- Email: [email protected]
Coronary Ostial Stenosis After Aortic Valve Replacement, Revisited
CASE REPORT PILLAI ET AL CORONARY OSTIAL STENOSIS AFTER AORTIC VALVE REPLACEMENT
In addition, we chose to add bivalirudin to the bypass pump priming solution on the basis of experience with lepirudin [2]. Dose adjustments were empirically based on trends seen in ACT measurements. Several observations may explain the differences observed in our 2 patients. Initial ACT targets were derived from the few previous reports [4, 5]. We then lowered the target ACT because of concern about excessive anticoagulation as a result of loss of effective dose-response correlation with ACT more than 500 seconds. Differences in renal function may account for some of the variability observed. Renal dysfunction requires dose reduction to avoid excessive anticoagulation. As with lepirudin, reduction or discontinuation of the maintenance infusion before separation from CPB or use of ultrafiltration may accelerate normalization of ACT and reduce the risk of severe hemorrhage after CPB [2]. Similarly, normal renal function requires more aggressive dosing to achieve and maintain adequate anticoagulation. Maintenance infusions can be continued until separation from CPB to avoid thrombosis of the bypass circuit in these patients. The potential effect of aprotinin, a protease inhibitor, on bivalirudin elimination is unknown. The potential for aprotinin to slow the degradation of bivalirudin and prolong its anticoagulant effect remains to be identified. The appearance of thrombus in the bypass circuit is of major concern. Increased temperature during rewarming may cause a decreased level of anticoagulation and require supplemental dosing. A terminal warm dose of cardioplegia was not used because of potential thrombus formation in the cardioplegia circuit. Thrombus formation in the circuit after CPB must be avoided if return to CPB is necessary. Rapid transfer of blood components in the circuit to a cell-saving device or continued anticoagulation of the bypass circuit by recirculation are possible solutions. Bivalirudin, with its short half-life and ease of monitoring during CPB, is a promising alternative to heparin. Further experience is necessary to standardize this technique.
References 1. Follis F, Schmidt CA. Cardiopulmonary bypass in patients with heparin-induced thrombocytopenia and thrombosis. Ann Thorac Surg 2000;70:2173–81. 2. Koster A, Hansen R, Kuppe H, Hetzer R, Crystal GJ, Mertzlufft F. Recombinant hirudin as an alternative for anticoagulation during cardiopulmonary bypass in patients with heparin-induced thrombocytopenia type II: a 1-year experience in 57 patients. J Cardiothorac Vasc Anesth 2000;14:243–8. 3. Sciulli TM, Mauro VF. Pharmacology and clinical use of bivalirudin. Ann Pharmacother 2002;36:1028 –41. 4. Vasquez JC, Vichiendilokkul A, Mahmood S, Baciewicz A. Anticoagulation with bivalirudin during cardiopulmonary bypass in cardiac surgery. Ann Thorac Surg 2002;74:2177–9. 5. Davis Z, Anderson R, Short D, Garber D, Valgiusti A. Favorable outcome with bivalirudin anticoagulation during cardiopulmonary bypass. Ann Thorac Surg 2003;75:264 –5. 6. Warkentin TE, Barkin RL. Newer strategies for the treatment of heparin-induced thrombocytopenia. Pharmacotherapy 1999;19:181–95. © 2004 by The Society of Thoracic Surgeons Published by Elsevier Inc
2169
Coronary Ostial Stenosis After Aortic Valve Replacement, Revisited Jain B. Pillai, FRCS, Thasee M. Pillay, FRCS, and Javed Ahmad, MRCP Departments of Cardiothoracic Surgery and Cardiology, Freeman Hospital, Newcastle Upon Tyne, United Kingdom
Coronary artery occlusive disease that develops after an uncomplicated aortic valve replacement is well recognized. We present a case that required two further coronary operations and two salvage angioplasty procedures for a continuing fibrotic process in the ascending aorta. The literature and pathology are reviewed. (Ann Thorac Surg 2004;78:2169 –71) © 2004 by The Society of Thoracic Surgeons
I
