Spontaneous Late Rupture of an Aortocoronary Saphenous Vein Graft Philip E. Werthman, MD, Francis P. Sutter, DO, Stephanie Flicker, MD, and Scott M. Goldman, MD Division of Thoracic Surgery and Cardiovascular Surgery, The Lank.enau Hospital and Medical Research Center, Philadelphia, Pennsylvania
A case is presented of vein graft rupture leading to myocardial infarction and subsequent pseudoaneurysm formation. (Ann Thorac Surg 1991;51:664-6)
T
he late complications of aortocoronary arterysaphenous vein bypass grafting include stricture at the anastomotic site, occlusion of the graft by atheromatous plaques, fibrous intimal hyperplasia of the graft [l], coronary steal syndrome, disruption of the proximal anastomosis, and aneurysm formation at any cannulation site. Aneurysmal dilatation of the vein graft is rare [2, 31, and rupture of the body of the graft is very unusual [4,5]. We present a case of late rupture of the body of an aortocoronary artery-saphenous vein bypass graft with subsequent pseudoaneurysm formation. A 63-year-old man with a medical history of atherosclerotic coronary artery disease and peripheral vascular disease was admitted for coronary artery bypass reoperation because of unstable angina. In 1977 the patient underwent uncomplicated triple aortocoronary arterysaphenous vein bypass grafting. He remained asymptomatic until 3 years before admission, when he again experienced chest pain. He then suffered a myocardial infarction. Chest roentgenogram (Fig 1) showed an additional density in the region of the left hilum. Because of postinfarction angina, cardiac catheterization was done. This revealed a 50% occlusion of the left main coronary artery and a clinically significant lesion of the left anterior descending artery. All bypass grafts were occluded. Of note was a short aneurysmal stump of vein graft (Fig 2). Computed tomographic scan of the chest with contrast medium (Fig 3) showed a large mediastinal mass to the left of the main pulmonary artery descending to the base of the heart and down into the atrioventricular groove. A small portion of this mass opacified, indicating that it was of vascular origin. A thoracic aortogram was performed to
determine the site of origin of the aneurysm. A small area of double density was seen in the ascending aorta. His operation was done 4 months after his infarct. The patient was placed on hypothermic cardiopulmonaiy bypass. A short stump of the saphenous vein graft proximal to a pseudoaneurysm was ligated. The mediastinal mass was found to be secondary to a ruptured vein graft. The neck of the pseudoaneurysm involved 35% of the free wall of the saphenous vein graft just beyond the proximal anastomosis. Organized clot and free blood was seen to travel over the pulmonary artery and down into the posterior atrioventricular groove just beyond the left atrial appendage, clearly molded by the heart structures and pericardium. Interestingly, the distal portion of the graft was also patent (Fig 4). Double coronary artery bypass was then performed with saphenous vein and left internal mammary artery grafts. The patient was easily taken off bypass on low dose inotropic support. The remainder of the hospital course was uneventful. Pathologic evaluation of the remaining portion of sa-
Accepted for publication Sep 19, 1990. Address reprint requests to Dr Sutter, Division of Thoracic and Cardiovascular Surgery, The Lankenau Hospital and Medical Research Center, 558 Lankenau Medical Building East, Lancaster Ave West of City Line, Philadelphia, PA 19151.
0 1991 by The Society of Thoracic Surgeons
Fig I . Chest roentgenogram showing left hilur muss. 0003-4975/91/$3.50
Ann Thorac Surg 1991;51:664-6
CASE REPORT
WERTHMAN ET AL VEIN GRAFT RUPTURE
665
Fig 2 . Cardiac catheterization revealing pseudoaneuy s m of proximal vein graft.
phenous vein at the site of rupture showed an adherent thrombus (0.9 cm in diameter) sitting in the vascular channel. There were marked changes of the intima consisting of fibrous and secondary hyalinization. The media and adventitia were both congested.
Comment Aneurysmal dilatation of the body of an aortocoronary saphenous vein graft is a rare complication of bypass grafting [2, 31. This may be the result of atheromatous or nonatheromatous processes. Early aneurysm formation occurring at 4 and 6 months postoperatively has been
Fig 3 . Computed tomographic scan revealing left hilar mass (see text).
