• Save
Anesthesia and perioperative care for aortic surgery
Upcoming SlideShare
Loading in...5
×
 

Anesthesia and perioperative care for aortic surgery

on

  • 468 views

 

Statistics

Views

Total Views
468
Views on SlideShare
468
Embed Views
0

Actions

Likes
0
Downloads
0
Comments
0

0 Embeds 0

No embeds

Accessibility

Categories

Upload Details

Uploaded via as Adobe PDF

Usage Rights

© All Rights Reserved

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
    Processing…
Post Comment
Edit your comment

Anesthesia and perioperative care for aortic surgery Anesthesia and perioperative care for aortic surgery Document Transcript

  • K. Subramaniam et al. (eds.), Anesthesia and Perioperative Care for Aortic Surgery,DOI 10.1007/978-0-387-85922-4_2, © Springer Science+Business Media, LLC 2011Acute aortic syndrome is a modern term thatdescribes the acute presentation of patients withcharacteristic “aortic” pain caused by one of thelife-threatening thoracic aortic conditions includ-ing aortic dissection, intramural hematoma, andpenetrating atherosclerotic ulcer (Fig. 2.1). Thisentity involves acute lesions of the aorta involvingthe tunica media and can be distinguished by theiretiopathogenesis and characteristic appearanceusing various diagnostic imaging modalities.Recent advances in imaging techniques and ther-apeutic interventions have increased awareness ofthese pathological conditions and emphasized theimportance of early diagnosis and treatment.Definition and EpidemiologyAcute aortic syndrome includes five classes ofaortic disease (Table 2.1).1While being distinctpathological processes, there is the possibility ofprogression from one entity to another (Fig. 2.2).Each of these processes also shares the Stanfordclassification that defines the location and extent ofaortic involvement. Stanford type A begins in theascending aorta, while type B originates distal tothe left subclavian artery to involve the descendingthoracic aorta (Fig. 2.3). This classification systemis popular since it directs different managementstrategies and correlates with patient prognosis.Aortic dissections can also be classified as acute orchronic, depending on whether the dissection isless or greater than 2 weeks old.Aortic DissectionClassic aortic dissections (class I) are the mostcommon cause of acute aortic syndromes (70%).Aortic dissection is the most common aorticcatastrophe occurring two to three times more fre-quently than abdominal aortic rupture. The exactincidence is unknown but studies quote it to be2.6–3.5 per 100,000 person-years.2Informationgathered from the International Registry of AcuteAortic Dissection (IRAD) shows that two thirdsof patients are male with a mean age of 63.Women are affected less often and present at amean age of 67. Patients with dissections involv-ing the ascending aorta tend to present at ayounger age (50–55 years) than those with dis-sections of the descending aorta (60–70 years).Table 2.2 outlines multiple risk factors for thedevelopment of aortic dissection with hyperten-sion being the most common predisposing factor(72%). Following this is a history of atherosclero-sis (31%), cardiac surgery (18%), and Marfan’ssyndrome (5%). Younger patients (<40 years ofage) who present with aortic dissection most oftenhave associated Marfan’s syndrome, a bicuspidaortic valve or a history of aortic surgery.3Acute Aortic SyndromeCynthia M. Wells and Kathirvel SubramaniamC.M. Wells( )Department of Anesthesiology, University of PittsburghMedical Center – Presbyterian Hospital,Pittsburgh, PA, USAe-mail: wellsc2@upmc.edu217
  • C.M. Wells and K. SubramaniamPathologically, classic aortic dissections(class I) are characterized by an intimal tear withseparation of the aortic media into two layers, theinner two thirds and outer one third. This separa-tion extends for a variable distance in bothcircumferential and longitudinal fashion. Thevast majority of dissections originate from inti-mal tears in the ascending aorta within severalcentimeters of the sinuses of Valsalva where tor-sional movement of the aortic annulus provokesadditional downward traction in the aortic rootand increases longitudinal stress in that segmentof aorta. The other common site for an intimaltear to originate is in the descending aorta justdistal to the origin of the subclavian artery at theFig. 2.1 Classification of acute aortic syndromes (Reprinted with permission from Berger F et al.30)Table 2.1 Classification of acute aortic syndromeClass I – Classic aortic dissectionClass II – Intramural hematomaClass III – Localized dissection, intimal tear withoutextensive intimal flap formation, localized bulge in theaortic wallClass IV – Penetrating aortic ulcersClass V – Iatrogenic or post-traumatic dissectionFig.2.2 Progression of one type of acute aortic syndrometo another type18
  • 2 Acute Aortic Syndromesite of the ligamentum arteriosum. Tears occur inthe isthmus area because of increased tension atthe union of the relatively mobile aortic arch withthe fixed descending thoracic aorta. From thispoint, blood under pressure extends the dissec-tion in an antegrade direction although retrogradeextension is also possible, thus forming a falselumen and double channel aorta. A further reen-trance tear allows blood to circulate in the falselumen and communicate with the true lumen.Reentry tears are often located in the abdominalaorta, iliac arteries, or other aortic branches.These small communications, normally less than2 mm in diameter, represent intercostal andlumbar arteries severed by the dissection pro-cess.4The true lumen is most often the smaller ofthe two and is surrounded by calcifications ifpresent. The false lumen is located along theouter curve of the aortic arch and from the aorticisthmus, a dissection adopts a spiral route involv-ing the left border of the descending thoracicaorta and the left posterior region of the infradia-phragmatic and infrarenal aorta (Fig. 2.4). Fromthere, a dissection may involve any branches ofaorta including the arch vessels, the left intercos-tal, renal, and iliac vessels, most often, it is theleft renal and iliac artery which are involved.The celiac, superior mesenteric, and right renalarteries usually communicate with the true lumen.Dissections rarely extend to the common femoralarteries.Class III dissections are characterized by thepresence of an intimal tear without a flap orhematoma formation. Patients often present withthe classic symptoms of dissection and may haveassociated aneurysms, aortic regurgitation, orFig. 2.3 Types of acuteaortic syndromes based onthe site of aortic involve-ment (Reprinted withpermission fromSpringer4)Table 2.2 Risk factors for aortic dissectionLong-standing hypertensionMaleAdvanced agePrior cardiac surgeryKnown aortic aneurysm or prior dissectionCardiac catheterization/surgeryConnective tissue disordersMarfan’s syndromeEhlers−Danlos syndromeBicuspid aortic valveCoarctation of the aortaHereditary thoracic aortic diseaseVascular inflammationDeceleration injuryCocainePeripartum19