n 1968, Trimble and colleagues [1] recognized coronary ostial stenosis as a significant delayed complication after aortic valve replacement. Literature review disclosed approximately 120 cases with a consistent clinical pattern. Recurring episodes of acute coronary syndrome persisted despite saphenous vein bypass grafting in our patient. Our sequence of events, although unreported until now, revisits and appears to be unified by the pathology noted by Roberts and Morrow [2] within the ascending aorta after aortic valve replacement. A 73-year-old man underwent an uncomplicated 21-mm Carpentier Edwards Perimount valve replacement for calcific aortic stenosis with a gradient of 96 mm Hg, preserved ventricular function, and normal coronaries. Myocardial protection with intermittent direct coronary cold blood cardioplegia was used. He presented 3 months later with myocardial infarction and unstable angina from a subtotal occlusion of the ostium and proximal 1 cm of the left main coronary stem. Echocardiography confirmed a normal aortic prosthesis. A successful coronary bypass grafting was performed using a bifurcating saphenous vein graft to the left anterior descending artery and obtuse marginal branch with a single aortic anastomosis. Recurrent unstable angina after 2 months again resulted from severe stenosis at the aorto-saphenous anastomosis extending 1 cm into the proximal vein trunk. The vein to vein anastomosis at the Y-bifurcation and both coronary insertion sites were widely patent. There was also a new severe stenosis of the right coronary ostium. The patient underwent successful percutaneous stenting of the right coronary ostium and the proximal aortosaphenous anas-
Accepted for publication Aug 1, 2003. Address reprint requests to Dr Pillai, Department of Cardiothoracic Surgery, Freeman Hospital, Newcastle Upon Tyne NE7 7DN, UK; e-mail: [email protected].
0003-4975/04/$30.00 doi:10.1016/S0003-4975(03)01536-4
FEATURE ARTICLES
Ann Thorac Surg 2004;78:2169 –71
2170
CASE REPORT PILLAI ET AL CORONARY OSTIAL STENOSIS AFTER AORTIC VALVE REPLACEMENT
Fig 1. Elastic van Gieson’s stain showing intense fibrosis (pink) disrupting the lamellar elastic fibers (blue) in the aortic media. (Original magnification, ⫻40.)
FEATURE ARTICLES
tomosis. Although cardiopulmonary bypass was anticipated, it was not required, and he made an excellent recovery. He was again readmitted after 1 month with acute coronary syndrome and broad complex tachycardia with severe aorto-saphenous stent stenosis. The right ostial stent and all other vein anastomoses were unaffected. Bail-out balloon angioplasty of the stent stenosis with complete restoration of flow down the left sided grafts was consolidated the day after with an off-pump pedicled left internal mammary artery anastomosis to the anterior descending vein graft segment. Adequate retrograde flow down the obtuse marginal vein graft was assumed as the vein graft bifurcation site was uninvolved and intraoperatively it was at least 2 cm distal to the involved aortic stent site. Autoantibody screen and Treponema pallidum tests were negative. During the last operation, a punch biopsy from a surgically untouched site on the ascending aorta showed an intense fibrosis replacing the lamellar elastic fibers in the media (Fig 1).
Comment Coronary ostial stenosis should be suspected when ischemic symptoms typically present within 3 to 6 months after aortic valve replacement. The symptoms range from accelerated angina, refractory ventricular arrhythmias, and congestive cardiac failure to sudden cardiac death. There is a predisposition for the left ostium. Two major mechanisms have been proposed. In 1958, Earle B. Kay introduced an important milestone in aortic valve surgery with the technique of direct coronary artery perfusion. In the pre-cardioplegia era, coronary cannulation for continuous blood perfusion was implicated in various forms of immediate damage, viz dissection, and thrombosis as well as in late ostial stenosis [1, 3]. Excessive coronary cannula tip-perfusion pressure caused ruptures in the media and intimal jet injury lesions distal to the orifice. Prolonged occlusion of the vasa vasorum with balloon tipped catheters produce necrosis and ostial scarring. Tight fitting cannulas and retaining ostial sutures are also sited. Improved catheter design has reduced the damage potential. The basket type cannula minimizes the area of contact in the ostium and delivers a dispersed flow rather than a single high-pressure stream.
