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Pulmonary artery compression by a giant aortocoronary vein graft aneurysm
948
CASE REPORT MITCHELL AND CAMPBELL AORTOCORONARY VEIN GRAFT ANEURYSM
Ann Thorac Surg 2000;69:948 –9
References 1. Meacham RR III, Headly AS, Bronze MS, Lewis JB, Rester MM. Impending paradoxical embolism. Arch Intern Med 1998;158:438– 48. 2. Thompson T, Evans W. Paradoxical embolism. QJM 1930;23: 135–50. 3. Wilhelm MJ, Schmid C, Hammel D, et al. Cardiac pacemaker infection: surgical management with and without extracorporeal circulation. Ann Thorac Surg 1997;64:1707–12. 4. AbuRahma AF, Lucente FC, Boland JP. Paradoxical embolism: an underestimated entity. A plea for comprehensive work-up. J Cardiovasc Surg 1990;31:685–92. 5. Loscalzo J. Paradoxical embolism: clinical presentation, diagnostic strategies, and therapeutic options. Am Heart J 1986; 112:141–5. 6. Ward R, Jones D, Haponik EF. Paradoxical embolism: an underrecognized problem. Chest 1995;108:549–58. 7. Nellessen U, Daniel WG, Matheis G, Oelert H, et al. Impending paradoxical embolism from atrial thrombus: correct diagnosis by transesophageal echocardiography and prevention by surgery. J Am Coll Cardiol 1985;5:1002– 4.
Pulmonary Artery Compression by a Giant Aortocoronary Vein Graft Aneurysm
Fig 1. Coronary angiogram demonstrating a large fusiform aneurysm of the sequential saphenous vein graft to the obtuse marginal and diagonal coronary arteries.
Max B. Mitchell, MD, and David N. Campbell, MD Division of Cardiothoracic Surgery, University of Colorado Health Sciences Center, Denver, Colorado
Late failure of saphenous vein aortocoronary bypass grafts is predominantly due to vein graft atherosclerotic disease. Rarely, saphenous vein aortocoronary bypass grafts undergo aneurysmal degeneration. We report a case of a giant true aneurysm of a saphenous vein aortocoronary bypass graft producing right heart failure from main pulmonary artery compression. (Ann Thorac Surg 2000;69:948 –9) © 2000 by The Society of Thoracic Surgeons
intervention was refused. Three months later the patient returned with chest pain, dyspnea, abdominal distention, and peripheral edema. Physical examination revealed jugular venous distension, ascites, an enlarged liver, and lower extremity edema. Chest roentgenogram was remarkable for a wide mediastinum and moderate cardiomegaly. Electrocardiogram revealed inferior ST segment depression and anteroseptal T-wave inversion with junctional bradycardia that was attributed to atrioventricular nodal ischemia. The chest pain abated with transvenous pacing and heparin. Echocardiography estimated an ejection fraction of 30% and right ventricular dilation with poor contractility.
A
neurysms of saphenous vein aortocoronary bypass grafts have been reported by several authors [1, 2]. This report presents a patient with a giant saphenous vein graft aneurysm causing compression of the main pulmonary artery and right heart failure. A 54-year-old man presented with increasing exertional angina 17 years after a four-vessel coronary artery bypass. Arteriographic examination revealed 80% stenosis of the left main coronary artery, occluded left anterior descending (LAD), circumflex and right coronary arteries, and occluded saphenous vein grafts to the LAD and posterior descending (PDA) arteries. A patent sequential vein graft to a high obtuse marginal artery and a proximal diagonal artery with a large fusiform aneurysm beginning just after the proximal anastomosis was identified (Fig 1). Computed tomographic (CT) scan confirmed a 7 cm aneurysm of this graft (Fig 2). Surgical
Accepted for publication July 30, 1999. Address reprint requests to Dr Mitchell, 1056 East 19th Ave, B200, Denver, CO 80218.