Fig 4. lntraoperative photograph (from patient’s right) revealing ligated proximal vein graft, open distal vein graft, and local extent of pseudoaneuysm (dotted line). Aortic cannula is to the left just proximal to innominate a r t e y , and the heart is to the right.
found to be the result of preexisting unrecognized vein wall weakness or injury at the time of harvest [2]. Vlodaver and Edwards [l] found that aneurysms of vein grafts in place for 3% months or longer consistently showed either organized thrombi or intimal fibrotic proliferation. Aneurysms discovered between 5 and 9 years postoperatively were all atherosclerotic in nature [3, 51. Late rupture of a vein graft aneurysm has only been reported in recent literature. The sequelae of this can include free rupture into the thoracic cavity, producing an acute hemothorax [4], and contained rupture with pseudoaneurysm formation and myocardial infarction [5]. In our patient, the contained rupture of the graft took place 12 years postoperatively and resulted in myocardial infarction. We are uncertain as to the cause of rupture. Undetected injury at the time of operation can be ruled out because of the prolonged time frame. The most likely explanation is that intimal fibrosis and hyalinization developed with atherosclerotic changes imposed on the inherent vein wall weakness in valvar areas. At the valves, the usual circular smooth muscle layer of the media gives way to a longitudinal layer of muscle. This is a potential site of weakness [6]. We believe this combina-
666
CASE REPORT WERTHMAN ET AL VEIN GRAFT RUPTURE
tion of events led to the formation of an atherosclerotic aneurysm, which spontaneously ruptured.
References 1. Vlodaver Z, Edwards JE. Pathologic changes in aortocoronary arterial saphenous vein grafts. Circulation 1971;44:719-28. 2. Riahi M, Vasu CM, Tomatis LA, Schlosser RJ, Zimmerman G. Aneurysm of saphenous vein bypass graft to coronary artery. J Thorac Cardiovasc Surg 1975;70:35&9. 3. Pintar K, Barboriak JJ, Johnson WD, Co ED. Atherosclerotic
Ann Thorac Surg 1991;51:66p6
aneurysm in aortocoronary vein graft. Arch Pathol Lab Med 1978;102287-8. 4. Murphy JP, Shabb B, Nishikawa A, Adams PR, Walker WE. Rupture of an aortocoronary saphenous vein graft aneurysm. Am J Cardiol 1986;58555-7. 5. Shapeero LG, Guthaner DF, Swerdlow CW, Wexler L. Rupture of a coronary bypass graft aneurysm: CT evaluation and coil occlusion therapy. Am J Roentgen01 1983;141:1060-2. 6. Benchimol A, Harris CL, Desser KB, Fleming H. Aneurysms of an aortocoronary artery-saphenous vein bypass graft: a case report. Vasc Surg 1975;9:261-4.
REVIEW OF RECENT BOOKS
Heart and Brain, Brain and Heart Edited by Prof Dr(Med) Helge Refsum, Prof Dr(Med) Ilmar A . Sulg, and Prof Dr(Med) Knut Rasrnussen New York, Springer-Verlag, 1989 470 pp, illustrated, $117.90 Reviewed by Bruce W . Lytle, M D The cerebral complications of cardiac operations have by necessity been of interest to cardiac surgeons. With today's older and aging cardiac surgical patient population, cerebral complications remain one of the most vexing problems with which cardiac surgeons are faced. Heart and Brain, Brain and Heart is a book that is based on a symposium held at the University of Tromso in Norway in June of 1987. The authors state that the purpose of this effort was to integrate basic and clinical aspects of cardiology, neurology, cardiovascular surgery, and neurosurgery, and to a certain extent that has been accomplished. This book is really not
likely to be very helpful to practicing cardiac surgeons who are not involved with research. The chapters that pertain to cerebral function and cardiac surgery constitute less than 20% of the book. There are interesting data presented that relate to cerebral blood flow during nonpulsatile cardiopulmonary bypass, but little clinical correlation. Those chapters that do pertain to clinically related studies involve younger groups of patients, a subset not at particularly high risk for cerebral complications. The chapter by John and colleagues that addresses electroencephalographic monitoring during cardiopulmonary bypass contains pertinent data relating to the monitoring of cerebral function, but again, only anecdotal clinical correlation. Two important problems cardiac surgeons face today are cerebral complications resulting from atheroembolism and the issues of cerebral protection during deep hypothermia and circulatory arrest. Unfortunately, neither of these subjects is addressed in any detail. I do not think the practicing cardiac surgeon will find this book to be a great deal of help. Cleveland, Ohio