Ann Thorac Surg 2004;78:2169 –71
Brief cannulation times with intermittent cardioplegia have considerably minimized but not eliminated the ostial trauma potential. Rath and colleagues [4] first reported the occurrence without coronary cannulation. In a seminal pathologic study, Roberts and Morrow [2] described intimal fibrous thickening in the aortic root and proximal coronary artery. This differed from atherosclerosis [2] and was attributed to the turbulence of blood flow in the root from the Starr Edwards ball valve. More laminar central flow through tilting disc valves has not, however, eliminated this complication. Removal of the protective aortic cusps instead exposes the coronary ostia, usually the left to the direct flow of blood from the left ventricle, resulting in stenosing ostial jet lesions. Force and colleagues [5], however, first described this entity with cusped bioprosthesis. The gradient across a bioprosthesis leading to turbulence in the aortic root is implicated. Other infrequent causes have been reported. Coronary syndromes can also occur acutely postoperatively. Right ostial occlusion from aortotomy sutures, ostial thrombosis from aortic retractor trauma, and coronary artery spasm and calcific embolus have been described. Teflon pledget granuloma compressing the right coronary and left main involvement from prosthetic endocarditis present later. Prosthetic oversizing and improper positioning can cause turbulence from the disc occluder moving in front of the ostium. De Scheerder and colleagues [6] reported an association with the postpericardiotomy syndrome and the deposition of circulating immune complexes on vascular walls. Apart from the obligatory vestibulo-auditory symptoms and interstitial keratitis, cardiovascular involvement in the Cogan’s syndrome due to an autoimmune vasculitis has led to delayed coronary ostial stenosis. Steroids have been used in the previously described situations. The apolipo-protein E phenotype predisposes to an accelerated proliferative repair response to arterial injury. Winkelmann and colleagues [7] described intimal and smooth muscle cell proliferation in the coronary artery indistinguishable from re-stenotic lesions after balloon angioplasty. Coronary bypass operations have used vein grafts in most cases. Isolated reports of coronary angioplasty also exist [8]. The recurring stenosis in our patient involved all native ostia and surgical neo-orifice created at the aortic end (vein and stent) and conspicuously spared all nonaortic anastomoses. Our aortic histology favors Roberts and Morrow’s [2] diffuse aortic pathology as opposed to Trimble and colleagues’ [1] isolated ostial pathology. However, this important prognostic distinction is impossible on initial presentation. Our experience here compels us to believe that a pedicled and composite internal mammary artery, rather than vein grafts, should be the safer definitive procedure for this complication. Even if it has less etiologic incidence, this would completely avoid a presumed pathologic ascending aorta and prevent such an extraordinary and potentially fatal recurrence. Direct coronary perfusion should be minimized or eliminated either by aortic root perfusion of cardioplegia or retrograde cardioplegia [9], plus right coronary ostial cannulation alone may be used in patients with aortic regurgitation.
Ann Thorac Surg 2004;78:2171–3
CASE REPORT GAO ET AL MITRAL VALVE ANEURYSM WITH INFECTIVE ENDOCARDITIS
2171
In recent years the knowledge of biomolecular aspects of cell cycle regulation had led to interventions in different phases of the stent re-stenotic process. The concept of local drug delivery through drug-eluting stents instead could possibly minimize the injury process [7] in the high-risk patient.
References
Mitral Valve Aneurysm With Infective Endocarditis Changqing Gao, MD, Cangsong Xiao, MD, and Bojun Li, MD
Fig 1. The 3-mm perforation on the noncoronary leaflet.