  • C.M. Wells and K. Subramaniampericardial effusion. Imaging techniques such asCT, MRI, or TEE may fail to detect this type ofdissection since each of these modalities dependson the presence and identification of an intimalflap or true and false lumen for diagnosis.Aortography may show an eccentric bulge in theaorta, which should raise the suspicion of thisclass of dissection. Treatment is similar to thatfor classic aortic dissection.1Class V aortic dissections are caused bytraumatic or iatrogenic injury. Traumatic dissec-tions are described in detail in another chapter.Iatrogenic aortic dissections may result fromcardiac surgery, percutaneous coronary interven-tions, or endovascular procedures. Dissectionsresulting from cardiac surgical procedures mayoccur during the procedure, early in the postop-erative period, or their presentation may bedelayed for years.5,6The incidence varies between0.12% and 0.35% of cardiac surgeries, but themortality is high unless recognized early. Injuryto the aorta can occur at the site of cross-clampplacement, cannulation and decannulation, aorto-tomy, cardioplegic cannulation, or aortocoronaryanastomosis. Preexisting atherosclerotic or con-nective tissue disease, increased aortic diameter,previous heart surgery, a history of hypertensionand elevated CPB pressures are all risk factors.There is a growing concern of an increased inci-dence of aortic dissection following off-pumpcoronary artery bypass grafting compared to on-pump CABG related to the application of a side-biting clamp under higher blood pressure andpulsatility.7Intraoperative TEE and epiaorticultrasound may help in the prevention andearly diagnosis of this potentially lethal compli-cation. Type A dissections have been reportedafter diagnostic coronary angiography (0.01%)and other percutaneous interventions (0.03%).8,9Isolated coronary artery dissections and localizedaortic dissections (less than 40 mm of ascendingaortic involvement) can be treated with intracoro-nary or aortic stenting. However, a failed stentingprocedure or progression of a dissection must besurgically treated. Retrograde type A dissectionsafter endograft placement for type B dissectionshavebeenreportedwithanincidenceof10–27%.10The presentation may be acute or delayed for sev-eral months. Various etiological factors includewire and sheath manipulation in the arch, repeatedballoon dilatations, oversizing of grafts, injury toa diseased aorta at the margin of inflexible grafts,and progression of disease unrelated to stentgrafting. Surgical replacement with tube grafts isrecommended in these patients and mortality ishigh (27%). Other procedures associated with anincreased risk of aortic dissection include theinsertion of intra-aortic balloon pumps, percuta-neous angioplasty, and stenting for coarctation ofthe aorta.11Fig. 2.4 CT reconstruction of a type A dissection follow-ing graft placement in the ascending aorta. The dissectionthat extends into the descending aorta demonstrates howthe defects spiral around the aorta20
  • 2 Acute Aortic SyndromeIntramural HematomaAortic intramural hematomas (IMH) account forup to 20% of all cases of AAS and represent avariant of dissection characterized by the absenceof an intimal flap, reentrant tear, or doublechannel with false lumen flow. IMH often occurin patients with severe atherosclerotic disease inwhich penetrating aortic ulcers or atheroscleroticplaques rupture causing intimal injury with bloodentering the media. In patients with mild or noatherosclerosis, spontaneous rupture of the vasavasorum may initiate aortic wall degeneration,which leads to hematoma formation in the aorticwall, splitting of the medial layer, and dissectionformation without an intimal tear (Class II).12Patients in the first group tend to be older andhave coexisting coronary and peripheral vasculardisease. Absence of intimal tears is not manda-tory in the diagnosis of IMH since small com-munications may be seen indicating rupture as adecompressing mechanism.13The presence oflarge intimal erosions or deep ulcer-like lesionsin the intima is associated with a progressive dis-ease course and poor outcome.14IMH evolution is difficult to predict (Fig. 2.5).In some cases, the hematoma does not change insize. Resolution occurs in fewer than 10% ofcases, but is more likely with less hematoma andaortic wall thickness.2When an IMH resolves, alocalized aneurysm may develop because of aweakened media and remodeling, requiring closesurveillance. Progression of IMH may lead toweakening and disruption of the intimal layercausing a classic dissection. Progression to dis-section has been shown to occur in 16–47% ofpatients with IMH.15A few patients may demon-strate IMH and dissection in different segments ofaorta, known as a hybrid case. Increasing aorticdiameter (>50 mm) causing aneurysm formationis a poor prognostic factor associated with IMH.16In addition, increased permeability of the aorticwall may lead to pericardial or pleural effusionsor a mediastinal hemorrhage. Most effusions willresolve. However, large and progressive fluidaccumulations are an ominous signs. Weakeningof the adventitial layer may lead to aortic rupture,while a contained rupture from disintegration ofthe outer medial layers with intact adventitia isnot uncommon.17Similar to aortic dissections, theFig. 2.5 Evolution ofintramural hematoma(Reprinted with permis-sion from Springer4)21
  • C.M. Wells and K. Subramaniammost common underlying condition associatedwith IMH is hypertension.Penetrating Aortic UlcerThe term penetrating atherosclerotic ulcer (PAU)describes a condition in which ulceration of anatherosclerotic lesion penetrates the intima andextends into the media, eroding the inner elasticlayer of the aortic wall. The reason why most ath-erosclerotic ulcers do not penetrate the internalelastic lamina and few penetrate the media andadventitia is not clear. PAUs are focal lesionsmost often located in the descending thoracicaorta, which correlates with a greater disease bur-den in that region. These patients tend to be olderwith severe systemic atherosclerosis but withoutconnective tissue diseases. Multiple PAUs areoften found in a single patient. Imaging of PAUmost often reveals extensive atherosclerosis withsevere intimal calcification and plaque. A crateror extravasation of contrast is often visualized.18Occasionally, PAU may progress (Fig. 2.6).This may precipitate a localized, intramural hem-orrhage following progressive erosion and ruptureof the vasa vasorum.19Further penetration to theadventitia may lead to the formation of a saccularaneurysm or pseudoaneurysm.20Symptomaticulcers with signs of deep erosion are more prone toaortic rupture.21In rare cases, PAU may lead toaortic dissection, but those dissections arising froma PAU tend to be less extensive and demonstrate athick, calcified static flap in a location atypical forentrance tears. Longitudinal spread of aortic dis-sections arising from PAU is limited by medialfibrosis and calcification.20Acute Expanding AneurysmsAlso included in many discussions of acute aorticpathology are symptomatic aortic aneurysmswhich may represent impending rupture. Theacute expansion of an aortic aneurysm accountsfor a significant number of patients who presentwith the sudden onset of chest pain. As aneu-rysms increase in size, the dilatation results ingreater wall tension and a more rapid rate ofexpansion. In addition, aneurysms may be associ-ated with progressive dissections, IMH, or PAU,all of which cause weakening of the aortic wall.EtiopathogenesisThe physiopathological mechanism that precipi-tates the appearance of each of these entities var-ies somewhat; however, both acquired and geneticconditions share an underlying pathology thatinvolves breakdown of the intimal layer andweakening of the aortic media, both of whichlead to higher wall stress. In addition, it iscommon for there to be progression from oneFig. 2.6 Evolution ofpenetrating aortic ulcers(Reprinted with permis-sion from Springer4)22
