Ann Thorac Surg 2010;89:277-279. doi:10.1016/j.athoracsur.2009.06.081
© 2010 The Society of Thoracic Surgeons
Case Reports
Aortic Bioprosthetic Valve Deterioration 8 Months After Implantation
Dominik Wiedemann, MD*,
Nikolaos Bonaros, MD,
Günther Laufer, MD,
Alfred Kocher, MD
University Clinic of Cardiac Surgery, Innsbruck Medical University, Innsbruck, Austria
Accepted for publication June 15, 2009.
* Address correspondence to Dr Wiedemann, University Clinic of Cardiac Surgery, Innsbruck Medical University, Anichstr. 35, Innsbruck, A-6020, Austria (Email: dominik.wiedemann{at}i-med.ac.at).
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Abstract
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One year after aortic bioprosthetic valve replacement with a 23-mm Epic bioprosthesis (St. Jude Medical, St. Paul, MN) with concomitant coronary artery bypass grafting, early valve degeneration with leaflet calcification and stiffening was documented in a 61-year-old man. A possible reason for this extremely early deterioration could not be identified, although a xenograft reaction could be a plausible hypothesis. Consequently, a successful redo aortic valve replacement with a 21-mm Magna Ease (Carpentier-Edwards, Irvine, CA) was performed.
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Introduction
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The Epic stented porcine prosthesis (St. Jude Medical, St. Paul, MN) in the aortic position has demonstrated excellent long-term durability and hemodynamic stability [1]. Low rates of valve-related events and structural failure prove that the Epic bioprostheses is a good choice for patients with calcified aortic stenosis. Degeneration of bioprostheses usually occurs rather late in an age-dependent manner. St. Jude bioprostheses are at risk of structural valve degeneration beginning as soon as 7 years postoperatively for patients aged younger than 65 years. Therefore, aortic valve replacement with a bioprosthesis is a reliable option, especially for elderly patients. We describe a patient with early valve deterioration of a St. Jude Medical bioprostheses 1 year postoperatively.
A 61-year-old man with coronary artery disease (CAD) and severe aortic stenosis combined with moderate aortic insufficiency was admitted to our hospital. His preoperative echocardiogram confirmed severe aortic stenosis (maximum pressure gradient, 98 mm Hg; mean gradient, 57 mm Hg), moderate aortic regurgitation, and normal left ventricular function. He had 80% stenosis of the left anterior descending artery (LAD) and 60% stenosis of the right coronary artery, after two percutaneous coronary interventions with unsatisfactory long-term results. Both coronary arteries were excellent target vessels for coronary artery bypass grafting (CABG).
The patient opted for a biologic valve because he objected to lifelong anticoagulation. He underwent aortic valve replacement with a 23-mm St. Jude Epic bioprosthesis with concomitant CABG with the left internal mammary artery (LIMA) to the LAD and a saphenous vein graft to the posterior descending artery. His postoperative course was uneventful and he could be discharged after 6 days.
By 8 months after the operation, dyspnea symptoms had already reappeared. An echocardiogram showed reappearance of severe aortic stenosis, with a maximum gradient of 100 mm Hg that rapidly progressed to a maximum gradient of 170 mm Hg. He had mean gradient of 90 mm Hg at 11 months.
A redo aortic replacement was performed with a 21-mm Carpentier-Edwards Magna Ease bioprosthesis (Edwards Lifesciences, Irvine, CA). The St. Jude valve (St. Jude Medical) presented as strongly degenerated, the leaflets were restricted with a fibrous layer on both sides, and the opening surface of the valve was reduced to a minimum (Fig 1). The valve was sent for histologic evaluation, which showed mild infiltration of granulocytes together with signs of calcification.
The patient's postoperative course was again uneventful. A transesophageal echocardiogram revealed a mean gradient over the aortic valve of 28 mm Hg (maximum, 33 mm Hg). This is in the acceptable range for this patient, with a patient prosthesis match of 0.91 cm2/m2. No further intervention was necessary, and the patient is doing well 6 months postoperatively.
