Ann Thorac Surg 1999;68:1849-1850
© 1999 The Society of Thoracic Surgeons
Case Reports
Accelerated allograft degeneration after aortic valve endocarditis
Ashraf Osman, MDa,
James McCann, PAa,
Richard J. Shemin, MDa,
Harold L. Lazar, MDa
a Department of Cardiothoracic Surgery, Boston Medical Center, Boston University School of Medicine, Boston, Massachusetts, USA
Address reprint requests to Dr Lazar, Department of Cardiothoracic Surgery, Boston Medical Center, 88 E Newton St, Suite B404, Boston, MA 02118
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Abstract
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Early calcification of aortic allografts is usually seen in children less than 3 years of age. We describe a case of a 22-year-old intravenous drug user who developed calcific aortic valve stenosis less than 3 years after an allograft root replacement for endocarditis.
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Introduction
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Aortic allografts have emerged as the valve of choice for patients with complex aortic root pathology after endocarditis [1, 2]. Long-term results have been good with less than 10% of implanted valves requiring reoperation at 5 years [1]. In this report, we describe the case of an intravenous drug user who developed calcific aortic valve stenosis less than 3 years after an allograft root replacement for endocarditis.
A 22-year-old white male intravenous drug user was admitted to the Boston Medical Center with Staphylococcus aureus septicemia and congestive heart failure. A transesophageal echocardiogram revealed a 2-cm vegetation on the right coronary leaflet of the aortic valve with 4+ aortic insufficiency. There was evidence of an abscess cavity burrowing into the membranous septum and into the right ventricular outflow tract. A cranial computed tomographic scan revealed multiple lacunar emboli. At the time of operation, the right coronary leaflet of the aortic valve was virtually replaced by a 2-cm vegetation extending into a large abscess cavity that burrowed through the septum and into the right ventricular outflow tract. The cavity and septum were thoroughly debrided and a pericardial patch was used to close the ventricular septal defect. A No. 25 cryopreserved homograft, procured from a 54-year-old man with a warm ischemic time of 675 minutes, was inserted using the full root replacement technique. The patient tolerated the procedure well, remained in normal sinus rhythm without neurologic deficits, and had no evidence of any aortic insufficiency or intracardiac shunts on a predischarge transesophageal echocardiogram. He received a 6-week course of nafcillin and was referred to a drug rehabilitation center. After his release from rehabilitation, he continued to use intravenous drugs for 6 months. He was readmitted to another drug rehabilitation center where he remained drug free. Thirty months after the homograft insertion, he began to experience dyspnea on exertion and had several episodes of congestive heart failure. A repeat transesophageal echocardiogram showed a heavily calcified aortic valve with a mean gradient of 60 mm Hg and an aortic valve area of 0.6 cm2. There were no vegetations or intracardiac shunts. Serum calcium and blood urea nitrogen and creatinine levels were within normal limits. Thirty-three months after the original homograft insertion, he was taken back to the operating room where the entire homograft, except for the coronary ostia, were found to be calcified. The valve leaflets were heavily calcified (Fig 1), with calcium extending into the annulus. The leaflets were excised, the annulus debrided, and a No. 25 St. Jude HP (St. Jude Medical, Inc, St. Paul, MN) mechanical prosthesis inserted. He tolerated the procedure well and had an uncomplicated postoperative course. The valve pathology revealed an acellular material with nodular calcifications and fibrosis. There was no evidence of any vegetations and all cultures were negative. At 10 months after operation he remains drug free with an active lifestyle. A transesophageal echocardiogram shows a normal functioning prosthesis with no paravalvular leaks.
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Comment
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The mode of failure of aortic allografts can be related to valve conditions (processing techniques, age of the donor) [3], patient factors (renal failure, hyperparathyroidism, younger age) [3–5], surgical technique (freestyle versus full root replacement) [6], or a combination of these factors. Although as many of 70% of all aortic allograft recipients less than 3 years of age have been noted to have extensive allograft calcification or insufficiency [4], we know of no other instance of accelerated allograft calcification in an adult in the absence of renal dysfunction, hyperparathyroidism, or recurrent endocarditis. Yacoub and colleagues [3], in their 14-year series with allograft aortic valves, showed that donor age less than 25 years and more than 55 years, and recipient age less than 30 years increased the risk for late valve degeneration. However, this was manifested as valve deterioration due to structural failure with insufficiency and not as calcific aortic stenosis. In the absence of early recurrent endocarditis, calcific aortic stenosis was not observed in patients less than 15 years.