  • 2 Acute Aortic Syndrometype of lesion to another and some patients mayconcurrently manifest multiple types of lesions.Hypertension and Mechanical ForcesThe most common risk factor for aortic dissec-tion is hypertension. Chronic exposure of theaorta to high pressures leads to intimal thicken-ing, fibrosis, calcification, and extracellular fattyacid deposition. The extracellular matrix alsoundergoes accelerated degradation, apoptosis,and elastolysis. Both mechanisms lead to intimalweakening and medial degeneration.22At any sitewhere there is tissue thickening and fibrosis, thereis compromise of nutrient and oxygen supply tothe arterial wall. Eventually, there is necrosis ofsmooth muscle cells and fibrosis of elastic tissuein the vessel wall. The resulting stiffness increasesthe risk of aortic pathology when exposed to thechronic trauma of arterial hypertension.Genetic PredispositionMarfan’s syndrome, Ehlers–Danlos syndrome,familial forms of aortic aneurysm and dissection,as well as bicuspid aortic valve are genetic condi-tions that predispose patients to develop an acuteaortic syndrome and correlate with earlierpresentations. Among these, Marfan’s syndromeis the most prevalent connective tissue disorderwith an incidence of one in 7,000. The underly-ing defect is a mutation on the fibrillin-1 gene,which results in defective fibrillin in the extracel-lular matrix.22Ehlers–Danlos syndrome is another inheritedconnective tissue disorder characterized by tissuefragility. The familial form of aortic disease hasbeen localized to mutations on the fibrillin-1gene,similartoMarfan’ssyndrome.Characteristicto each of the different genetic disorders is a sim-ilar pathophysiology that includes a dedifferenti-ation of vascular smooth muscle cells andenhanced elastolysis of aortic wall components.In addition, increased expression of metallopro-teinases promotes fragmentation of elastic tissuein the medial layer.22Matrix MetalloproteinsThe matrix metalloproteins are a group of proteinswhose primary function is to degrade extracellu-lar matrix. Patients with thoracic aortic diseasehave been shown to have increased levels of theseenzymes, which favor proteolysis within the aor-tic wall. There are still many unanswered ques-tions related to the role these enzymes play inAAS; however, they may serve as a marker foraortic pathology or their inhibition may slow theprogression of disease.23Clinical PresentationAAS is characterized clinically by “aortic pain,”most often in a patient with a coexisting historyof hypertension. The early recognition of painassociated with progressive aortic lesions is ofparamount importance. Table 2.3 lists variouspresenting symptoms and signs of AAS andTable 2.4 lists the most common associated con-ditions. The characteristic findings listed mayTable 2.3 Presenting features of acute aortic syndromeChest pain – abrupt, severe, tearing, radiatingAnterior pain or radiation to neck – associated withascending aortaRadiation to back or abdomen – associated withdescending aortaSyncope or cerebrovascular accidentHypertension – SBP > 150 mmHgShock or tamponadeDiastolic murmurPressure differential in upper extremitiesPulse deficitsEnd-organ ischemiaTable 2.4 Comorbid conditions associated with acuteaortic syndromeHistory of hypertensionSmokingKnown coronary artery diseaseThoracic or abdominal aortic aneurysmPeripheral arterial diseasePrior strokeChronic renal insufficiency23
  • C.M. Wells and K. Subramaniamvary or be absent, emphasizing the necessity of ahigh level of suspicion in order to avoid diagnos-tic delays and poor outcomes.The pain caused by PAU and IMH is similar toclassic aortic dissection. The various types ofAAS cannot be reliably differentiated on clinicalgrounds alone. Aortic pain is described asseverely intense, acute, tearing, throbbing, andradiating.24In contrast to the increasing intensityof dull cardiac pain, AAS is described as beingmore abrupt and at maximal intensity from theonset. In addition, 4.5% of patients deny havingany pain on presentation.25Pain located in theanterior chest and neck is related to involvementof the ascending aorta and may be easily con-founded with that of ischemic syndromes. Backand abdominal pain may indicate that there isinvolvement of the descending aorta. Syncopemay be the presenting symptom in up to 20% ofcases and is associated with a proximal dissec-tion. The onset of syncope or central neurologi-cal deficits indicates probable complications suchas obstruction of cerebral vessels, cardiac tam-ponade, or activation of cerebral baroreceptors.Other presenting features of AAS may includeend-organ ischemia or pulse deficits.3Two typesofdistalvisceralorganmalperfusionaredescribed(Fig. 2.7). In static obstruction, the dissectionflap enters the origin of the branch and encroacheson the lumen. If there is no reentry, then the truelumen will be narrowed to cause ischemia. Indynamic obstruction, the flap prolapses andobstructs the origin of the vessel without enteringthe vessel. Static and dynamic obstruction maybe combined to contribute to branch obstruction.Diagnostic EvaluationAs diagnostic modalities have improved over thepast 2 decades, the awareness of AAS hasincreased significantly. PAU and IMH were virtu-ally unknown in the prior era of aortic imaging byaortography. These disorders were not classifiedas being distinct entities until the mid-1980s.In the current era of three-dimensional, high-resolution imaging by computerized tomography(CT), magnetic resonance (MR) imaging, andFig. 2.7 Types of visceralorgan malperfusion withaortic dissections(Reprinted with permis-sion from Springer4)24