A case is presented of vein graft rupture leading to myocardial infarction and subsequent pseudoaneurysm formation. (Ann Thorac Surg 1991;51:664-6)
T
he late complications of aortocoronary arterysaphenous vein bypass grafting include stricture at the anastomotic site, occlusion of the graft by atheromatous plaques, fibrous intimal hyperplasia of the graft [l], coronary steal syndrome, disruption of the proximal anastomosis, and aneurysm formation at any cannulation site. Aneurysmal dilatation of the vein graft is rare [2, 31, and rupture of the body of the graft is very unusual [4,5]. We present a case of late rupture of the body of an aortocoronary artery-saphenous vein bypass graft with subsequent pseudoaneurysm formation. A 63-year-old man with a medical history of atherosclerotic coronary artery disease and peripheral vascular disease was admitted for coronary artery bypass reoperation because of unstable angina. In 1977 the patient underwent uncomplicated triple aortocoronary arterysaphenous vein bypass grafting. He remained asymptomatic until 3 years before admission, when he again experienced chest pain. He then suffered a myocardial infarction. Chest roentgenogram (Fig 1) showed an additional density in the region of the left hilum. Because of postinfarction angina, cardiac catheterization was done. This revealed a 50% occlusion of the left main coronary artery and a clinically significant lesion of the left anterior descending artery. All bypass grafts were occluded. Of note was a short aneurysmal stump of vein graft (Fig 2). Computed tomographic scan of the chest with contrast medium (Fig 3) showed a large mediastinal mass to the left of the main pulmonary artery descending to the base of the heart and down into the atrioventricular groove. A small portion of this mass opacified, indicating that it was of vascular origin. A thoracic aortogram was performed to
determine the site of origin of the aneurysm. A small area of double density was seen in the ascending aorta. His operation was done 4 months after his infarct. The patient was placed on hypothermic cardiopulmonaiy bypass. A short stump of the saphenous vein graft proximal to a pseudoaneurysm was ligated. The mediastinal mass was found to be secondary to a ruptured vein graft. The neck of the pseudoaneurysm involved 35% of the free wall of the saphenous vein graft just beyond the proximal anastomosis. Organized clot and free blood was seen to travel over the pulmonary artery and down into the posterior atrioventricular groove just beyond the left atrial appendage, clearly molded by the heart structures and pericardium. Interestingly, the distal portion of the graft was also patent (Fig 4). Double coronary artery bypass was then performed with saphenous vein and left internal mammary artery grafts. The patient was easily taken off bypass on low dose inotropic support. The remainder of the hospital course was uneventful. Pathologic evaluation of the remaining portion of sa-
Accepted for publication Sep 19, 1990. Address reprint requests to Dr Sutter, Division of Thoracic and Cardiovascular Surgery, The Lankenau Hospital and Medical Research Center, 558 Lankenau Medical Building East, Lancaster Ave West of City Line, Philadelphia, PA 19151.
0 1991 by The Society of Thoracic Surgeons
Fig I . Chest roentgenogram showing left hilur muss. 0003-4975/91/$3.50
Ann Thorac Surg 1991;51:664-6
CASE REPORT
WERTHMAN ET AL VEIN GRAFT RUPTURE
665
Fig 2 . Cardiac catheterization revealing pseudoaneuy s m of proximal vein graft.
phenous vein at the site of rupture showed an adherent thrombus (0.9 cm in diameter) sitting in the vascular channel. There were marked changes of the intima consisting of fibrous and secondary hyalinization. The media and adventitia were both congested.
Comment Aneurysmal dilatation of the body of an aortocoronary saphenous vein graft is a rare complication of bypass grafting [2, 31. This may be the result of atheromatous or nonatheromatous processes. Early aneurysm formation occurring at 4 and 6 months postoperatively has been
Fig 3 . Computed tomographic scan revealing left hilar mass (see text).