(Ann Thorac Surg 2004;78:2171–3) © 2004 by The Society of Thoracic Surgeons
M
itral valve aneurysm (MVA) is uncommon and reported cases are rare and often the consequence of infective endocarditis. The mechanism of the aneurysm evolvement is not clearly established.
A case of MVA associated with infective endocarditis is reported. The patient, a 37-year-old man, was suffering from febrile (⬎ 38°C) and fatigue after a cold, who was intermittently prescribed antibiotic therapy. The patient’s temperature fluctuated, but his complaints gradually deteriorated. Eight months later he came to our hospital because of shortness of breath and palpitation after slight exertion and finally nocturnal dyspnea. Physical examination found diastolic murmur along the left sternal border and systolic murmur at the apex implying aortic and mitral regurgitation. Several Osler’s nodes were also documented. Moderate cardiomegaly was
Department of Cardiovascular Surgery, PLA General Hospital, PLA Institute of Cardiac Surgery, Beijing, China
A case of mitral valve aneurysm associated with infective endocarditis is reported. Two-dimensional echocardiography revealed a saccular structure in the anterior leaflet that bulged into the left atrium throughout the cardiac cycle. During operation, the vegetation on the commissure of the right and left aortic leaflet and a 3-mm perforation on the noncoronary leaflet were found. The mitral valve and aortic valve were replaced with mechanical prosthesis. Pathology of the excised valves showed inflammation. For this patient, we considered that the infected aortic regurgitant jet striking the ventricular surface of the anterior mitral leaflet could be the mechanism of the leaflet aneurysm. Accepted for publication Aug 6, 2003. Address reprint requests to Dr Gao, Department of Cardiovascular Surgery, PLA General Hospital, 28 Fuxing Rd, Beijing 100853, China; e-mail: [email protected].
© 2004 by The Society of Thoracic Surgeons Published by Elsevier Inc
Fig 2. Mitral valve aneurysm with oval deficit of 5 mm in diameter on the anterior mitral leaflet (shown from the aortic incision). 0003-4975/04/$30.00 doi:10.1016/S0003-4975(03)01602-3
FEATURE ARTICLES
1. Trimble AS, Bigelow WG, Wigle ED, Silver MD. Coronary ostial stenosis. A late complication of coronary perfusion in open heart surgery. J Thorac Cardiovas Surg 1969;57:792–5. 2. Roberts WC, Morrow AG. Late postoperative pathological findings after cardiac valve replacement. Circulation 1967;35 (4 Suppl):I48-62. 3. Fishman NH, Youker JE, Roe BB. Mechanical injury to the coronary arteries during operative cannulation. Am Heart J 1968;75:26 –33. 4. Rath S, Goor DA, Har-Zahav Y, Buttler A, Ziskind Z. Coronary ostial stenosis after aortic valve replacement without coronary cannulation. Am J Cardiol 1988;61:1156 –7. 5. Force TL, Raabe DS Jr, Coffin LH, DeMeules JD. Coronary ostial stenosis following aortic valve replacement without continuous coronary perfusion. J Thorac Cardiovas Surg 1980;80:637–41. 6. De Scheerder I, De Buyzere M, Clement D. Association between post-pericardiotomy syndrome and coronary occlusion after aortic valve replacement. Br Heart J 1985;54:445–7. 7. Winkelmann BR, Ihnken K, Beyersdorf F, et al. Left main coronary artery stenosis after aortic valve replacement: genetic disposition for accelerated arteriosclerosis after injury of intact human coronary artery? Coronary Artery Dis 1993;4:659 –67. 8. Marti V, Auge JM, Picart J, et al. Percutaneous transluminal coronary angioplasty as alternative treatment to coronary artery bypass in iatrogenic stenosis of the left main coronary artery. J Interv Cardiol 1995;8:229 –31. 9. Menasche P, Kural S, Fauchet M, et al. Retrograde coronary sinus perfusion. A safe alternative for ensuring cardioplegic delivery in aortic valve surgery. Ann Thorac Surg 1982;34:647–58.