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Comment
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This patient presented with leaflet fibrosis within a 1 year. The Epic stented bioprosthesis has been used in Europe for almost 9 years and received United States Food and Drug Administration approval in 2004. It has a proven history of excellent durability and long-term stability of hemodynamic performance in both the aortic and mitral positions. Valve dysfunction rates are low.
Classic reasons for deterioration of bioprosthetic valves are calcification, infection, degeneration, instrument trauma, and leaflet detachment from the valve strut. There were a few reports of early calcification of bioprosthetic valves [2, 3]. The crucial pathologic process of valve degeneration is leaflet calcification [4]. Glutaraldehyde pretreatment-devitalized residual cells often initiate leaflet calcification. The following mechanism leads to reaction of calcium rich extracellular fluid with membrane-bound phosphorus to build calcium phosphate mineral deposits. Calcification of the leaflets leads to leaflet stiffening and finally failing of the valve. The rate of valve deterioration in older patients is lower and the process is accelerated in younger patients. Reasons for this age dependency are unclear [5].
A recent study showed that valve calcification can be induced or inhibited by special factors [6]. Dialysis patients often have early valve degeneration together with vascular calcification. Risk factors for the vascular calcification include calcium or vitamin D supplementation. One may speculate that higher systemic calcium levels can also trigger early bioprosthetic valve degeneration. There is a potential relation between calcium consumption and early leaflet calcification. Reduced kidney function may increase the deposition of calcium.
Our patient had none of these risk factors for early degeneration. His serum calcium levels were normal preoperatively and postoperatively, with no calcium supplementation perioperatively. Renal function was only slightly reduced, with maximum creatinine levels of 1.4 mg/dL. The serum calcium levels were always within the normal reference range in the routine blood samples.
A rather new hypothesis for early bioprosthetic valve degeneration is xenograft reaction [7]. Although glutaraldehyde fixation decreases the antigenicity of bioprosthesis, it does not eliminate antigens completely. Rejection and as consequence, calcification, may be a reason why bioprosthetic valves fail, especially in young patients. In an experimental study, Manji and colleagues [7] showed that glutaraldehyde-fixed xenografts show cellular and humoral signs of rejection. The histologic evaluation in our patient showed a rather unspecific granulocyte infiltration and only a few signs of inflammation. Therefore, we could not prove xenograft rejection as reason for the early failure of the bioprosthetic valve; nevertheless, this might be a possible explanation.
Despite the early valve degeneration, the patient did not receive a mechanical heart valve, because of his attitude to life-long anticoagulation. In view of the possible mechanisms of deterioration, we switched from a porcine valve to a bovine pericardial bioprosthesis because we believed this change provided the best possible antigenic diversity to preclude a second immune-mediated xenograft rejection.
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References
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- Eichinger WB, Hettich IM, Ruzicka DJ, et al. Twenty-year experience with the St. Jude medical Biocor bioprosthesis in the aortic position Ann Thorac Surg 2008;86:1204-1210.[Abstract/Free Full Text]
- Polo ML, Legarra JJ, Vilar M, Cabrera A, Duran D, Pradas G. Early calcification of a Carpentier-Edwards Perimount mitral valve in an elderly woman J Thorac Cardiovasc Surg 2002;124:1043-1044.[Free Full Text]
- Izutani H, Shibukawa T, Kawamoto J, Mochiduki S, Nishikawa D. Early aortic bioprosthetic valve deterioration in an octogenarian Ann Thorac Surg 2008;86:1369-1371.[Abstract/Free Full Text]
- Butany J, Nair V, Leong SW, Soor GS, Feindel C. Carpentier-Edwards Perimount valves—morphological findings in surgical explants J Card Surg 2007;22:7-12.[Medline]
- Schoen FJ, Levy RJ. Calcification of tissue heart valve substitutes: progress toward understanding and prevention Ann Thorac Surg 2005;79:1072-1080.[Abstract/Free Full Text]
- Speer MY, Giachelli CM. Regulation of cardiovascular calcification Cardiovasc Pathol 2004;13:63-70.[Medline]
- Manji RA, Zhu LF, Nijjar NK, et al. Glutaraldehyde-fixed bioprosthetic heart valve conduits calcify and fail from xenograft rejection Circulation 2006;114:318-327.[Abstract/Free Full Text]
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Abstract
Introduction