  • 2 Acute Aortic Syndrometransesophageal echocardiography (TEE), thesetwo disorders have become increasingly recog-nized. The sensitivity and specificity of differentimaging techniques and their comparison aregiven in Table 2.5.26The goals of diagnosticimaging in patients with suspected AAS are con-firmation of the diagnosis, classification and typeof aortic pathology, tear localization, and identifi-cation of signs indicating the need for emergentintervention (pericardial, mediastinal, or pleuralhemorrhage).2Additional information includesarch and branch vessel involvement. Each imag-ing modality has distinct advantages (Table 2.6)and most patients require multiple imaging stud-ies to diagnose and characterize the underlyingaortic pathology.27ElectrocardiogramAn ECG is an important first diagnostic testperformed for all patients presenting with acutechest pain, whether typical or atypical for anacute aortic syndrome. The differentiation ofAAS from acute coronary syndrome (ACS) isimportant; however, it must be remembered theACS may occur as a result of AAS.Chest RadiographyWhile rapid imaging plays a crucial role in thediagnosis of AAS, the role of chest radiographyhas become limited, especially for conditionsTable2.5 Results of meta-analysis – diagnostic accuracy of different imaging modalities for suspected aortic dissection(Reprinted with permission from American Medical Association16)ImagingtechniqueNumberof studies Sensitivity SpecificityPositivelikelihood ratioNegativelikelihood ratioTEE 10 98 (95–99) 95 (92–97) 14.1 (6.0–33.2) 0.04 (0.02–0.08)Helical CT 3 100 (96–100) 98 (87–99) 13.9 (4.2–46.0) 0.02 (0.01–0.11)MRI 7 98 (95–99) 98 (95–100) 25.3(11.1–57.1) 0.05 (0.03–0.10)Data reported with 95% confidence intervals. Likelihood ratios greater than 10 and less than 0.1 are considered strongevidence to confirm or ruling out the diagnosis of aortic dissectionTable 2.6 Comparison of imaging modalities (Reproduced with permission from Oxford University press and theprimary author Professor Raimund Erbel56)TTE/TEE CT MRI Angiography IVUSSensitivity ++ ++ +++ ++ +++Specificity +++ ++ +++ ++ +++Classification +++ ++ ++ + ++Tear localization +++ − ++ + +Aortic regurgitation +++ − ++ ++ −Pericardial effusion +++ ++ ++ − −Mediastinal hematoma ++ +++ +++ − +Side branchinvolvement+ ++ ++ +++ +++Coronary arteryinvolvement++ − + +++ ++X-ray exposure − ++ − +++ −Patient comfort + ++ + + +Follow-up studies ++ ++ +++ − −Intraoperativeavailability+++ − − (+) (+)TTE/TEE – transthoracic/transoesophageal echocardiography; CT – computed tomography; MRI – magnetic resonanceimaging; IVUS – intravascular ultrasound25
  • C.M. Wells and K. Subramaniamconfined to the ascending aorta. In a study of 216patients over a 6-year period, the sensitivity foraortic disease was 64%, with a specificity of 86%.The sensitivity for lesions of the ascending aortawas 47%, while that for disease involving distalaortic segments was 77%.28A chest X-ray mayshow widening of the aortic contour, displacedcalcification, aortic kinking, or opacification ofthe aortopulmonary window (Fig. 2.8a and b).Computerized Tomography (CT)When AAS is suspected based on clinical presen-tation and an acute coronary syndrome has beenexcluded, cardiac-gated, contrast-enhanced mul-tidetector CT angiography is nearly 100% sensi-tive and specific in the diagnosis, differentiationand staging of AAS.29Modern CT machines haveup to 64 rows of detectors, and this enables themto generate multiple simultaneous images with aslice thickness of less than 1 mm. MultidetectorCT is also extremely fast with spiral imagingof the entire thorax can be done in a singlebreath-hold, which eliminates respiratory motionartifact. Cardiac gating is done to avoid artifactsproduced because of the imaging being obtainedduring different phases of cardiac cycle. CTallows for a complete diagnostic evaluation of thethoracic aorta, including the lumen, aortic wall,and periaortic region. Both unenhanced andenhanced images are valuable. Unenhanced scansdepict intramural hematoma (crescent shaped orcircumferential wall thickening) and thrombosisof the false lumen. Contrast-enhanced imagingallows demonstration of an intimal flap, which isthe most reliable finding in the diagnosis of dis-section (Fig. 2.9a and b). Contrast differencesbetween arterial and venous phase can helpdifferentiate true and false lumens. Interestingly,it can be difficult to differentiate an aneurysmwith thrombus from a dissection with a throm-bosed false lumen. Intimal calcifications aredisplaced by a false lumen in the latter case.30The diagnosis of IMH and PAU are also highlyaccurate with CT.31,32The diagnosis of PAU ismade by the demonstration of an outpouchingof the aortic wall with rough edges (Fig. 2.10).Fig. 2.8 PA (a) and lateral Chest X-Rays (b) demonstrating a dilated thoracic aorta and widened mediastinum26
  • 2 Acute Aortic SyndromeThe ulcer is usually surrounded by extensive ath-erosclerotic plaques. CT imaging of the aortashould include the iliac arteries for possible endo-vascular intervention and aortic arch branches toevaluate the extent of dissection and possibleneurological complications. Other benefits of CTare its availability and noninvasiveness. Themajor drawbacks of CT are the exposure to largedoses of ionizing radiation and contrast agents.29In addition, CT does not offer the capability toassess for aortic insufficiency or involvement ofthe coronary arteries.Magnetic Resonance Imaging (MRI)MRI is a valuable diagnostic tool for the diagno-sis of acute aortic syndrome. MRI can be highlyaccurate even without the use of contrast.Although MRI has the highest sensitivity andspecificity for the detection of all forms of aorticpathology and provides superior anatomic detailwhen compared to other imaging modalities, it islimited by availability, expense, and patientrestrictions such as pacemakers, aneurysm clips,or other metal devices. Prolonged scanning timeand limited access to unstable patients are otherlimitations. For these reasons, MRI is not awidely used tool (<5% of patients in IRAD)3(Fig. 2.11).Fig. 2.9 Contrast-enhanced chest CT clearly depicting a type A dissection. The intimal flap is seen in the ascendingand descending aorta (a) as well as the aortic arch (b)Fig. 2.10 CT reconstructions demonstrating PAU of thearch and descending aorta as indicated by arrows27
  • C.M. Wells and K. SubramaniamEchocardiographyTransthoracic echocardiography (TTE) can beused as screening tool for the diagnosis of AASof the proximal aorta. TTE is useful in the rapidevaluation of aortic insufficiency, pericardialtamponade, arch vessel involvement, and leftventricular systolic function. Hemodynamicallyunstable patients in whom TTE has shown peri-cardial effusion to be present should be taken tothe operating room for airway stabilization andfurther TEE evaluation. Thus, cardiac surgeonsrely on echocardiography more than otherimaging modalities including CTA in emer-gency situations.33A TEE can be done whilethe surgeon simultaneously prepares to openthe chest.Transesophageal echocardiography (TEE) ishighly sensitive and specific in diagnosing tho-racic aortic pathologies. The only limitation is inthe distal ascending aorta and proximal archwhich are not clearly visualized by TEE inmost patients. Evaluation of the aortic valve andsuitability for repair can be done with TEE.The diagnosis of an IMH is characterized bycrescentric aortic wall thickening, the absence ofan intimal flap and a lack of false lumen colorflow typical of dissection. The primary limitingfactor in the use of TEE is the requirement for askilled echocardiographer to be immediatelyavailable to perform and interpret results in emer-gency situations.29A further detailed descriptionof TEE examinations for aortic