In addition, we chose to add bivalirudin to the bypass pump priming solution on the basis of experience with lepirudin [2]. Dose adjustments were empirically based on trends seen in ACT measurements. Several observations may explain the differences observed in our 2 patients. Initial ACT targets were derived from the few previous reports [4, 5]. We then lowered the target ACT because of concern about excessive anticoagulation as a result of loss of effective dose-response correlation with ACT more than 500 seconds. Differences in renal function may account for some of the variability observed. Renal dysfunction requires dose reduction to avoid excessive anticoagulation. As with lepirudin, reduction or discontinuation of the maintenance infusion before separation from CPB or use of ultrafiltration may accelerate normalization of ACT and reduce the risk of severe hemorrhage after CPB [2]. Similarly, normal renal function requires more aggressive dosing to achieve and maintain adequate anticoagulation. Maintenance infusions can be continued until separation from CPB to avoid thrombosis of the bypass circuit in these patients. The potential effect of aprotinin, a protease inhibitor, on bivalirudin elimination is unknown. The potential for aprotinin to slow the degradation of bivalirudin and prolong its anticoagulant effect remains to be identified. The appearance of thrombus in the bypass circuit is of major concern. Increased temperature during rewarming may cause a decreased level of anticoagulation and require supplemental dosing. A terminal warm dose of cardioplegia was not used because of potential thrombus formation in the cardioplegia circuit. Thrombus formation in the circuit after CPB must be avoided if return to CPB is necessary. Rapid transfer of blood components in the circuit to a cell-saving device or continued anticoagulation of the bypass circuit by recirculation are possible solutions. Bivalirudin, with its short half-life and ease of monitoring during CPB, is a promising alternative to heparin. Further experience is necessary to standardize this technique.
References 1. Follis F, Schmidt CA. Cardiopulmonary bypass in patients with heparin-induced thrombocytopenia and thrombosis. Ann Thorac Surg 2000;70:2173–81. 2. Koster A, Hansen R, Kuppe H, Hetzer R, Crystal GJ, Mertzlufft F. Recombinant hirudin as an alternative for anticoagulation during cardiopulmonary bypass in patients with heparin-induced thrombocytopenia type II: a 1-year experience in 57 patients. J Cardiothorac Vasc Anesth 2000;14:243–8. 3. Sciulli TM, Mauro VF. Pharmacology and clinical use of bivalirudin. Ann Pharmacother 2002;36:1028 –41. 4. Vasquez JC, Vichiendilokkul A, Mahmood S, Baciewicz A. Anticoagulation with bivalirudin during cardiopulmonary bypass in cardiac surgery. Ann Thorac Surg 2002;74:2177–9. 5. Davis Z, Anderson R, Short D, Garber D, Valgiusti A. Favorable outcome with bivalirudin anticoagulation during cardiopulmonary bypass. Ann Thorac Surg 2003;75:264 –5. 6. Warkentin TE, Barkin RL. Newer strategies for the treatment of heparin-induced thrombocytopenia. Pharmacotherapy 1999;19:181–95. © 2004 by The Society of Thoracic Surgeons Published by Elsevier Inc
2169
Coronary Ostial Stenosis After Aortic Valve Replacement, Revisited Jain B. Pillai, FRCS, Thasee M. Pillay, FRCS, and Javed Ahmad, MRCP Departments of Cardiothoracic Surgery and Cardiology, Freeman Hospital, Newcastle Upon Tyne, United Kingdom
Coronary artery occlusive disease that develops after an uncomplicated aortic valve replacement is well recognized. We present a case that required two further coronary operations and two salvage angioplasty procedures for a continuing fibrotic process in the ascending aorta. The literature and pathology are reviewed. (Ann Thorac Surg 2004;78:2169 –71) © 2004 by The Society of Thoracic Surgeons
I
