Extrinsic Coronary Artery Obstruction by Chronic Aortic Dissection

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1 Extrinsic Coronary Artery Obstruction by Chronic Aortic Dissection Alexander S. Giritsky, M.D., Michael T. Ricci, M.D., Bruce A. Reitz, M.D., and Norman E. Shumway, M.D., Ph.D. ABSTRACT Chronic type A aortic dissection due to cannulation injury is an unusual entity which in this patient was seen as extrinsic left main coronary artery obstruction four years following valve operation. This is an unusual manifestation of coronary artery involvement by dissection, and successful management did not require simultaneous myocardial revascularization. The clinical and pathological characteristics of this condition are presented, and the spectrum of lesions associated with iatrogenic dissection is reviewed. In 1968, the incidence of aortic dissection was reported as one per 10,000 hospital admissions and as one per 400 postmortem examinations [l]. The relative incidence of chronic type A dissection is 16% of all cases of dissection reported in selected large series of medically and surgically treated patients since 1970 [21. In these studies, 68% of dissections were acute when defined as less than fourteen days old. Thus, only approximately one-third of type A dissections are chronic, which reflects the high early mortality of this disease. Although it is known that acute dissection may develop as a consequence of aortic cannulation or clamping [3-71, it is not generally appreciated that chronic dissection may have a similar iatrogenic etiology. In addition, extrinsic coronary artery obstruction by a chronic aortic dissection has not been previously described. Our experience in the successful management of a patient seen with both of these rare entities is the subject of this communication. From the Departments of Cardiovascular Surgery and Radiology, Stanford University Medical Center, Stanford, CA. Accepted for publication Sept 29, Address reprint requests to Dr. Reitz, Department of Cardiovascular Surgery, A206, Stanford University Medical Center, Stanford, CA A 61-year-old truck driver was admitted to Stanford University Hospital with congestive heart failure in November, He was known to have had rheumatic fever as a child and was rejected for military service because of a cardiac murmur. When he was 38 years old, physical examination revealed signs of aortic stenosis, aortic insufficiency, and left ventricular enlargement. At the age of 56 years, he was noted to have atrial fibrillation and congestive heart failure. Electrocardioversion failed, and congestion worsened despite aggressive management with digoxin and diuretics. Cardiac catheterization revealed severe aortic valve disease with stenosis and insufficiency. Selective coronary angiography revealed normal vessels. When he was 57 years old, in 1974, the patient underwent aortic valve replacement with a 27 mm Hancock porcine bioprosthesis (model 242) and mitral valve commissurotomy. The patient s postoperative course was uncomplicated. He returned to work and was well until he was 60 years old when he sustained an occlusion of the left iliac artery, which required balloon catheter embolectomy and subsequent management with warfarin. There was no left atrial thrombus by ultrasound examination. When he was seen at the age of 61 years, the patient gave a history of increasing dyspnea and orthopnea. The electrocardiogram showed atrial fibrillation. Cardiac catheterization demonstrated markedly elevated right-sided resting pressures and a low cardiac index (Table). There were no aortic or mitral gradients. Ventriculography showed diffuse hypocontractility of the left ventricle, and grade 314 mitral regurgitation. Selective coronary angiography showed severe narrowing (estimated at 95%) of the left main coronary artery caused by extrinsic compression from an abnormality of the aortic root (Figs 1-3). Operation was performed on November 27, by The Society of Thoracic Surgeons

2 290 The Annals of Thoracic Surgery Vol 32 No 3 September 1981 Cardiac Catheterization Data Obtained Preoperatively and Postoperatively in a Patient with Chronic Type A Dissection and Extrinsic Compression of the Left Main Coronary Artery Postop Preop Pressure Pressure Catheterization November, 1978 June, 1979 Data (mm Hg) (mm Hg) Right atrium /16/14 ( A/V/M) Pulmonary artery 65/35/51 50/20/31 (SIDIM) Pulmonary arterial -/48/31 18/28/20 wedge (NVIM) Left ventricle /27 NA (SIDIED) Aorta (SIDIM) 100/73/81 159/92/114 Cardiac index (L1m/m2) Fig 2. Selective left coronary arteriogram (shallow left Rhythm atrial fibrillation sinus anterior oblique projection) demonstrates a smooth, tubular narrowing of the left main coronary artery A = wave; v = wave; M = mean; s = systolic; D = (large arrow) and absence of the circumflex coronary diastolic; ED = end-diastolic; NA = not available. artery. The left anterior descending coronary artery is indicated by the small arrow. Fig 1. Thoracic aortogram in the right posterior oblique projection. Extrinsic compression with near occlusion of the left main coronary artery (black arrow) is caused by an aortic dissection with aneurysmal formation. Fig 3. Selective left coronary arteriogram (right anterior oblique projection) demonstrates severe narrowing of the left main coronary artery proxiinal to the left anterior descending and circumflex coronary bifurcation (large arrow) and markedly diminished flow in the circumflex coronary artery (small arrow).