pathology isdescribed elsewhere in this textbook.AortographySince the development of newer, noninvasiveimaging modalities, there has been a shift awayfrom invasive techniques for imaging the aorta.Traditionally, aortography had been the goldstandard for the diagnosis of aortic dissection. Itsprimary limitations include its invasive natureand further risk of intimal damage, the use ofcontrast agents, as well as limited visualization ofthrombosed dissections, IMH, and occludedbranch vessels. The specificity for diagnosingaortic dissection is >95%, but the sensitivity onlyaverages 90%.2Intravascular ultrasound (IVUS)with high-frequency transducers (8–10 MHz) hasbeen used to complement conventional angiogra-phy in the diagnosis of acute dissection. IVUSprobes are advanced through guidewire and guid-ing catheters under fluoroscopy to evaluate theaorta from inside and provide useful informationabout the vessel wall and pathology.ManagementOnce there is a suspicion of AAS, patients shouldbe rapidly stabilized and transported to a tertiarycare center with adequate aortic surgical andendovascular surgical expertise. It is there thatfurther imaging and management should takeplace. Figure 2.12 provides an algorithm for therapid evaluation and treatment of patientspresenting with a suspected AAS.29,34Fig. 2.11 MRI of the chest showing a descending aorticdissection28
  • 2 Acute Aortic SyndromePatientsPresentingwithAcuteChestPainandHistoryofHypertensionHistory&PhysicalExamEKG,CXR,ABG,LabteststoruleoutacutecoronarysyndromeConsiderothercausesofchestpainObtainlargeboreIVAccess&invasivebloodpressuremonitoringBloodpressurecontrolSendbloodforcrossmatchObtainemergentTransthoracicEcho(TTE)inemergencyroom,ifavailable,whilearrangingforCT,OR,orICUtransportHemodynamicallyStableHemodynamicallyUnstableNoDissectionNohighriskfeaturesConfirmedDissectionorHighriskfeatures1.Pencardialtamponade2.Aorticinsufficiency3.Regionalwallmotionabnormalities4.DilatedaorticrootTocardiacORforairwayprotectionTEEexamination&surgicalexplorationTransfertotheOperatingRoomforsurgeryCTSurgicalConsultAggressivemedicaltherapySurgicalconsultif:-Visceralischemia-Thrombus-Aneurysmaldelation-Pain-Uncontrolledhtnarepresent-Marfan’sdiseaseissuspectedAcuteTypeBDissectionorIMHPenetratingUlcerUnstableThoracicAneurysmTypeADissectionorIMHObtaincardiacgated,multidetectorCTangiographyofchest,abdomen,&pelvisFig.2.12Acuteaorticsyndromemanagementalgorithm(Modifiedandreprintedwithpermissionfromthefollowingresources29,34)29
  • C.M. Wells and K. SubramaniamAlthough the treatment of AAS remains a ther-apeutic challenge, diverse surgical and percutane-ous strategies continue to evolve. There are manyfactors that affect management decision as listedin Table 2.7. One third of the mortality associatedwith AAS is the result of end-organ failure, whichemphasizes the importance of early intervention.The goal of treatment is to prevent the progres-sion of the disease and its lethal complications.The initial management of all patients withAAS involves pain relief and aggressive bloodpressure control. In normalizing the blood pres-sure, the goal is to reduce the force of left ven-tricular ejection (dP/dt), which is the primarycause of dissection extension and aortic rupture.Beta-blockers are the preferred agents becausethey not only reduce systemic pressure but alsolower heart rate. For most patients, the goal is asystolic pressure between 100 and 120 mmHgand heart rate <60 bpm or the lowest tolerablelevels that provide adequate cerebral, coronary,and renal perfusion. Less is known about the roleof calcium channel blockers for patients who are-blocker intolerant, but they should reduceblood pressure without causing reflex tachycar-dia. If neither of the above agents is adequate tocontrol the blood pressure, vasodilators may beadded. However, they should never be used as aninitial form of therapy before starting -blockersbecause of the reflex tachycardia and increase inthe force of left ventricular ejection leading toincreased aortic wall stress.Type A Aortic DissectionAcute ascending aortic pathology (acute dissec-tion, IMH, and PAU) should be treated as a surgi-cal emergency because of the possible risk oflife-threatening complications including aorticrupture, pericardial tamponade, and high earlymortality (Fig. 2.13). Surgery is also aimedto relieve aortic regurgitation and reestablishcoronary and branch vessel perfusion. Acute typeA dissection has a mortality rate of 1–2% perhour during the first hours of symptom onset andwithout surgical treatment, the mortality rate is20% by 24 h, 30% by 48 h, 40% at 1 week, and50% at 1 month.35Even with surgical treatment,Table 2.7 Patient factors affecting managementdecisionsDisease location – type A or BRetrograde extension into the arch and/or ascendingaortaRupture or impending ruptureSite of entry and reentryInvolvement of side branchesBranch origin from true or false lumenRisk of end-organ damageComplications – rupture, coronary occlusion, aorticinsufficiency, neurologicalDiameters of the true and false lumensAreas of normal vessel for stent-graft placementFig. 2.13 Management ofacute aortic dissection(Reprinted with permis-sion from Springer4)30
  • 2 Acute Aortic Syndromethe mortality rate is as high as 10% by 24 h and20% at 1 month.36,37Aortic arch and descending thoracic intimaltears are seen in 20–30% of patients with type Adissection and if left untreated predisposes tolater distal reoperation.38,39Patients who requirepartial or total arch replacement with reconnec-tion of supraaortic vessels to the graft must oftenundergo deep hypothermic circularoty arrest withantegrade or retrograde cerebral perfusion. If adissection extends into the descending thoracicaorta, an elephant trunk extension of the archgraft is an option.40In a later procedure, the ele-phant trunk portion of the graft may be connectedto the distal descending aorta, a tubular graft orendovascular graft. There are reports of endovas-cular repair of the ascending aorta in highlyselected patients, but this has most often been forthe purpose of temporizing symptoms and pre-venting disease progression before a more defini-tive open repair could be performed. It is mostoften not possible due to the anatomic restrictionsof securing the graft in the ascending aorta. Theplacement of stent grafts has been applied to treataortic branch occlusions in both type A and Bacute aortic dissections. In type A dissectionswith visceral malperfusion, treatment of the leak-ing aorta and aortic valve take precedence overvisceral malperfusion. However, patients withprolonged limb or bowel ischemia may beunsuitable for proximal aortic surgery, and endo-vascular treatment to restore perfusion to criticalorgans is recommended.Type B Aortic DissectionUncomplicated Type B DissectionMedical management (analgesics and antihyper-tensive therapy) still remains the main stay oftherapy for patients with uncomplicated type Bdisease. It is safe to treat these patients medicallywith close follow-up for ischemic complications,disease progression, or aneurysmal enlargement.In a group of 384 patients