© 2000 by The Society of Thoracic Surgeons Published by Elsevier Science Inc
Fig 2. Computed tomographic scan demonstrating a large vein graft aneurysm compressing the main pulmonary artery. Note the large intraluminal aneurysm thrombus. 0003-4975/00/$20.00 PII S0003-4975(99)01425-3
Ann Thorac Surg 2000;69:949 –51
At operation the central venous pressure (CVP) was 23 mm Hg, right ventricular pressures were 65/14 mm Hg, pulmonary artery pressures were 28/18 mm Hg, and the pulmonary artery wedge pressure was 16 mm Hg. The right femoral vessels were exposed before sternotomy because of the elevated right heart pressures. The left internal mammary artery (LIMA) was prepared as a pedicle graft. The right femoral artery and right atrium were cannulated and cardiopulmonary bypass was established. The distal ascending and proximal transverse aorta was freed from the densely adherent innominate vein avoiding manipulation of the aneurysmal graft, which originated 2 cm proximal to the innominate artery. The aorta was clamped, and retrograde cold blood cardioplegia was administered to minimize possible graft embolization. The graft was opened longitudinally at the origin of the aneurysm and intraluminal thrombus was removed. The aneurysm had eroded through the anterior wall of the main pulmonary artery. The pulmonary artery was repaired with a 3 cm circular patch of autologous pericardium. The remaining adherent posterior wall of the aneurysmal vein graft was left in place. Gram stain of the thrombus revealed no organisms and cultures were sterile. The distal anastomoses were taken down and a new sequential vein graft was constructed to the diagonal and obtuse marginal arteries. The PDA was not graftable. The LAD was bypassed using the LIMA. After reperfusion the patient easily weaned from bypass with a CVP ranging from 8 to 12 mm Hg and normal-appearing right ventricular contractility. Pullback pressures indicated no right ventricular-pulmonary artery gradient. Histologic section of the aneurysm wall revealed fibrous tissue and fibrin deposition consistent with an aneurysm and intraluminal thrombus. The patient made an uneventful recovery and was discharged home.
CASE REPORT NAIR ET AL ARTERIAL SWITCH: BILATERAL ITA GRAFTING
949
most commonly complicated by myocardial infarction either from graft embolization or occlusion [1, 2]. The unusual feature of our case was the compression of the main pulmonary artery limiting right ventricular ejection resulting in right heart failure. Fistula formation into the pulmonary artery did not occur because of the large thrombus separating the pulmonary artery and aneurysm lumina. Vein graft aneurysms warrant reintervention to prevent ischemic and compressive complications. Intraluminal thrombus may lead to significant underestimation of the size of an aneurysm as determined by angiography. CT scan more accurately estimates aneurysm size. In addition, knowledge of the relation between the aneurysm and adjacent structures provided by the CT scan may be useful in planning surgical intervention as safe mammary artery harvest and the need for femoral artery cannulation were predictable in our case (Fig 2).
References 1. Liang BT, Antman EM, Taus R, et al. Atherosclerotic aneurysms of aortocoronary vein grafts. Am J Cardiol 1988;61: 185– 8. 2. Johnson PR, Truitt TD. Saphenous vein coronary artery bypass graft aneurysm demonstrated by electron beam CT scan. J Comput Assist Tomogr 1994;18:488–91. 3. Kallis P, Keogh BE, Davies MJ. Pseudoaneurysm of aortocoronary vein graft secondary to late venous rupture: case report and literature review. Br Heart J 1993;70:189–92. 4. Mohara J, Konishi H, Kato M, et al. Saphenous vein graft pseudoaneurysm rupture after coronary artery bypass grafting. Ann Thorac Surg 1998;65:831–2. 5. Riahi M, Stone KS, Hanni CL, et al. Right ventricular-saphenous vein graft fistula. Unusual complication of aortocoronary bypass grafting. J Thorac Cardiovasc Surg 1984;87:626 – 8.