3 291 Case Report: Giritsky et al: Extrinsic Coronary Artery Obstruction The patient was found to have an aortic dissection (type A) with a false lumen between the ascending aorta and main pulmonary artery. The intimal tear was 9 cm distal to the aortic prosthesis, in a left posterolateral position. The false lumen extended 4 cm distal to the intimal tear and proximally in a retrograde fashion to the left main coronary artery, which was visible at the base of the dissection cavity. There was no evidence of false aneurysm at the sites of previous aortic cannulation or aortotomy. The ostium of the left coronary artery was widely patent, and the vessel lumen easily accepted an 8F catheter. The porcine aortic bioprosthesis was normal without evidence of fibrosis, thrombus, or fenestration. The sinuses of Valsalva were normal. The mitral valve was thickened, and the chordae tendineae were fibrotic and foreshortened, without evidence of chordal rupture. The mitral valve was replaced with a 29 mm porcine bioprosthesis (Hancock model 342AV), and the ascending aorta was resected and replaced with a 35 mm woven Dacron tubular graft. No coronary artery bypass grafts were considered necessary. The patient's initial postoperative course was complicated by ventricular tachyarrhythmias, low cardiac output syndrome, respiratory failure, and azotemia. Management included pharmacological afterload reduction, intraaortic balloon counterpulsation, tracheotomy, and parenteral nutrition. He made a good recovery and was discharged home six weeks postoperatively. Cardiac catheterization and angiography seven months later confirmed an intact repair and a normal left main coronary artery without evidence of stenosis or external obstruction (Figs 4, 5; see Table). The patient has been followed for more than twenty-six months postoperatively and remains asymptomatic. Comment Aortic dissection is a condition in which blood is found between layers of the arterial wall. In 1756, William Hunter described aortic dissection in his presentation "History of Aneurysms of the Aorta, with Some Remarks on Aneurysms in General" to the Society of Physicians in London [81. He called this condition "mixed Fig 4. Left coronary arteriogram (left anterior oblique projection) made seven months postoperatively demonstrates a patent left main coronary artery (large arrow) with a normal caliber. Note the normal filling of the circumflex coronary artery (small arrow). Fig 5. Left coronary arteriogram (right anterior oblique projection) made seven months postoperatively demonstrates restoration of normal flow in the circumjlex coronary artery (large arrow). The left anterior descending coronary artery is indicated by the small arrow.