n 1968, Trimble and colleagues [1] recognized coronary ostial stenosis as a significant delayed complication after aortic valve replacement. Literature review disclosed approximately 120 cases with a consistent clinical pattern. Recurring episodes of acute coronary syndrome persisted despite saphenous vein bypass grafting in our patient. Our sequence of events, although unreported until now, revisits and appears to be unified by the pathology noted by Roberts and Morrow [2] within the ascending aorta after aortic valve replacement. A 73-year-old man underwent an uncomplicated 21-mm Carpentier Edwards Perimount valve replacement for calcific aortic stenosis with a gradient of 96 mm Hg, preserved ventricular function, and normal coronaries. Myocardial protection with intermittent direct coronary cold blood cardioplegia was used. He presented 3 months later with myocardial infarction and unstable angina from a subtotal occlusion of the ostium and proximal 1 cm of the left main coronary stem. Echocardiography confirmed a normal aortic prosthesis. A successful coronary bypass grafting was performed using a bifurcating saphenous vein graft to the left anterior descending artery and obtuse marginal branch with a single aortic anastomosis. Recurrent unstable angina after 2 months again resulted from severe stenosis at the aorto-saphenous anastomosis extending 1 cm into the proximal vein trunk. The vein to vein anastomosis at the Y-bifurcation and both coronary insertion sites were widely patent. There was also a new severe stenosis of the right coronary ostium. The patient underwent successful percutaneous stenting of the right coronary ostium and the proximal aortosaphenous anas-
Accepted for publication Aug 1, 2003. Address reprint requests to Dr Pillai, Department of Cardiothoracic Surgery, Freeman Hospital, Newcastle Upon Tyne NE7 7DN, UK; e-mail: [email protected].
0003-4975/04/$30.00 doi:10.1016/S0003-4975(03)01536-4
FEATURE ARTICLES
Ann Thorac Surg 2004;78:2169 –71
2170
CASE REPORT PILLAI ET AL CORONARY OSTIAL STENOSIS AFTER AORTIC VALVE REPLACEMENT
Fig 1. Elastic van Gieson’s stain showing intense fibrosis (pink) disrupting the lamellar elastic fibers (blue) in the aortic media. (Original magnification, ⫻40.)
FEATURE ARTICLES
tomosis. Although cardiopulmonary bypass was anticipated, it was not required, and he made an excellent recovery. He was again readmitted after 1 month with acute coronary syndrome and broad complex tachycardia with severe aorto-saphenous stent stenosis. The right ostial stent and all other vein anastomoses were unaffected. Bail-out balloon angioplasty of the stent stenosis with complete restoration of flow down the left sided grafts was consolidated the day after with an off-pump pedicled left internal mammary artery anastomosis to the anterior descending vein graft segment. Adequate retrograde flow down the obtuse marginal vein graft was assumed as the vein graft bifurcation site was uninvolved and intraoperatively it was at least 2 cm distal to the involved aortic stent site. Autoantibody screen and Treponema pallidum tests were negative. During the last operation, a punch biopsy from a surgically untouched site on the ascending aorta showed an intense fibrosis replacing the lamellar elastic fibers in the media (Fig 1).
Comment Coronary ostial stenosis should be suspected when ischemic symptoms typically present within 3 to 6 months after aortic valve replacement. The symptoms range from accelerated angina, refractory ventricular arrhythmias, and congestive cardiac failure to sudden cardiac death. There is a predisposition for the left ostium. Two major mechanisms have been proposed. In 1958, Earle B. Kay introduced an important milestone in aortic valve surgery with the technique of direct coronary artery perfusion. In the pre-cardioplegia era, coronary cannulation for continuous blood perfusion was implicated in various forms of immediate damage, viz dissection, and thrombosis as well as in late ostial stenosis [1, 3]. Excessive coronary cannula tip-perfusion pressure caused ruptures in the media and intimal jet injury lesions distal to the orifice. Prolonged occlusion of the vasa vasorum with balloon tipped catheters produce necrosis and ostial scarring. Tight fitting cannulas and retaining ostial sutures are also sited. Improved catheter design has reduced the damage potential. The basket type cannula minimizes the area of contact in the ostium and delivers a dispersed flow rather than a single high-pressure stream.
