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Ann Thorac Surg 1997;63:1463-1465
© 1997 The Society of Thoracic Surgeons

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Case Report

Mitral Valve Replacement and Tricuspid Valve Repair After Cardiac Transplantation

Division of Cardiothoracic Surgery, Department of Surgery, College of Physician & Surgeons, Columbia University, New York, New York

Accepted for publication December 3, 1996.

	Abstract

Top Footnotes Abstract Introduction Comment References

 
Efforts aimed at limiting the pool of cardiac retransplantation candidates have focused increasingly on attempts to preserve cardiac allograft function. The present report reviews the course of a patient who underwent mitral valve replacement and tricuspid annuloplasty for bivalvular incompetence after cardiac transplantation and examines the limited reported world experience with valve replacement after transplantation. The limited yet successful experiences with these and other operations in cardiac allograft recipients suggest that worsening donor organ shortages will likely lead to increased clinical experience with conventional operations in the transplanted heart.

	Introduction

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Valvular incompetence after heart transplantation is not an infrequent finding. In most instances, medical management with vasodilators and diuretics is successful. We report a case of severe mitral and tricuspid insufficiency after transplantation requiring mitral valve replacement and tricuspid valve repair and review the limited worldwide experience with posttransplantation surgical management of valvular incompetence.

A 60-year-old man with ischemic dilated cardiomyopathy underwent orthotopic heart transplantation for end-stage heart failure. A donor heart was obtained from a 53-year-old man who had suffered spontaneous intracranial bleeding. At the time of the harvest, echocardiography revealed mild left ventricular hypertrophy with evidence of mild to moderate mitral regurgitation. No segmental wall motion abnormalities were noted, and normal overall left ventricular systolic function was seen. Examination of the donor heart intraoperatively revealed mild myxomatous degenerative changes of the mitral valve. Biatrial anastomotic implantation was performed using a paraseptal donor right atrial incision to prevent distortion of the right atrium. The total ischemic time was 2 hours, the cross-clamp time was 52 minutes, and the cardiopulmonary bypass time was 136 minutes. Intraoperative transesophageal echocardiography performed shortly after separation from cardiopulmonary bypass confirmed mild concentric hypertrophy of the left ventricle without wall motion abnormality while on a regimen of low-dose norepinephrine and dopamine. However, moderate anteriorly directed mitral valve regurgitation and mild to moderate tricuspid regurgitation were seen. The patient's early postoperative course was complicated by bradycardia necessitating placement of a permanent pacemaker. A predischarge echocardiogram revealed moderate mitral and tricuspid regurgitation, a severely dilated left ventricle with an end-diastolic diameter of 6.8 cm, and an estimated ejection fraction of 0.35. He was discharged 2 weeks postoperatively without evidence of cellular rejection.

Within 3 weeks of transplantation the patient returned to an active lifestyle including daily walks of more than 1 km and stationary bicycle exercises. He underwent routine endomyocardial biopsies without significant rejection episodes. During the first 3 months after transplantation, physical examinations revealed a persistent 3/6 holosystolic murmur. Transesophageal echocardiography 2 months postoperatively demonstrated a persistently dilated left ventricle with an ejection fraction of 0.30 to 0.40, a ruptured mitral valve chorda, and moderate to severe tricuspid regurgitation. Increasing doses of captopril (Bristol-Myers Squibb, Princeton, NJ) and diuretics were required to maintain compensated New York Heart Association class II heart failure symptoms.

Four months after transplantation he was admitted to the hospital with a diarrheal syndrome and abdominal pain. Exploratory laparoscopy was unrevealing. Right heart catheterization documented a cardiac output of 2.4 L/min, a pulmonary capillary wedge pressure of 13 mm Hg, and a pulmonary artery saturation of 46%. The low output state was clinically manifested by worsening renal function, acidosis, and sepsis. An endomyocardial biopsy was performed, and no evidence of cellular or humoral rejection was documented. Despite this, he was empirically treated for rejection and started on a regimen of dopamine, dobutamine (Eli Lilly & Co, Indianapolis, IN) and milrinone (Sanofi Winthrop, New York, NY) with only mild improvement in clinical status. Echocardiography demonstrated malcoaptation of the tricuspid valve, a ruptured chorda, and severe tricuspid incompetence in addition to ruptured mitral chordae and severe mitral incompetence. The estimated left ventricular ejection fraction was 0.35 with an end-diastolic diameter of 5.5 cm. It was thought that his biventricular failure and low output state were largely due to valvular incompetence, and plans were made for valvular replacement.

He was taken to the operating room 155 days after transplantation. At operation, severe mitral regurgitation secondary to myxomatous degeneration was found. In addition, the tricuspid annulus was very dilated and the septal tricuspid leaflet was perforated, likely due to endomyocardial biopsy. The patient underwent mitral valve replacement with a Carpentier-Edwards 29-mm porcine prosthesis, pericardial patch repair of the tricuspid leaflet, and DeVega tricuspid annuloplasty. Intraaortic balloon pump support was required for separation from cardiopulmonary bypass.

His early postoperative course was marked by tenuous hemodynamics, multiple inotropic and pressor requirements, and development of perioperative acute tubular necrosis necessitating continuous venovenous hemofiltration. He remained hospitalized for management of heart failure and inpatient rehabilitation. He was discharged 2 months postoperatively. No evidence of mitral regurgitation, mild to moderate tricuspid regurgitation, and residual biventricular dysfunction were documented at that time. Thirteen months after operation, he remains alive and well leading an active lifestyle. Recent right heart catheterization showed a right atrial pressure of 7 mm Hg, pulmonary artery pressure of 25/12 mm Hg (mean, 16 mm Hg), capillary wedge pressure of 8 mm Hg, and pulmonary artery oxygen saturation of 61% with a cardiac index of 2.1 L•min^-1•m^-2. He remains off the transplant waiting list.