Comment Graft atherosclerosis, technical errors, and native coronary artery disease progression are common causes of saphenous vein aortocoronary graft failure. Aneurysmal degeneration of these grafts appears to be rare. There are several reports of pseudoaneurysm formation in saphenous vein grafts [3, 4]. True aneurysms tend to occur late postoperatively, whereas pseudoaneurysms present earlier [1– 4]. Possible mechanisms of pseudoaneurysm formation include hypertension, inadequate hemostasis, vein graft trauma, side branch weakness, and mycotic vasculitis [2– 4]. True aneurysms have been attributed to hypertension, weakness in the wall of the vein (eg, at valves), and more commonly as a sequela of atherosclerosis [1, 2]. Varicosities may predispose to aneurysm formation. Hypertension, hypercholesterolemia, and a long history of smoking may have led to atherosclerotic degeneration and aneurysm formation in our patient. Previous reports of true and false aneurysms of saphenous vein aortocoronary bypass grafts emphasize an association with complications suggesting that the presence of an aneurysm indicates intervention. Pseudoaneurysms most frequently rupture or present with associated infections dictating urgent reoperation [3, 4]. Fistula formation into adjacent cardiac structures has been reported with pseudoaneurysms [5]. True aneurysms are © 2000 by The Society of Thoracic Surgeons Published by Elsevier Science Inc
Arterial Switch Operation: Successful Bilateral Internal Thoracic Artery Grafting Kiron Kumar Somasekharan Nair, MD, Kak Chen Chan, FRCP, and Mark St. John Hickey, FRCSI Departments of Cardiac Surgery and Cardiology, Glenfield Hospital, Leicester, United Kingdom
Internal thoracic artery grafting in arterial switch operations for transposition of great arteries has been reported for salvage of myocardial ischemia after initial coronary transfer. We report a situation where we opted for primary coronary bypass grafting to avoid an obviously difficult coronary transfer, with successful outcome. (Ann Thorac Surg 2000;69:949 –51) © 2000 by The Society of Thoracic Surgeons
Accepted for publication July 17, 1999. Address reprint requests to Dr Hickey, Department of Cardiothoracic Surgery, Glenfield Hospital, Groby Rd, Leicester LE3 9QP, United Kingdom.
0003-4975/00/$20.00 PII S0003-4975(99)01411-3
CASE REPORT MITCHELL AND CAMPBELL AORTOCORONARY VEIN GRAFT ANEURYSM
Ann Thorac Surg 2000;69:948 –9
References 1. Meacham RR III, Headly AS, Bronze MS, Lewis JB, Rester MM. Impending paradoxical embolism. Arch Intern Med 1998;158:438– 48. 2. Thompson T, Evans W. Paradoxical embolism. QJM 1930;23: 135–50. 3. Wilhelm MJ, Schmid C, Hammel D, et al. Cardiac pacemaker infection: surgical management with and without extracorporeal circulation. Ann Thorac Surg 1997;64:1707–12. 4. AbuRahma AF, Lucente FC, Boland JP. Paradoxical embolism: an underestimated entity. A plea for comprehensive work-up. J Cardiovasc Surg 1990;31:685–92. 5. Loscalzo J. Paradoxical embolism: clinical presentation, diagnostic strategies, and therapeutic options. Am Heart J 1986; 112:141–5. 6. Ward R, Jones D, Haponik EF. Paradoxical embolism: an underrecognized problem. Chest 1995;108:549–58. 7. Nellessen U, Daniel WG, Matheis G, Oelert H, et al. Impending paradoxical embolism from atrial thrombus: correct diagnosis by transesophageal echocardiography and prevention by surgery. J Am Coll Cardiol 1985;5:1002– 4.
Pulmonary Artery Compression by a Giant Aortocoronary Vein Graft Aneurysm
Fig 1. Coronary angiogram demonstrating a large fusiform aneurysm of the sequential saphenous vein graft to the obtuse marginal and diagonal coronary arteries.