4 292 The Annals of Thoracic Surgery Vol 32 No 3 September 1987 aneurysm in order to distinguish it from the features of true aneurysm and false aneurysm, as defined in the second century by Galen. In 1826 Laennec [9] introduced the designation dissecting aneurysm, but the development of angiography permitted antemortem demonstration of the lesion and revealed that aneurysmal dilatation is not a consistent feature. Similarly, dissecting hematoma is often a misleading designation for a condition in which the false lumen may be devoid. of clot. Aortic dissection accurately describes the pathological process, without speculation regarding the ultimate pathological morphology. In fact, the pathological morphology of aortic dissection is so variable that a number of detailed anatomical classifications have been proposed [9, 101. Therapeutic strategy, however, is determined by the presence or absence of ascending aortic involvement by the dissection [2, 111. The Stanford classification system thus categorizes aortic dissection in two groups: type A and type B. Type A dissections involve the ascending aorta, irrespective of the site of intimal tear, and type B dissections do not [ll]. In each category the dissections may occur acutely or chronically, and the clinical characteristics and results of management of these categories have been reported previously [2,11, 121. In the patient presented in this report, a chronic type A dissection developed following aortic valve replacement and mitral commissurotomy. The striking feature was the left coronary artery obstruction due to extrinsic compression by the retrograde dissection. To our knowledge, this complication has not been reported previously. The common lethal complications of type A dissection are well known and include the following: intrapericardial rupture with cardiac tamponade, with or without prodromal acute pericarditis [131; left ventricular failure due to acute aortic regurgitation; myocardial infarction due to occlusion of a coronary ostium; and cerebral infarction due to carotid artery occlusion [14]. Unusual complications of type A dissections include obstruction of the superior vena cava or pulmonary artery; fistulous communication to the right or left atrium, right ventricle, pulmonary artery, or esophagus; and hematoma of the interatrial septum [ In addition, chronic type A dissection may cause stenosis of right or left coronary arteries by intramural extension of the retrograde dissection [18, 191. This lesion must be distinguished from primary coronary artery dissection which may occur idiopathically [20], iatrogenically as a complication of selective coronary angiography, coronary balloon angioplasty, or myocardial revascularization, and degeneratively as a consequence of intimal injury due to coronary atherosclerosis. Histological examination of the resected ascending aorta of our patient confirmed intramural aortic dissection, but did not demonstrate cystic medial necrosis. This is consistent with the view that no specific medial defect can be held responsible for the pathogenesis of aortic dissection and that dissection is part of a spectrum of lesions having as the common denominator the process of injury and repair that renders defective the muscle or elastic tissue or both within the vessel wall [21, 221. In our patient, the intimal tear involved the left posterolateral third of the aortic circumference at the level of the previous aortic cannulation site. Spontaneous type A dissection usually involves the convexity of the ascending aorta, that is, the right anterolateral portion of the cross-sectional circumference [12]. It seems most likely, therefore, that intimal injury occurred at the time of the previous aortic cannulation. Acute type A dissection due to cannulation is a rare but well-known complication of cardiopulmonary bypass [15, 231. The tip of the perfusion cannula is inadvertently introduced between the layers of the ves8sel wall, and the propagation of dissection is caused by mechanical pumping at the initiation of bypass. The incidence of this complication at major cardiovascular centers is less than o.04 /~ [6,71, and it can be avoided by observing prompt blood return from the perfusion cannula at the time of its insertion, ensuring intraluminal placement. This maneuver, however, does not protect against the development of chronic dissection should the cannula merely lacerate the posterior aortic wall from within the vessel lumen. The true incidence of this complication remains unknown, presumably since small localized dis-