The mechanism for accelerated calcification in aortic allografts remains unclear. Clarke and co-workers [4] postulated that early allograft calcification in patients less than 3 years of age might be immunologic, and suggested antiinflammatory agents or low-dose immunosuppression in children less than 3 years of age. Vogt and co-workers [2] used immunochemistry techniques to demonstrate the presence of B-cell lymphocytes in patients with accelerated allograft degeneration giving more support to an immunologic cause. However, Mitchell and associates [7] showed a marked paucity of viable cells in cryopreserved allografts explanted after 2 months. They concluded that there was no evidence that cell-medicated immune reactions caused pathologic changes in the cryopreserved allograft valve. Calcification was noted to be most prominent in the aortic walls and less likely to be found on the leaflets. The calcified deposits seen in the leaflets appeared to originate in residual nonviable cells. They postulate that intracellular Ca2+ concentration in these nonviable cells, normally kept low by energy-requiring pumps in the cell membranes, is now increased because the membranes are disrupted and Ca2+ exclusion is impaired. This allows high concentrations of intracellular Ca2+ to react with membrane phosphorous, resulting in the calcification of collagen fibers.
The pathologic findings in our patient provide no insight into the cause of the development of accelerated calcification. No vegetations were noted, and the material was acellular making it less likely to have been attributable to an immunologic reaction. Dystrophic calcification is a common end stage for necrotic tissue and it is conceivable that this patient’s early return to intravenous drug use could have precipitated an immunologic response to any viable cells still present in the leaflets at that time. It is also possible that the older age of the donor (54 years) may have played a role in the accelerated calcification of this valve.
Despite the early failure of this allograft, we continue to favor the use of cryopreserved allografts for aortic root reconstruction in patients with endocarditis. More clinical follow-up will be necessary to determine whether intravenous drug abusers may be more susceptible to accelerated valvular calcification of cryopreserved allografts after implantation for endocarditis.
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References
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Dearani J.A., Orszulak T.A., Schaff H.V., Daly R.C., Anderson B.J., Danielson G.K. Results of allograft aortic valve replacement for complex endocarditis. J Thorac Cardiovasc Surg 1997;113:285-291.[Abstract/Free Full Text]
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Vogt P.R., von Segesser L.K., Jenni R., et al. Emergency surgery for acute infective aortic valve endocarditis. Euro J Cardiothorac Surg 1997;11:53-61.[Abstract]
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Yacoub M., Rasmi N.R.H., Sundt T.M., et al. Fourteen year experience with homovital homografts for aortic valve replacement. J Thorac Cardiovasc Surg 1995;110:186-194.[Abstract/Free Full Text]
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Clarke D.R., Campbell D.N., Hayward A.R., Bishop D.A. Degeneration of aortic valve allografts in young recipients. J Thorac Cardiovasc Surg 1993;105:934-942.[Abstract]
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Sundt T.M., Rasmi N., Wong K., Radley-Smith R., Khaghani A., Yacoub M.H. Reoperative aortic valve operation after homograft root replacement. Ann Thorac Surg 1995;60:S95-S106.
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Doty J.R., Salazar J.D., Liddicoat J.R., Flores J.H., Doty D.B. Aortic valve replacement with cryopreserved aortic allograft. J Thorac Cardiovasc Surg 1997;115:371-380.[Abstract/Free Full Text]
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Mitchell R.N., Jonas R.A., Schoen F.J. Pathology of explanted cryopreserved allograft heart valves. J Thorac Cardiovasc Surg 1998;115:118-127.[Abstract/Free Full Text]
Accepted for publication April 16, 1999.
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Abstract
Introduction
