drugs) 26 valvuloplasty 29–30, 45–6, 45, 46 see also clopidogrel; ticlopidene ventricular septal defects 23, 30–1, 32, 32, 46, 48, 48thrombin inhibitors 26 ventricular tachycardia 37, 40, 41–2, 43thrombocytopenia, heparin–induced 25, 26thrombolytic drugs 19, 19, 23–4 Wolff-Parkinson-White syndrome 37, 38, 39, 39thrombosis 7, 22, 25–8, 25 thrombus formation 1, 16, 16, 35 x ray, chest pain 2, 3 51