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Ann Thorac Surg 1995;59:477-480
© 1995 The Society of Thoracic Surgeons

Tricuspid Valve Dysfunction in the Transplanted Heart

Utah Cardiac Transplant Program, Salt Lake City, Utah

Accepted for publication September 17, 1994.

	Abstract

Top Footnotes Abstract Introduction Case Reports Comment Addendum References

 
Mild degrees of tricuspid regurgitation are common in the orthotopically transplanted heart, probably secondary to the geometry of the right atrial anastomosis. At the University of Utah, 5 (0.95%) of 526 patients with transplantations performed from March 1985 to December 1993 have presented with severe tricuspid regurgitation requiring operative intervention. Echocardiographic findings confirmed at the time of operation consisted of ruptured chordae to the tricuspid valve. Standard tricuspid valve repair and replacement techniques were used with good results. We postulate the chordal disruption found in these patients is secondary to injuries incurred at the time of endomyocardial biopsy.

	Introduction

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See also page 480.

Mild degrees of tricuspid regurgitation are known frequently to accompany orthotopically transplanted hearts [1, 2]. This degree of tricuspid regurgitation is well tolerated and tends to decrease with time [3]. A more severe degree of tricuspid regurgitation has been noted in a very small number of transplant recipients at the University of Utah. This may be due to traumatic disruption of the subvalvular support mechanism during routine endomyocardial biopsy.

Since March 1985, 526 orthotopic cardiac transplantations have been performed by the Utah Cardiac Transplant Program. Five patients (0.95%) have presented with severe tricuspid regurgitation refractory to medical management and have required surgical intervention to correct their tricuspid regurgitation. Their brief clinical histories are as follows.

	Case Reports

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Patient 1
Patient 1 was a 55-year-old man who underwent orthotopic cardiac transplantation in October 1988 for ischemic dilated cardiomyopathy. Initial postoperative echocardiograms showed mild tricuspid regurgitation, but an echocardiogram performed 2 months postoperatively revealed 3+/4+ tricuspid regurgitation with a flail septal leaflet. Physical examination revealed hepatomegaly with laboratory results significant for elevated transaminase levels and a macrocytic anemia. He was admitted in April 1989 with acute symptoms consistent with a transient ischemic attack. Head computed tomographic and carotid duplex scans were normal. Right heart catheterization showed 4+ tricuspid regurgitation with an enlarged patent foramen ovale and a right-to-left shunt. We believed that the patient had suffered from a paradoxical embolus in part related to an enlarging patent foramen ovale and elevated right atrial pressures. On April 17, 1989 (6 months after transplantation), the patient underwent closure of the patent foramen ovale and a De Vega valvuloplasty for correction of a flail septal leaflet and dilated tricuspid annulus. The patient made an uneventful recovery with complete symptomatic recovery from his tricuspid regurgitation. The patient continued to suffer from restrictive lung disease and hypoxia, renal insufficiency, and myelodysplastic pancytopenia. He eventually died on March 20, 1990, secondary to multiorgan system failure.

Patient 2
Patient 2 was a 65-year-old man who underwent orthotopic cardiac transplantation in April 1987 for ischemic dilated cardiomyopathy. Pretransplantation right heart catheterization showed pulmonary arterial pressures (PAP) of 56/28 (mean, 39 mm Hg), a pulmonary capillary wedge pressure (PCWP) of 24 mm Hg, a cardiac output of 2.8 L/min, and a pulmonary vascular resistance of 5.4 Wood units. An echocardiogram 15 months after transplantation documented the new presence of severe tricuspid regurgitation with biatrial enlargement. The patient continued to do well with medical treatment; however, a cardiac catheterization performed in November 1990 showed severe tricuspid regurgitation with V waves to 22 mm Hg and ventricularization of the right atrial pressure tracing. Pulmonary artery and wedge pressures remained normal. Subsequently increasing peripheral edema and shortness of breath developed necessitating surgical intervention. In November 1991 (55 months after transplantation), the patient underwent valve repair with a 35-mm Carpentier ring. Chordae to the posterior and septal leaflets were ruptured. The patient's postoperative course was unremarkable, and he was discharged on postoperative day 6. Soon after discharge, obstructive jaundice developed. A periampullary villous adenoma with a focus of adenocarcinoma was discovered on endoscopy. Successful resection with a Whipple procedure was performed. The patient remains alive and well without symptoms of tricuspid regurgitation to date.

