Ann Thorac Surg 2000;70:1723-1725
© 2000 The Society of Thoracic Surgeons
Case report
Mitral valve repair in a transplanted heart via right thoracotomy
Joseph S. Ladowski, MDa
a Lutheran Hospital of Indiana, Fort Wayne, Indiana, USA
Address reprint requests to Dr Ladowski, Lutheran Hospital of Indiana, 7910 W Jefferson Blvd, Suite 102, Fort Wayne, IN 46804
e-mail: jsl{at}ioheart.com
 |
Abstract
|
|---|
With increasing longevity of many heart transplant recipients, the need for cardiac surgery upon the transplanted heart will become more common. Herein is presented an illustrative case that reinforces the utility of a right-side thoracotomy to approach valve repair in the transplanted heart.
|
Introduction
|
|---|
The transplanted heart is subject to many of the usual degenerative disorders, such as coronary artery disease and valvular degeneration. In addition, diseases unique to heart transplantation may affect the implanted organ and lead to graft atherosclerosis or tricuspid damage from biopsies. Approaches to these disorders will likely become more common. Often, they will require utilization of accepted techniques for the nontransplanted heart.
A 54-year-old woman underwent orthotopic heart transplantation for idiopathic cardiomyopathy on 30 May 1994. The donor was a 34-year-old woman, and a predonation echocardiogram revealed no valvular lesions with a left ventricular ejection fraction (LVEF) of 50%. The transplant was performed with standard atrial and great vessel anastomoses. The recipient’s postoperative course was complicated by pulmonary hypertension, which ultimately responded to isoproterenol, dobutamine, and nitroglycerin. A single rejection episode occurred during her first postoperative month and this was successfully treated with "pulse" steroid intervention. Routine annual cardiac catheterization in 1996 demonstrated mild proximal right coronary artery atherosclerosis, hypokinesia of the inferoapical left ventricle, and mild mitral regurgitation. Subsequent annual catheterization demonstrated development of moderate allograft vasculopathy in all three major coronary systems, with LVEF of 50%. Echocardiography at that time demonstrated mild left ventricular hypertrophy with mild mitral regurgitation. She had no symptoms of heart failure. In April of 1998, she developed orthopnea and dyspnea with daily activities. Physical examination and echocardiogram revealed severe mitral regurgitation with LVEF of 38%. There was no evidence of aortic insufficiency. An electrocardiogram demonstrated chronic right bundle branch block. Creatine phosphokinase levels failed to demonstrate myocardial injury. Cardiac catheterization revealed atherosclerotic lesions in the septal perforator branches and a diagonal branch. These resulted in separate areas of stenosis of approximately 75%. The three major coronary arteries had no obstructing lesions but did demonstrate distal tapering in all terminal branches, with "pruning" of the usual terminal arborization. Her left ventricular end-diastolic pressure was 22 mm Hg with pulmonary artery pressures of 50/30 mm Hg. An endomyocardial biopsy demonstrated no significant rejection (ISHLT-IA).
Because of satisfactory previous experience with right thoracotomy for mitral valve repair in our institution, a "moderately invasive" parasternal right anterior thoracotomy was employed with a transverse incision and entry via the fourth interspace. The patient was placed on cardiopulmonary bypass with bicaval and ascending aortic cannulation. The intraatrial groove was widely mobilized and the left atrium was opened, after cooling the patient to 24°C. With the heart in ventricular fibrillation, coronary perfusion was uninterrupted and the aorta was not clamped. The mitral valve was inspected and found to have thickened but mobile leaflets. All cords and both papillary muscles were structurally sound. Annular dilatation was corrected with insertion of a 25-mm Duran ring. Following closure of the atriotomy, the heart was de-aired with a catheter through the repaired valve. Subsequent deairing through the ascending aorta was then performed and the patient was then rewarmed. Separation from cardiopulmonary bypass was uneventful and postrepair transesophageal echocardiogram confirmed the presence of mild mitral regurgitation with an LVEF of 35%. Intercostal nerve blocks afforded good pain control and her postoperative course was benign. Echocardiography 3 months following mitral repair confirmed only mild mitral regurgitation, along with improvement of the LVEF to 58%. No further symptoms of heart failure were noted. In an attempt to discourage further allograft vasculopathy, she is being treated with intermittent methotrexate in addition to steroids, cyclosporin, azathioprine, and pravastatin.
|
Comment
|
|---|
Replacement of the mitral valve of a transplanted heart as been reported in 4 cases [1–4]. Additionally, "bench" repair of the mitral valve has been described at the time of transplantation [5]. The cause of mitral regurgitation was thought to be iatrogenic (secondary to endomyocardial biopsies) in most of these cases. In the patient reported herein, the etiology of the mitral regurgitation is not certain. Although mitral regurgitation may arise from malalignment of the donor and recipient left atria, the patient did not manifest mitral regurgitation during the first 4 posttransplant years, suggesting that the technique of implantation (atrium-to-atrium instead of pulmonary venous anastomosis) did not induce mitral regurgitation. She has had no left ventricular endomyocardial biopsies and had no evidence of chordal detachment at the time of surgical exploration. Progressive allograft vasculopathy may have contributed to ventricular dysfunction with consequent mitral annular dilatation.
It has previously been demonstrated that mitral replacement (with chordal transection) reduces LVEF because of increases in end-systolic wall stress. Conversely, mitral repair reduces end-systolic wall stress with improvement in LVEF [6]. In accord with these findings, our patient demonstrated improvement in LVEF following mitral repair.
The surgical approach to the transplanted heart is similar to that for the native heart. To date our center has utilized median sternotomy for coronary artery bypass revascularization of the transplanted heart on three occasions. We have performed myocardial laser revascularization on the transplanted heart by means of video–assisted thoracoscopy and limited left thoracotomy (1 case each). This case further confirms that exposure of the transplanted heart can be achieved with standard approaches, including right thoracotomy for mitral valve repair.
|
References
|
|---|
-
Copeland J.G., Rosado L.J., Sethi G., Huston C., Lee R.W. Mitral valve replacement six years after cardiac transplantation. Ann Thorac Surg 1991;51:1014-1016.[Abstract]
-
Cavero M.A., Pulpon L.A., Rubio J.A., et al. Mitral valve replacement in a heart transplant recipient with iatrogenic mitral regurgitation. Ann Thorac Surg 1996;61:1530-1532.[Abstract/Free Full Text]
-
Myers J.C., Coopwood J.B. Mitral valve replacement in the transplanted heart. Ann Thorac Surg 1996;61:1832-1833.[Abstract/Free Full Text]
-
Goldstein D.J., Garfein E.S., Aaronson K., Zuech N., Michler R.E. Mitral valve replacement and tricuspid valve repair after cardiac transplantation. Ann Thorac Surg 1997;63:1463-1465.[Abstract/Free Full Text]
-
Massad M.G., Smedira N.G., Hobbs R.E., Hoercher R., Vandervoort P., McCarthy P.M. Bench repair of donor mitral valve before heart transplantation. Ann Thorac Surg 1996;61:1833-1835.[Abstract/Free Full Text]
-
Tischler M.D., Cooper K.A., Rowen M., et al. Mitral valve replacement versus mitral valve repair. Circulation 1994;89:132-134.[Abstract/Free Full Text]
Accepted for publication February 25, 2000.
Top
Abstract
Introduction