with type B dissec-tions, 73% were treated medically with a 10%in-hospital mortality. Long-term survival is60–80% at 5 years.3Surgical repair has not beenshown to improve outcomes in this group ofpatients. Recently, a completed randomized study(Investigation of stent grafts in patients with typeB aortic dissection-INSTEAD) examined the useof endografts versus medical therapy in uncom-plicated dissections. The results did not show anysurvival benefit at 2 years.41Complicated Type B DissectionsComplicated type B aortic disease is differentiatedby the presence of a distal malperfusion syndromeor rapid disease progression. Indications for inter-vention are similar to those for type A diseases;the prevention of life-threatening complicationssuch as organ or limb ischemia, aneurysm expan-sion and risk of rupture, periaortic blood collec-tion, intractable pain, aneurysm expansion oruncontrolled hypertension. The mortality rate foropen surgical repair (graft replacement, fenestra-tion, or bypass procedures) is 30–35% and evenhigher with the presence of visceral malperfu-sion.42,43Aortic endovascular grafting may be par-ticularly beneficial in this group and has shownimproved mortality rates (16%). The goals ofendograft treatment include reconstruction of theaortic segment containing the entry tear, inductionof thrombosis in the false lumen, and thereestablishment of flow in the true lumen andbranches.44In one series, false lumen thrombosiswas achieved in 85–100% of patients.An additional benefit of stent grafts is the abil-ity to relieve dynamic and combined static anddynamic obstructions successfully in compli-cated acute type B dissections.45,46Static obstruc-tions are relieved by placing the graft in thebranch vessel and dynamic obstructions maybenefit from stents in the true lumen. Endograftshave also been used in patients with retrogradetype A dissection with intimal tear in the descend-ing aorta to induce false lumen thrombosis.47Surgical treatment may be the only option inpatients with failed endografts or patients unsuit-able for this less-invasive technique.With either surgical, endograft, or medicalmanagement, the risk of further dissection isnever eliminated. Therefore, close, regular moni-toring, most likely with CT imaging, is necessaryto assess for progression or complications.31
  • C.M. Wells and K. SubramaniamIntramural HematomaType A DiseaseThe recommended treatment for patients withType A IMH is prompt surgical intervention.Proximal IMH are independently associated withpotential progression to dissection, aneurysm,and rupture as well as poor clinical outcomes.17The risk of a nonsurgical approach to type A IMHdemonstrates an early mortality of 55% comparedwith 8% following surgical repair.17However, forpatients with significant comorbidities anduncomplicated type A IMH (no dissection or inti-mal tear, thickness less than 11 mm, aortic diam-eter less than 50 mm), medical treatment withfollow-up imaging and timed surgical interven-tion has been recommended.Type B DiseaseThe management of IMH involving the descend-ing aorta is similar to that recommended for typeB dissections. The current literature supportsmedical management. However, if complicationsarise (ulceration, expansion, and dilatation),endograft placement may be considered althoughlimited data exists. Endografts may cause erosionof the intima during the acute phase. IMH of thedescending aorta have been associated with anin-hospital mortality rate of 10%, similar to thatof type B aortic dissection, further emphasizingthe importance of correct diagnosis and propertreatment.Penetrating Aortic UlcersThere are multiple important factors to identifywhen diagnosing PAU. One must determine thenumber (single or multiple), location (type A orB), and associated complications (IMH, dissec-tion, pseudoaneurysm, and rupture). Type A PAUshould be treated surgically. Medical therapy isindicated in stable patients with type B PAU.48Very few centers advocate any surgical interven-tion in uncomplicated type B patients becausethere is a high risk of organ failure and poorprognosis due to the high likelihood of extensiveatherosclerotic disease. For patients with symp-tomatic or progressive disease, focal PAU in thedescending aorta are ideal targets for endograftplacement. In a meta-analysis of 58 patients from13 studies, complete sealing of the ulcer was pos-sible in 94% of patients. Neurologic complica-tions were present in 6% and the in-hospitalmortality rate was 5%.49Long-term results arenot known at this time.Natural History and PrognosisThe outcomes of patients treated for AAS haveimproved significantly, although there stillremains a high mortality rate in the acute phase.Table 2.8 lists predictors of in-hospital death.50Early clinical suspicion and greater surgicalexpertise appear to be the most important factorsin reducing mortality.Type A aortic dissections are highly lethal.Overall, mortality at 1 month is 20% with and50% without surgical treatment for type A dis-sections. The risk of death is higher if there arecomplications of pericardial tamponade, involve-ment of the coronary arteries causing acute myo-cardial ischemia, or a malperfusion syndrome.Age greater than 70 has been identified as anindependent risk factor for hospital death foracute type A dissection. Shock, hypotension, andtamponade are other risk factors for increasedmortality.37For type B dissections, the overall mortalityrate is 10% with medical treatment. Circulatoryshock and visceral ischemia predispose to ahigher mortality in type B dissection.51Table 2.8 Predictors of in-hospital deathAge >70Abrupt onset of painHypotension/cardiac tamponade/shockAbnormal EKGKidney failurePulse deficitsIatrogenic cause32
  • 2 Acute Aortic SyndromeFollowing the acute-phase, mid- to long-termsurvival depends not only on the underlyingaortic disease but also other comorbidities. Inpatients with surgically corrected type A dissec-tions, survival differences were based on thepresence or absence of distal false lumen flow. Inone study, the absence of a false lumen wasachieved in 53% of patients compared to 10–20%in most series. In patients with absent false lumenflow, the survival was 85% at 6 years comparedto 62% in patients with persistent false lumenflow.37At 10 years, the survival rate was 44% forcorrected type A dissections compared to 32% inmedically treated type B dissections.51The pri-mary reasons for higher, long-term mortality intype B dissections were aneurysmal expansionand rupture. Dilatation in the descending aortawas greater in medically treated type B dissec-tions compared to operated type A dissections.Dilatation occurs at a faster rate in patients withfalse lumen flow when compared to absent falselumen flow in type B dissections.52Junoven et al.described rupture in 18% and rapid expansionrequiring surgery in 20% of patients with type Bdissection at 3 years.53The impact of early endo-vascular treatment on the long-term survival oftype B dissections is yet to be determined.In patients with type A IMH, Kaji et al.54reported that surgery was required in 43% ofpatients during