Max B. Mitchell, MD, and David N. Campbell, MD Division of Cardiothoracic Surgery, University of Colorado Health Sciences Center, Denver, Colorado
Late failure of saphenous vein aortocoronary bypass grafts is predominantly due to vein graft atherosclerotic disease. Rarely, saphenous vein aortocoronary bypass grafts undergo aneurysmal degeneration. We report a case of a giant true aneurysm of a saphenous vein aortocoronary bypass graft producing right heart failure from main pulmonary artery compression. (Ann Thorac Surg 2000;69:948 –9) © 2000 by The Society of Thoracic Surgeons
intervention was refused. Three months later the patient returned with chest pain, dyspnea, abdominal distention, and peripheral edema. Physical examination revealed jugular venous distension, ascites, an enlarged liver, and lower extremity edema. Chest roentgenogram was remarkable for a wide mediastinum and moderate cardiomegaly. Electrocardiogram revealed inferior ST segment depression and anteroseptal T-wave inversion with junctional bradycardia that was attributed to atrioventricular nodal ischemia. The chest pain abated with transvenous pacing and heparin. Echocardiography estimated an ejection fraction of 30% and right ventricular dilation with poor contractility.
A
neurysms of saphenous vein aortocoronary bypass grafts have been reported by several authors [1, 2]. This report presents a patient with a giant saphenous vein graft aneurysm causing compression of the main pulmonary artery and right heart failure. A 54-year-old man presented with increasing exertional angina 17 years after a four-vessel coronary artery bypass. Arteriographic examination revealed 80% stenosis of the left main coronary artery, occluded left anterior descending (LAD), circumflex and right coronary arteries, and occluded saphenous vein grafts to the LAD and posterior descending (PDA) arteries. A patent sequential vein graft to a high obtuse marginal artery and a proximal diagonal artery with a large fusiform aneurysm beginning just after the proximal anastomosis was identified (Fig 1). Computed tomographic (CT) scan confirmed a 7 cm aneurysm of this graft (Fig 2). Surgical
Accepted for publication July 30, 1999. Address reprint requests to Dr Mitchell, 1056 East 19th Ave, B200, Denver, CO 80218.
© 2000 by The Society of Thoracic Surgeons Published by Elsevier Science Inc
Fig 2. Computed tomographic scan demonstrating a large vein graft aneurysm compressing the main pulmonary artery. Note the large intraluminal aneurysm thrombus. 0003-4975/00/$20.00 PII S0003-4975(99)01425-3
Ann Thorac Surg 2000;69:949 –51
At operation the central venous pressure (CVP) was 23 mm Hg, right ventricular pressures were 65/14 mm Hg, pulmonary artery pressures were 28/18 mm Hg, and the pulmonary artery wedge pressure was 16 mm Hg. The right femoral vessels were exposed before sternotomy because of the elevated right heart pressures. The left internal mammary artery (LIMA) was prepared as a pedicle graft. The right femoral artery and right atrium were cannulated and cardiopulmonary bypass was established. The distal ascending and proximal transverse aorta was freed from the densely adherent innominate vein avoiding manipulation of the aneurysmal graft, which originated 2 cm proximal to the innominate artery. The aorta was clamped, and retrograde cold blood cardioplegia was administered to minimize possible graft embolization. The graft was opened longitudinally at the origin of the aneurysm and intraluminal thrombus was removed. The aneurysm had eroded through the anterior wall of the main pulmonary artery. The pulmonary artery was repaired with a 3 cm circular patch of autologous pericardium. The remaining adherent posterior wall of the aneurysmal vein graft was left in place. Gram stain of the thrombus revealed no organisms and cultures were sterile. The distal anastomoses were taken down and a new sequential vein graft was constructed to the diagonal and obtuse marginal arteries. The PDA was not graftable. The LAD was bypassed using the LIMA. After reperfusion the patient easily weaned from bypass with a CVP ranging from 8 to 12 mm Hg and normal-appearing right ventricular contractility. Pullback pressures indicated no right ventricular-pulmonary artery gradient. Histologic section of the aneurysm wall revealed fibrous tissue and fibrin deposition consistent with an aneurysm and intraluminal thrombus. The patient made an uneventful recovery and was discharged home.