Fig 4. lntraoperative photograph (from patient’s right) revealing ligated proximal vein graft, open distal vein graft, and local extent of pseudoaneuysm (dotted line). Aortic cannula is to the left just proximal to innominate a r t e y , and the heart is to the right.
found to be the result of preexisting unrecognized vein wall weakness or injury at the time of harvest [2]. Vlodaver and Edwards [l] found that aneurysms of vein grafts in place for 3% months or longer consistently showed either organized thrombi or intimal fibrotic proliferation. Aneurysms discovered between 5 and 9 years postoperatively were all atherosclerotic in nature [3, 51. Late rupture of a vein graft aneurysm has only been reported in recent literature. The sequelae of this can include free rupture into the thoracic cavity, producing an acute hemothorax [4], and contained rupture with pseudoaneurysm formation and myocardial infarction [5]. In our patient, the contained rupture of the graft took place 12 years postoperatively and resulted in myocardial infarction. We are uncertain as to the cause of rupture. Undetected injury at the time of operation can be ruled out because of the prolonged time frame. The most likely explanation is that intimal fibrosis and hyalinization developed with atherosclerotic changes imposed on the inherent vein wall weakness in valvar areas. At the valves, the usual circular smooth muscle layer of the media gives way to a longitudinal layer of muscle. This is a potential site of weakness [6]. We believe this combina-
666
CASE REPORT WERTHMAN ET AL VEIN GRAFT RUPTURE
tion of events led to the formation of an atherosclerotic aneurysm, which spontaneously ruptured.
References 1. Vlodaver Z, Edwards JE. Pathologic changes in aortocoronary arterial saphenous vein grafts. Circulation 1971;44:719-28. 2. Riahi M, Vasu CM, Tomatis LA, Schlosser RJ, Zimmerman G. Aneurysm of saphenous vein bypass graft to coronary artery. J Thorac Cardiovasc Surg 1975;70:35&9. 3. Pintar K, Barboriak JJ, Johnson WD, Co ED. Atherosclerotic
Ann Thorac Surg 1991;51:66p6
aneurysm in aortocoronary vein graft. Arch Pathol Lab Med 1978;102287-8. 4. Murphy JP, Shabb B, Nishikawa A, Adams PR, Walker WE. Rupture of an aortocoronary saphenous vein graft aneurysm. Am J Cardiol 1986;58555-7. 5. Shapeero LG, Guthaner DF, Swerdlow CW, Wexler L. Rupture of a coronary bypass graft aneurysm: CT evaluation and coil occlusion therapy. Am J Roentgen01 1983;141:1060-2. 6. Benchimol A, Harris CL, Desser KB, Fleming H. Aneurysms of an aortocoronary artery-saphenous vein bypass graft: a case report. Vasc Surg 1975;9:261-4.
REVIEW OF RECENT BOOKS
Heart and Brain, Brain and Heart Edited by Prof Dr(Med) Helge Refsum, Prof Dr(Med) Ilmar A . Sulg, and Prof Dr(Med) Knut Rasrnussen New York, Springer-Verlag, 1989 470 pp, illustrated, $117.90 Reviewed by Bruce W . Lytle, M D The cerebral complications of cardiac operations have by necessity been of interest to cardiac surgeons. With today's older and aging cardiac surgical patient population, cerebral complications remain one of the most vexing problems with which cardiac surgeons are faced. Heart and Brain, Brain and Heart is a book that is based on a symposium held at the University of Tromso in Norway in June of 1987. The authors state that the purpose of this effort was to integrate basic and clinical aspects of cardiology, neurology, cardiovascular surgery, and neurosurgery, and to a certain extent that has been accomplished. This book is really not
likely to be very helpful to practicing cardiac surgeons who are not involved with research. The chapters that pertain to cerebral function and cardiac surgery constitute less than 20% of the book. There are interesting data presented that relate to cerebral blood flow during nonpulsatile cardiopulmonary bypass, but little clinical correlation. Those chapters that do pertain to clinically related studies involve younger groups of patients, a subset not at particularly high risk for cerebral complications. The chapter by John and colleagues that addresses electroencephalographic monitoring during cardiopulmonary bypass contains pertinent data relating to the monitoring of cerebral function, but again, only anecdotal clinical correlation. Two important problems cardiac surgeons face today are cerebral complications resulting from atheroembolism and the issues of cerebral protection during deep hypothermia and circulatory arrest. Unfortunately, neither of these subjects is addressed in any detail. I do not think the practicing cardiac surgeon will find this book to be a great deal of help. Cleveland, Ohio