Ann Thorac Surg 2004;78:2169 –71
Brief cannulation times with intermittent cardioplegia have considerably minimized but not eliminated the ostial trauma potential. Rath and colleagues [4] first reported the occurrence without coronary cannulation. In a seminal pathologic study, Roberts and Morrow [2] described intimal fibrous thickening in the aortic root and proximal coronary artery. This differed from atherosclerosis [2] and was attributed to the turbulence of blood flow in the root from the Starr Edwards ball valve. More laminar central flow through tilting disc valves has not, however, eliminated this complication. Removal of the protective aortic cusps instead exposes the coronary ostia, usually the left to the direct flow of blood from the left ventricle, resulting in stenosing ostial jet lesions. Force and colleagues [5], however, first described this entity with cusped bioprosthesis. The gradient across a bioprosthesis leading to turbulence in the aortic root is implicated. Other infrequent causes have been reported. Coronary syndromes can also occur acutely postoperatively. Right ostial occlusion from aortotomy sutures, ostial thrombosis from aortic retractor trauma, and coronary artery spasm and calcific embolus have been described. Teflon pledget granuloma compressing the right coronary and left main involvement from prosthetic endocarditis present later. Prosthetic oversizing and improper positioning can cause turbulence from the disc occluder moving in front of the ostium. De Scheerder and colleagues [6] reported an association with the postpericardiotomy syndrome and the deposition of circulating immune complexes on vascular walls. Apart from the obligatory vestibulo-auditory symptoms and interstitial keratitis, cardiovascular involvement in the Cogan’s syndrome due to an autoimmune vasculitis has led to delayed coronary ostial stenosis. Steroids have been used in the previously described situations. The apolipo-protein E phenotype predisposes to an accelerated proliferative repair response to arterial injury. Winkelmann and colleagues [7] described intimal and smooth muscle cell proliferation in the coronary artery indistinguishable from re-stenotic lesions after balloon angioplasty. Coronary bypass operations have used vein grafts in most cases. Isolated reports of coronary angioplasty also exist [8]. The recurring stenosis in our patient involved all native ostia and surgical neo-orifice created at the aortic end (vein and stent) and conspicuously spared all nonaortic anastomoses. Our aortic histology favors Roberts and Morrow’s [2] diffuse aortic pathology as opposed to Trimble and colleagues’ [1] isolated ostial pathology. However, this important prognostic distinction is impossible on initial presentation. Our experience here compels us to believe that a pedicled and composite internal mammary artery, rather than vein grafts, should be the safer definitive procedure for this complication. Even if it has less etiologic incidence, this would completely avoid a presumed pathologic ascending aorta and prevent such an extraordinary and potentially fatal recurrence. Direct coronary perfusion should be minimized or eliminated either by aortic root perfusion of cardioplegia or retrograde cardioplegia [9], plus right coronary ostial cannulation alone may be used in patients with aortic regurgitation.
Ann Thorac Surg 2004;78:2171–3
CASE REPORT GAO ET AL MITRAL VALVE ANEURYSM WITH INFECTIVE ENDOCARDITIS
2171
In recent years the knowledge of biomolecular aspects of cell cycle regulation had led to interventions in different phases of the stent re-stenotic process. The concept of local drug delivery through drug-eluting stents instead could possibly minimize the injury process [7] in the high-risk patient.
References
Mitral Valve Aneurysm With Infective Endocarditis Changqing Gao, MD, Cangsong Xiao, MD, and Bojun Li, MD
Fig 1. The 3-mm perforation on the noncoronary leaflet.