5 293 Case Report: Giritsky et al: Extrinsic Coronary Artery Obstruction sections may remain asymptomatic or heal by the process of thrombosis and repair [24]. Similarly, acute dissections due to aortic clamping have been described. Based on published reports [4], aortic clamping appears to carry a higher risk of dissection than cannulation. In the series of Salama and Blesovsky 153, the incidence of dissection due to aortic crossclamping was 0.23%. The risk of dissection initiated by aortic injury caused by the application of partial-occlusion clamps, used in the performance of the proximal anastomosis of aortocoronary bypass grafts, may be as high as 0.9% [3]. Almost uniformly, these patients were noted to have arteriosclerotic aortas, in contradistinction to the relatively normal aorta of the patient reported here. In summary, our patient was seen with a combination of several unusual entities: a chronic type A dissection probably due to a complication of aortic cannulation, and aortic dissection causing extrinsic obstruction of the left main coronary artery. The condition in this patient illustrates another of the numerous manifestations of aortic dissection and its management by conventional operative techniques without the need for bypass grafting. References 1. Gore I: Diseases of noncoronary arteries. In Gould SE (ed): Pathology of the Heart and Blood Vessels. Third Edition. Springfield, 11, Thomas, 1968, p Miller DC, Stinson EB, Oyer PE, et al: Operative treatment of aortic dissections. J Thorac Cardiovasc Surg 78:365, Boruchow IB, Iyengar R, Jude JR: Injury to ascending aorta by partial-occlusion clamp during aorta-coronary bypass. J Thorac Cardiovasc Surg 73:303, Nicholson WJ, Crawley IS, Logue RB, et al: Aortic root dissection complicating coronary bypass surgery. Am J Cardiol41:103, Salama FD, Blesovsky A: Complications of cannulation of the ascending aorta for open heart surgery. Thorax 25:604, Taylor PC: Extracorporeal circulation-technical aspects. In Effler DB (ed): Blades Surgical Diseases of the Chest. Fourth edition. St. Louis, Mosby, 1978, p Taylor PC, Groves LK, Loop FD, et al: Cannulation of the ascending aorta for cardiopulmonary bypass. J Thorac Cardiovasc Surg 71:255, 1976 Chitwood WR: John and William Hunter on aneurysms. Arch Surg 112:829, 1977 Hume DA, Porter RR: Acute dissecting aortic aneurysms. Surgery 53:122, 1963 DeBakey ME, Henly WS, Cooley DA, et al: Surgical management of dissecting aneurysms of the aorta. J Thorac Cardiovasc Surg 49:130, 1965 Daily PO, Trueblood HW, Stinson EB, et al: Management of acute aortic dissections. Ann Thorac Surgery 10:237, 1970 Koster JK Jr, Cohn LH, Mee RBB, Collins JJ Jr: Late results of operation for acute aortic dissection producing aortic insufficiency. Ann Thorac Surg 26:461, 1978 Greenberg DI, Davia JE, Fenoglio J, et al: Dissecting aortic aneurysm manifesting as acute pericarditis. Arch Intern Med 139:108, 1979 Cipriano PR, Griepp RB: Acute retrograde dissection of the ascending thoracic aorta. Am J Cardiol43:520, 1979 Chamsangavej C: Occlusion of the right pulmonary artery by acute dissecting aortic aneurysm. AJR 132:274, 1979 Morris AL, Banvinsky J: Unusual vascular complications of dissecting thoracic aortic aneurysms. Cardiovasc Radio1 1:95, 1978 Roth JA, Parekh MA: Dissecting aneurysms perforating the esophagus. N Engl J Med 299:776, 1978 Guthaner DF, Miller DC, Silverman JF, et al: Fate of the false lumen following surgical repair of aortic dissections: an angiographic study. Radiology 133:1, 1979 Lantos G, Sos TA, Sniderman KW, et al: Disseding hematoma of the thoracic aorta extending into a coronary artery. Radiology 135:329, 1980 Ciravlo DA, Chesne RB: Coronary artery dissection. Chest 73:677, 1978 Hirst AE, Gore I: Is cystic medionecrosis the cause of dissecting aortic aneurysm? Circulation 53:915, 1976 Schlatmann TJM, Becker AE: Pathogenesis of dissecting aneurysm of aorta. Am J Cardiol39:21, 1977 Reinke RT, Harris RD, Klein AJ, Daily PO: Aortoiliac dissection due to aortic cannulation. Ann Thorac Surg 18:295, 1974 Ambos MA, Rothberg M, Lefleur RS, et al: Unsuspected aortic dissection: the chronic healed dissection. AJR 132:221, 1979