	Comment

Top Footnotes Abstract Introduction Comment References

 
Efforts aimed at limiting the pool of cardiac retransplant candidates have focused increasingly on attempts to preserve cardiac allograft function. To this effect, a significant number of transplant recipients are undergoing conventional cardiac operations.

The development of mitral regurgitation in our patient was likely due to the presence of myxomatous degeneration of the mitral valve in the donor organ. Although the etiology of tricuspid regurgitation in the transplanted heart remains controversial, it appears to be a common finding among transplant recipients [1]. Attention has been focused on the abnormal atrial anatomy that results from the biatrial anastomoses routinely used to approximate the donor atria with recipient atrial remnants [2]. A number of authors have recently favored bicaval anastomosis as it has been shown to preserve atrial geometry and size, reduce postoperative tachycardia and the need for temporary and permanent pacing, and reduce hospital stay [3, 4]. Additional factors that have been implicated in the development or worsening of tricuspid regurgitation include pretransplantation and posttransplantation pulmonary hypertension, endomyocardial biopsy-induced chordal damage [5], and right ventricular enlargement with subsequent annular dilatation. Despite a long postoperative course, our patient has markedly improved and has returned to a very active lifestyle.

The world experience with valvular replacement after cardiac transplantation, to our knowledge, is limited to 5 cases (Table 1). One patient underwent aortic valve replacement with a St. Jude Medical prosthesis for aortic insufficiency; the donor organ was noted to have a bicuspid valve at the time of transplantation, and severe aortic incompetence developed within 2 years of transplantation.

A third patient underwent tricuspid valve replacement with a porcine bioprosthesis. At the time of operation, multiple ruptured chordae with flail leaflets were found, and Votapka and associates [9] suggested endomyocardial biopsy-induced injury as the most likely explanation. Finally, 1 patient underwent tricuspid valve replacement with a porcine bioprosthesis and closure of a patent foramen ovale discovered after the patient presented with a paradoxical embolism and transient ischemic attack. Again, chordal rupture secondary to endomyocardial biopsy was thought to be the mechanism of valvar injury. The ensuing right ventricular pressure overload was believed to have led to the development of a right-to-left shunt through a patent foramen ovale.

The limited experience with valvular replacement precludes firm conclusions regarding the management of these difficult patients. However, several points deserve mention. First, valvular procedures after orthotopic heart transplantation can be safely performed with good short-term success. In all reported cases, patients have returned to normal activities. Importantly, these procedures have delayed and perhaps avoided retransplantation, theoretically providing a donor heart for other patients in need [6]. Second, due to the increasing awareness and potential problems of biopsy-induced tricuspid regurgitation, alternative protocols, including echocardiographic guided-endomyocardial biopsy, have been considered. The finding of myxomatous valve degeneration, bicuspid aortic valve, and patent foramen ovale in donor hearts underscores the importance of careful donor organ examination at the time of harvest. Worsening donor organ shortages will likely lead to increased clinical experience with conventional opeations in the transplanted heart.

	Footnotes

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Address reprint requests to Dr Goldstein, Department of Surgery, Milstein Hospital, 7GS, 177 Fort Washington Ave, New York, NY 10032. (e-mail: djg9{at}columbia.edu).

	References

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1. Lewen MK, Brugg J, Miller LW, Williams GA, Labovitz AJ. Tricuspid regurgitation by Doppler echocardiography after orthotopic cardiac transplantation. Am J Cardiol 1987;59:1371–4.[Medline]
2. Rees AP, Milani RV, Lavie CJ, Smart FW, Ventura HO. Valvular regurgitation and right sided pressures in hearttransplant recipients by complete Doppler and color flow evaluation. Chest 1993;104:82–7.[Abstract/Free Full Text]
3. Grant SCD, Khan MA, Faragher EB, Yonan N, Brooks NH. Atrial arrhythmias and pacing after orthotopic heart transplantation: bicaval versus standard atrial anastomosis. Br Heart J 1995;74:149–53.[Abstract/Free Full Text]
4. Czer LSC, Trento A, Blanche C, et al. Orthotopic heart transplantation: clinical experience with a new technique. J Am Coll Cardiol 1993;21(Suppl A):168A.
5. Huddleston CB, Rosenbloom M, Goldstein JA, Pasque MK. Biopsy-induced tricuspid regurgitation after cardiac transplantation. Ann Thorac Surg 1994;57:832–7.[Abstract]
6. Copeland JG, Rosado LJ, Sethi G, Huston C, Lee RW. Mitral valve replacement six years after cardiac transplantation. Ann Thorac Surg 1991;51:1014–6.[Abstract]
7. Weston MW, Vijayanagar R, Sastry NS. Closure of patent foramen ovale and tricuspid valve replacement after heart transplantation. Ann Thorac Surg 1996;61:717–9.[Abstract/Free Full Text]
8. Goenen MJ, Jacquet L, De Kock M, Van Dyck M, Schoevardis JC, Chalant CH. Aortic valve replacement thirty one months after orthotopic heart transplantation. J Heart Lung Transplant 1991;10:604–7.[Medline]
9. Votapka TV, Appleton RS, Pennington DG. Tricuspid valve replacement after orthotopic heart transplantation. Ann Thorac Surg 1994;57:752–4.[Abstract]

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This Article Abstract Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Daniel J. Goldstein Robert E. Michler Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Goldstein, D. J. Articles by Michler, R. E. Search for Related Content PubMed PubMed Citation Articles by Goldstein, D. J. Articles by Michler, R. E.