Patient 3
Patient 3 was a 64-year-old man who underwent orthotopic cardiac transplantation on November 25, 1991, for idiopathic dilated cardiomyopathy. Preoperative right heart pressures were as follows: PAP, 28/18 mm Hg (mean, 20 mm Hg); PCWP, 9 mm Hg; cardiac index, 2.4 L • min^-1 • m^-2; and pulmonary vascular resistance, 2.3 Wood units. His immediate postoperative course was complicated by markedly decreased right ventricular function and progressive renal insufficiency. Echocardiogram in the postoperative period revealed no significant tricuspid valvular disfunction. An endocardial biopsy excluded the possibility of rejection. The right ventricular dysfunction was believed to be due to a long donor ischemia time. His condition eventually improved and the patient was discharged from the hospital. He was readmitted with symptoms of weakness and dizziness. Right heart catheterization 2 months later was significant for a right atrial pressure of 20 mm Hg with V waves to 24 mm Hg (PAP, 28/19 mm Hg; PCWP, 22 mm Hg). Endocardial biopsy again showed no evidence of rejection. The patient was readmitted a second time for right ventricular failure 2 months later. The patient subsequently noticed a gradual decrease in exercise tolerance, increasing fatigue, and bilateral lower extremity edema. Hepatomegaly was also present on physical examination, along with an elevated alkaline phosphatase level (139 U/L). A transesophageal echocardiogram showed a flail septal leaflet with severe tricuspid regurgitation. The patient's tricuspid regurgitation was managed medically; however, he was admitted 9 months later with worsening right-sided congestive heart failure, believed to be secondary to tricuspid regurgitation. He was taken to the operating room on December 11, 1992 (13 months after transplantation), disrupted chordae to the anterior leaflet were found. A 32-mm Carpentier ring was used to repair the valve. A 10-L diuresis ensued postoperatively along with complete resolution of the lower extremity edema. Follow-up echocardiogram showed trace tricuspid regurgitation. The patient died suddenly at home 3 months later, presumably of graft atherosclerosis. An autopsy revealed 70% stenosis of the three major coronary arteries. The tricuspid valve prosthesis was in good condition.

Patient 4
Patient 4 was a 40-year-old man who underwent orthotopic cardiac transplantation for idiopathic dilated cardiomyopathy on March 19, 1988. (Pretransplantation right heart pressures were as follows: PAP, 62/34; mean, 46 mm Hg; PCWP, 38 mm Hg; cardiac index, 1.8 L • min^-1 • m^-2; pulmonary vascular resistance, 2.0 Wood units.) The patient had done well until he was admitted on July 20, 1993, with complaints of increasing lower extremity edema and increasing abdominal girth. Transesophageal echocardiography revealed marked right atrial enlargement, severe tricuspid regurgitation with a flail septal leaflet, and bulging of the interatrial septum toward the left atrium. On July 30, 1993 (64 months after transplantation), he underwent tricuspid valve replacement with a 35-mm Carpentier-Edwards porcine valve (because valve repair was deemed undesirable for technical reasons). Operative findings included right atrial enlargement with annular dilatation and a flail septal leaflet.

Patient 5
Patient 5 was a 55-year-old man who underwent orthotopic cardiac transplantation in April 1993 for ischemic cardiomyopathy. Pretransplantation right heart catheterization showed a right ventricular pressure of 26/2 mm Hg; PAP of 29/19 mm Hg (mean, 23 mm Hg); and PCWP of 9 mm Hg. The patient experienced three episodes of acute rejection documented by endomyocardial biopsy. After one biopsy procedure 2 months after transplantation, tricuspid regurgitation developed, documented by transthoracic echocardiogram. Symptoms of right heart failure increased over the ensuing 6 months despite medical treatment. Tricuspid valve replacement with a 29-mm Carpentier-Edwards porcine valve was performed 8 months after transplantation. Operative findings included a flail septal leaflet secondary to ruptured chordae. Right-sided heart failure resolved, and the patient made an uneventful recovery.