(Ann Thorac Surg 2004;78:2171–3) © 2004 by The Society of Thoracic Surgeons
M
itral valve aneurysm (MVA) is uncommon and reported cases are rare and often the consequence of infective endocarditis. The mechanism of the aneurysm evolvement is not clearly established.
A case of MVA associated with infective endocarditis is reported. The patient, a 37-year-old man, was suffering from febrile (⬎ 38°C) and fatigue after a cold, who was intermittently prescribed antibiotic therapy. The patient’s temperature fluctuated, but his complaints gradually deteriorated. Eight months later he came to our hospital because of shortness of breath and palpitation after slight exertion and finally nocturnal dyspnea. Physical examination found diastolic murmur along the left sternal border and systolic murmur at the apex implying aortic and mitral regurgitation. Several Osler’s nodes were also documented. Moderate cardiomegaly was
Department of Cardiovascular Surgery, PLA General Hospital, PLA Institute of Cardiac Surgery, Beijing, China
A case of mitral valve aneurysm associated with infective endocarditis is reported. Two-dimensional echocardiography revealed a saccular structure in the anterior leaflet that bulged into the left atrium throughout the cardiac cycle. During operation, the vegetation on the commissure of the right and left aortic leaflet and a 3-mm perforation on the noncoronary leaflet were found. The mitral valve and aortic valve were replaced with mechanical prosthesis. Pathology of the excised valves showed inflammation. For this patient, we considered that the infected aortic regurgitant jet striking the ventricular surface of the anterior mitral leaflet could be the mechanism of the leaflet aneurysm. Accepted for publication Aug 6, 2003. Address reprint requests to Dr Gao, Department of Cardiovascular Surgery, PLA General Hospital, 28 Fuxing Rd, Beijing 100853, China; e-mail: [email protected].
© 2004 by The Society of Thoracic Surgeons Published by Elsevier Inc
Fig 2. Mitral valve aneurysm with oval deficit of 5 mm in diameter on the anterior mitral leaflet (shown from the aortic incision). 0003-4975/04/$30.00 doi:10.1016/S0003-4975(03)01602-3
FEATURE ARTICLES
1. Trimble AS, Bigelow WG, Wigle ED, Silver MD. Coronary ostial stenosis. A late complication of coronary perfusion in open heart surgery. J Thorac Cardiovas Surg 1969;57:792–5. 2. Roberts WC, Morrow AG. Late postoperative pathological findings after cardiac valve replacement. Circulation 1967;35 (4 Suppl):I48-62. 3. Fishman NH, Youker JE, Roe BB. Mechanical injury to the coronary arteries during operative cannulation. Am Heart J 1968;75:26 –33. 4. Rath S, Goor DA, Har-Zahav Y, Buttler A, Ziskind Z. Coronary ostial stenosis after aortic valve replacement without coronary cannulation. Am J Cardiol 1988;61:1156 –7. 5. Force TL, Raabe DS Jr, Coffin LH, DeMeules JD. Coronary ostial stenosis following aortic valve replacement without continuous coronary perfusion. J Thorac Cardiovas Surg 1980;80:637–41. 6. De Scheerder I, De Buyzere M, Clement D. Association between post-pericardiotomy syndrome and coronary occlusion after aortic valve replacement. Br Heart J 1985;54:445–7. 7. Winkelmann BR, Ihnken K, Beyersdorf F, et al. Left main coronary artery stenosis after aortic valve replacement: genetic disposition for accelerated arteriosclerosis after injury of intact human coronary artery? Coronary Artery Dis 1993;4:659 –67. 8. Marti V, Auge JM, Picart J, et al. Percutaneous transluminal coronary angioplasty as alternative treatment to coronary artery bypass in iatrogenic stenosis of the left main coronary artery. J Interv Cardiol 1995;8:229 –31. 9. Menasche P, Kural S, Fauchet M, et al. Retrograde coronary sinus perfusion. A safe alternative for ensuring cardioplegic delivery in aortic valve surgery. Ann Thorac Surg 1982;34:647–58.