the acute phase and, among thosedischarged without surgery (57%), complete res-olution occurred in 40% of patients. Type B IMHhas a better long-term prognosis than type B dis-sections with 5-year survival reported between43% and 90%.17,55Close follow-up with imagingtechniques is recommended in patients undergo-ing medical treatment to look for complications(dilatation, pseudoaneurysm formation, anddissection).Prevention and Follow-UpAt a time when there is an increasing elderlypopulation, the awareness of such conditions asAAS is likely to continue to rise. This is due toimprovements in diagnostic modalities, longerlife expectancy, and longer exposure to elevatedblood pressure. In order to best treat thesepatients, continued improvements in diagnosticimaging and therapeutic strategies are necessary,and a focus on surveillance and prevention willfurther reduce the morbidity and mortality asso-ciated with aortic pathology.One possibility for the surveillance of patientsat risk for the development or progression ofAAS is the development of biomarkers, whichwould enable serum diagnosis. In addition, thiswould provide a fast and economic means of dif-ferentiating patients who present to the emer-gency room with chest pain. Possible markerscurrently include an assay for circulating smoothmuscle myosin heavy chain protein, soluble elas-tin fragments and acute-phase reactants such asC-reactive protein, fibrinogen, and D-dimer.All patients with a known aortic diseaserequire close surveillance following discharge.Lifelong treatment of hypertension is requiredand regular assessments of the aorta should beperformed at 1, 3, 6, 9, and 12 months as well asevery 6–12 months thereafter, depending on theaortic size. The most important findings on imag-ing are aortic diameter, signs of aneurysm forma-tion, and hemorrhage at surgical anastamosis orstent-graft sites. The close follow-up emphasizesthe fact that aortic disease progression is not easyto predict. Repeated surgery is required in12–30% of patients due to extension or recur-rence of dissection, aneurysm formation, graftdehiscence, aortic insufficiency, or infection.26ConclusionSignificant advances have been made in the diag-nosis and management of acute aortic dissectionsover the past 2 decades. These advancementshave led to a better understanding of aortic pathol-ogy and led to the discovery of variants that arecollectively termed acute aortic syndrome.Despite a persistent level of uncertainty in thediagnosis and management of this lethal disorder,advances are being made and patient outcomesare improving.33
  • C.M. Wells and K. SubramaniamKey Notes1. The clinical progress of patients with AAS isunpredictable. A high level of suspicion isrequired for early diagnosis and crucial forpatient survival.2. The most common risk factor for AAS ishypertension, with men being affected moreoften.3. Any mechanism that causes intimal damageand leads to weakening of the medial layersof the aortic wall can result in dissection,IMH, or PAU.4. Acute aortic dissection, the most commonetiology of AAS, is characterized by an inti-mal tear which is often preceded by medialwall degeneration or cystic medial necrosis.5. IMH, a variant of aortic dissection, originatesfrom a disruption of the vasa vasorum withinthe media. They are treated similar to dissec-tions and have a similar prognosis.6. PAU is associated with atherosclerotic dis-ease and can lead to dissection or perfora-tion. Both IMH and PAU are found mostoften in the descending aorta.7. AAS may present in many ways. Most oftenthere is the sudden onset of severe, sharpchest pain or back pain.8. Type A aortic dissections are associated withhigh mortality rates and without surgery,30-day mortality exceeds 50%.9. Uncomplicated type B dissections have a30-day mortality of 10% and may be man-aged medically. Complications require surgi-cal intervention or endovascular stenting.10. CT, MRI, and TEE are all accurate in thediagnosis of AAS.11. The initial treatment of all patients with AASis blood pressure control in order to decreasethe force of left ventricular contraction andlower the risk of dissection extension or rup-ture. Beta-blockers are the preferred first-lineagent to achieve a systolic pressure <120mmHg and heart rate <60 bpm.12. Surgery is the definitive treatment of type Aacute aortic pathology. The goal is to preventlife-threatening complications such as aorticrupture or pericardial tamponade.13. Medical therapy with -blockers andantihypertensive agents is the recommendedtherapy for patients with uncomplicated typeB aortic dissection, IMH, or PAU.14. The advent and incorporation of less-invasiveendovascular treatments has opened up newperspectives in the treatment of acute aorticdisease and continued advances will result inimproved patient outcomes.References1. Svensson LG, Labib SB, Eisenhauer AC, Butterly JR.Intimal tear without hematoma: an important variantof aortic dissection that can elude current imagingtechniques. Circulation. 1999;99:1331–1336.2. Tsai TT, Nienaber CA, Eagle KA. Acute aortic syn-dromes. Circulation. 2005;112:3802–3813.3. Hagan PG, Nienaber CA, Isselbacher EM, et al. TheInternational Registry of Acute Aortic Dissection(IRAD): new insights into an old disease. JAMA.2000;283:897–903.4. Evangelista A, Gonzalez-Alujas T. Pathophysiologyof aortic dissection. In: Rousseau H, Verhoye JP,Heautot JF, eds. Thoracic aortic Diseases. 1st ed.Berlin Heidelberg, Germany: Springer; 2006:33–53.5. Fleck T, Ehrlich M, Czerny M, et al. Intraoperativeiatrogenic type A aortic dissection and perioperativeoutcome. Interact Cardiovasc Thorac Surg. 2006;5:11–14.6. Elitz T, Kawohl M, Fritzsche D, et al. Aortic dissec-tion after previous coronary artery bypass grafting.J Card Surg. 2003;18:519–523.7. De Smet JM, Stefanidis C. Acute aortic dissectionafter off pump coronary artery surgery. EurJ Cardiothorac Surg. 2003;24:315–317.8. Okamoto R, Makino K, Saito K, et al. Aorto-coronary dissection during angioplasty in a patientwith myxedema. Jpn Circ J. 2000 Apr;64(4):316–320.9. Wyss CA, Steffel J, Lüscher TF. Isolated acute iatro-genic aortic dissection during percutaneous coronary-intervention without involvement of the coronaryarteries. J Invasive Cardiol. 2008 Jul;20(7):380–382.10. Kpodonu J, Preventza O, Ramaiah VG, et al.Retrograde type A dissection after endovascular stent-ing of the descendingthoracic aorta. Is the risk real?Eur J Cardiothorac Surg. 2008 Jun;33(6):1014–1018.Epub 2008 Apr 21.11. Panten RR, Harrison JK, Warner J, Grocott HP. Aorticdissection after angioplasty and stenting of an aorticcoarctation:detection by intravascular ultrasonogra-phy but not transesophageal echocardiography. J AmSoc Echocardiogr. 2001 Jan;14(1):73–76.12. Sheldon WS, Vandervoort PM, Black IW, Grimm RA,Stewart WJ. Aortic intramural hematoma inpatients evaluated for aortic dissection: clinical,34
