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Ann Thorac Surg 2004;78:2169-2171
© 2004 The Society of Thoracic Surgeons
a Department of Cardiothoracic Surgery, Freeman Hospital, Newcastle Upon Tyne, United Kingdom
b Department of Cardiology, Freeman Hospital, Newcastle Upon Tyne, United Kingdom
Accepted for publication August 1, 2003.
* Address reprint requests to Dr Pillai, Department of Cardiothoracic Surgery, Freeman Hospital, Newcastle Upon Tyne NE7 7DN, UK
jain_freeman{at}hotmail.com
| Abstract |
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| Introduction |
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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-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).
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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.
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.
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 pos-sibly minimize the injury process [7] in the high-risk patient.
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