CASE REPORT NAIR ET AL ARTERIAL SWITCH: BILATERAL ITA GRAFTING
949
most commonly complicated by myocardial infarction either from graft embolization or occlusion [1, 2]. The unusual feature of our case was the compression of the main pulmonary artery limiting right ventricular ejection resulting in right heart failure. Fistula formation into the pulmonary artery did not occur because of the large thrombus separating the pulmonary artery and aneurysm lumina. Vein graft aneurysms warrant reintervention to prevent ischemic and compressive complications. Intraluminal thrombus may lead to significant underestimation of the size of an aneurysm as determined by angiography. CT scan more accurately estimates aneurysm size. In addition, knowledge of the relation between the aneurysm and adjacent structures provided by the CT scan may be useful in planning surgical intervention as safe mammary artery harvest and the need for femoral artery cannulation were predictable in our case (Fig 2).
References 1. Liang BT, Antman EM, Taus R, et al. Atherosclerotic aneurysms of aortocoronary vein grafts. Am J Cardiol 1988;61: 185– 8. 2. Johnson PR, Truitt TD. Saphenous vein coronary artery bypass graft aneurysm demonstrated by electron beam CT scan. J Comput Assist Tomogr 1994;18:488–91. 3. Kallis P, Keogh BE, Davies MJ. Pseudoaneurysm of aortocoronary vein graft secondary to late venous rupture: case report and literature review. Br Heart J 1993;70:189–92. 4. Mohara J, Konishi H, Kato M, et al. Saphenous vein graft pseudoaneurysm rupture after coronary artery bypass grafting. Ann Thorac Surg 1998;65:831–2. 5. Riahi M, Stone KS, Hanni CL, et al. Right ventricular-saphenous vein graft fistula. Unusual complication of aortocoronary bypass grafting. J Thorac Cardiovasc Surg 1984;87:626 – 8.
Comment Graft atherosclerosis, technical errors, and native coronary artery disease progression are common causes of saphenous vein aortocoronary graft failure. Aneurysmal degeneration of these grafts appears to be rare. There are several reports of pseudoaneurysm formation in saphenous vein grafts [3, 4]. True aneurysms tend to occur late postoperatively, whereas pseudoaneurysms present earlier [1– 4]. Possible mechanisms of pseudoaneurysm formation include hypertension, inadequate hemostasis, vein graft trauma, side branch weakness, and mycotic vasculitis [2– 4]. True aneurysms have been attributed to hypertension, weakness in the wall of the vein (eg, at valves), and more commonly as a sequela of atherosclerosis [1, 2]. Varicosities may predispose to aneurysm formation. Hypertension, hypercholesterolemia, and a long history of smoking may have led to atherosclerotic degeneration and aneurysm formation in our patient. Previous reports of true and false aneurysms of saphenous vein aortocoronary bypass grafts emphasize an association with complications suggesting that the presence of an aneurysm indicates intervention. Pseudoaneurysms most frequently rupture or present with associated infections dictating urgent reoperation [3, 4]. Fistula formation into adjacent cardiac structures has been reported with pseudoaneurysms [5]. True aneurysms are © 2000 by The Society of Thoracic Surgeons Published by Elsevier Science Inc
Arterial Switch Operation: Successful Bilateral Internal Thoracic Artery Grafting Kiron Kumar Somasekharan Nair, MD, Kak Chen Chan, FRCP, and Mark St. John Hickey, FRCSI Departments of Cardiac Surgery and Cardiology, Glenfield Hospital, Leicester, United Kingdom
Internal thoracic artery grafting in arterial switch operations for transposition of great arteries has been reported for salvage of myocardial ischemia after initial coronary transfer. We report a situation where we opted for primary coronary bypass grafting to avoid an obviously difficult coronary transfer, with successful outcome. (Ann Thorac Surg 2000;69:949 –51) © 2000 by The Society of Thoracic Surgeons
Accepted for publication July 17, 1999. Address reprint requests to Dr Hickey, Department of Cardiothoracic Surgery, Glenfield Hospital, Groby Rd, Leicester LE3 9QP, United Kingdom.
0003-4975/00/$20.00 PII S0003-4975(99)01411-3