  • 2 Acute Aortic Syndromeechocardiographic,radiologicandpathologicfindings.Circulation. 1994;90(Suppl I):I385.13. Vilacosta I, de Dios RM, Pinto AG. Aortic intramuralhematoma during coronary angioplasty: insights intothe pathogenesis of intramedial hemorrhage. J AmSoc Echocardiogr. 2000;13:403–406.14. Ganaha F, Miller DC, Sugimoto K, et al. Prognosis ofaortic intramural hematoma with and without pene-trating atherosclerotic ulcer: a clinical and radiologi-cal analysis. Circulation. 2002 Jul 16;106(3):342–348.15. Nienaber CA, Sievers HH. Intramural hematoma inacute aortic syndrome: more than on variant of dissec-tion? Circulation. 2002;106:284–285.16. Kaji S, Nishigami K, Akasaka T, et al. Prediction ofprogression or regression of type A aortic intramuralhematoma bycomputed tomography. Circulation.1999 Nov 9;100(19 Suppl):II281–II286.17. Von Kodolitsch Y, Csösz SK, Koschyk DH, et al.Intramural hematoma of the aorta: predictors of pro-gression to dissection and rupture. Circulation. 2003Mar 4;107(8):1158–1163.18. Hayashi J, Matsuoka Y, Sakamoto I, et al. Penetratingatherosclerotic ulcer of the aortoa: imaging featuresand disease concept. RadioGraphics. 2000;20:995–1005.19. Stanson AW, Kazmier FJ, Hollier LH, et al. Penetratingatherosclerotic ulcers of the thoracic aorta: naturalhistory and clinicopathologic correlations. Ann VascSurg. 1986;1:15–23.20. Vilacosta I, San Román JA, Aragoncillo P, et al.Penetrating atherosclerotic aortic ulcer: documenta-tion by transesophagealechocardiography. J Am CollCardiol. 1998;32:83–89.21. Ando Y, Minami H, Muramoto H, Narita M, Sakai S.Rupture of thoracic aorta caused by penetrating aorticulcer. Chest. 1994;106:624–626.22. Nienaber CA. Pathophysiology of acute aortic syn-dromes. In: Baliga RR, Nienaber CA, IsselbacherEM, Eagle KA, eds. Aortic Dissection and RelatedSyndromes. 1st ed. NewYork: Springer Science;2007:17–44.23. Botta DM, Elefteriades JA. Matrix metalloproteinasesin aortic aneurysm and dissection. In: Elefteriades JA,ed. Acute Aortic Disease. 1st ed. NewYork: InformaHealthcare; 2007:131–146.24. Wooley CF, Sparks EH, Boudoulas H. Aortic pain.Prog Cardiovasc Dis. 1998;40:563–589.25. Ahmad F, Cheshire N, Hamady M. Acute aortic syn-drome: pathology and therapeutic strategies. PostgradMed J. 2006;82:305–312.26. Shiga T, Wajima Z, Apfel CC, Inoue T, Ohe Y.Diagnostic accuracy of transesophageal echocardiog-raphy, helical computed tomography, and magneticresonance imaging for suspected thoracic aortic dis-section: systematic review and meta-analysis. ArchIntern Med. 2006;166:1350–1356.27. Kapustin AJ, Litt HI. Diagnostic imaging for aorticdissection. Semin Thorac Cardiovasc Surg. 2005;17:214–223.28. Von Kodolitsch Y, Nienbar CA, Dieckmann C, et al.Chest radiography for the diagnosis of acute aorticsyndrome. Am J Med. 2004;116:73–77.29. Smith AD, Schoenhagen P. CT imaging for acuteaortic syndrome. Cleve Clin J Med. 2008;75:7–9.30. Berger F, Smithuis R, van Delden O. Thoracic Aorta –the Acute Aortic Syndrome. www.radiologyassistant.nl/en. Accessed May 25, 2009.31. Reddy GP. Multidetector CT of acute aortic syndrome.Imag Decision. 2006;2:22–26.32. Manghat NE, Morgan-Hughes GJ, Roobottom CA.Multi-detector row computed tomography: imaging inacute aortic syndrome. Clin Radiol. 2005;60:1256–1267.33. Svensson LG. Acute aortic syndromes: time to talk ofmany things. Cleve Clin J Med. 2008;75:25–29.34. Meredith EL, Masani ND. Echocardiography in theemergency assessment of acute aortic syndromes. EurJ Echocardiogr. 2009;10:i31–i39.35. Hagan PG, Nienaber CA, Isselbacher EM, et al. TheInternational Registry of Acute Aortic Dissection(IRAD): new insights into an old disease. JAMA.2000;283:897–903.36. Mehta RH, O’Gara PT, Bossone E, et al. Acute type Aaortic dissection in the elderly: clinical characteris-tics, management, and outcomes in the current era.J Am Coll Cardiol. 2002;40:685–692.37. Mehta RH, Suzuki T, Hagan PG, et al. Predictingdeath in patients with acute type A aortic dissection.Circulation. 2002;105:200–206.38. Ergin MA, O’Connor J, Guinto R, Griepp RB.Experience with profound hypothermia and circula-tory arrest in the treatment of aneurysms of the aorticarch. Aortic arch replacement for acute arch dissec-tions. J Thorac Cardiovasc Surg. 1982;84:649–655.39. Nguyen B, Müller M, Kipfer B, et al. Different tech-niques of distal aortic repair in acute type A dissec-tion: impacton late aortic morphology and reoperation.Eur J Cardiothorac Surg. 1999;15:496–500.40. Borst HG, Walterbusch G, Schaps D. Extensive aorticreplacement using elephant trunk prosthesis. ThoracCardiovasc Surg. 1983;31:37–40.41. Isselbacher EM. Dissection of the descending thoracicaorta: looking into the future. J Am Coll Cardiol.2007;50:805–807.42. Heinemann MK, Buehner B, Schaefers HJ, JurmannMJ, Laas J, Borst HG. Malperfusion of the thoracoab-dominal vasculature in aortic dissection. J Card Surg.1994;9:748–755.43. Borst HG, Laas J, Heinemann M. Type A aortic dis-section: diagnosis and management of malperfusionphenomena. Semin Thorac Cardiovasc Surg.1991;3:238–241.44. Ince H, Nienaber CA. The concept of interventionaltherapy in acute aortic syndrome. J Card Surg.2002;17:135–142.45. Slonim SM, Miller DC, Mitchell RS, Semba CP,Razavi MK, Dake MD. Percutaneous balloon fenes-tration and stenting for life-threatening ischemiccomplications in patients with acute aortic dissection.J Thorac Cardiovasc Surg. 1999;117:1118–1126.35
  • C.M. Wells and K. Subramaniam46. Slonim SM, Nyman UR, Semba CP, Miller DC,Mitchell RS, Dake MD. True lumen obliteration incomplicated aortic dissection: endovascular treat-ment. Radiology. 1996;201:161–166.47. Kato N, Shimono T, Hirano T, Ishida M, Yada I,Takeda K. Transluminal placement of endovascularstent-grafts for the treatment of type A aortic dissec-tion with an entry tear in the descending thoracicaorta. J Vasc Surg. 2001;34:1023–1028.48. Tittle SL, Lynch RJ, Cole PE, et al. Midterm follow-upof penetrating ulcer and intramural hematoma of theaorta. J Thorac Cardiovasc Surg. 2002;123:1051–1059.49. Eggebrecht H, Baumgart D, Schmermund A, et al.Penetrating atherosclerotic ulcer of the aorta: treat-ment by endovascular stent-graft placement. CurrOpin Cardiol. 2003;18:431–435.50. Song JK, Kang SJ, Song JM, et al. Factors associatedwith in-hospital mortality in patients with acute aorticsyndrome involving the ascending aorta. Int J Cardiol.2007;115:14–18.51. Nienaber CA, Eagle KA. Aortic dissection:newfrontiers in diagnosis and management. Circulation.2003;108:628–635.52. Sueyoshi E, Sakamoto I, Hayashi K, Yamaguchi T,Imada T. Growth rate of aortic diameter in patientswith type B aortic dissection during the chronic phase.Circulation. 2004;110(11 Suppl 1):II256–II261.53. Junoven T, Ergin MA, Galla JD, et al. Risk factors forrupture of chronic type B dissections. J ThoacCardiovasc Surg. 1999;117:776–786.54. Kaji S, Akasaka T, Boribata Y, et al. Long term prog-nosis of patients with type A intramural hematoma.Circulation. 2002;106:248–252.55. Kaji S, Akasaka T, Katayama M, et al. Long termprognosis of patients with type B intramural hema-toma. Circulation. 2003;108:307–331.56. Erbel R, Alfonso F, Boileau C, et al. Diagnosis andmanagement of aortic dissection: task force on aorticdissection, European society of cardiology. Eur HeartJ. 2001;22:1642–1681.36
  • http://www.springer.com/978-0-387-85921-7