	Comment

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In the general population, isolated tricuspid regurgitation is rare. Studies using Doppler echocardiography have noted a 17% incidence in the general population [4]. When color Doppler studies are performed in normal subjects, the incidence of tricuspid regurgitation is found to be 15% to 70% [5]. Although functional causes of tricuspid regurgitation are more common, organic causes may include trauma, endocarditis, carcinoid heart disease, or rheumatic heart disease. Although the orthotopically transplanted heart usually has mild to moderate degrees of tricuspid regurgitation (probably due to the abnormal atrial anatomy), other contributory causes may include pretransplantation or posttransplantation pulmonary hypertension, right ventricular enlargement, or valvular damage incurred at the time of endomyocardial biopsy. Rees and associates [6] have reported mild tricuspid regurgitation in 29% and moderate tricuspid regurgitation in 17% of orthotopic transplant patients [6, 7]. Our 5 patients had severe degrees of tricuspid regurgitation that appears to have arisen secondary to traumatic disruption of the chordal supporting mechanism. We postulate that this occurred secondary to repeated, multiple endomyocardial biopsies used in the routine surveillance of graft rejection. In addition, damage incurred to the chordae at the time of endomyocardial biopsy may place increased stress upon the remaining chordae until they fail, resulting in a flail leaflet.

Endomyocardial biopsies were performed using the Stanford technique [8] by transplant and cardiology staff. Routine biopsies were performed every week for the first 8 weeks, every 2 weeks for the next 2 months, every 3 weeks for the following 2 months, every 4 weeks for the next 2 months, every 6 weeks for the next 2 months after that, and then every 3 months thereafter. This biopsy schedule was varied according to the presence of acute rejection. Echocardiographic examinations were performed routinely every week for the first 4 weeks, every 2 weeks for the next month, and every month thereafter.

Symptomatically, all 5 patients presented with classic signs of right-sided heart failure including progressive fatigue, lower extremity edema, hepatomegaly, and jugular venous distention. Patient data are summarized in Table 1. Interestingly, 1 patient (patient 1) presented with a paradoxic embolic event through a progressively enlarging patent foramen ovale secondary to elevated right atrial pressures and a right-to-left shunt. The onset of symptoms in these patients varied from 2 months to 64 months after transplantation, which may support the contention of acute onset of tricuspid regurgitation secondary to a traumatic event or repeated events. One such event occurred in patient 4 and was believed to be temporally related to and even induced by endomyocardial biopsy with the immediate onset of severe, symptomatic tricuspid regurgitation. Each patient also had relatively normal tricuspid valve function, documented by echocardiogram before their admissions for severe tricuspid regurgitation.

Treatment in these patients consisted of medical management for periods ranging from 0 to 40 months after the time of diagnosis. The presence of sudden, severe tricuspid regurgitation required immediate repair in 1 patient. This degree of tricuspid regurgitation was tolerated in the remaining 4 patients for varying periods of time until progressive right-sided failure ensued or a paradoxic embolus occurred.

Surgical intervention consisted of valve repair in 3 patients and valve replacement in 2. A simple repair with a Carpentier ring provided a durable repair with good results, as documented by serial echocardiograms. The De Vega repair was used in 1 patient. This provided good immediate results with resolution of symptoms but did not prove to be a durable repair, as documented by echocardiogram before the patient's death secondary to unrelated causes. A porcine valve was used in 2 patients for technical reasons and has provided good short-term results. A porcine valve would also allow future endomyocardial biopsy to be performed. It appears that this lesion can be corrected using standard techniques and good results can be obtained.

To date, severe tricuspid valve regurgitation in the transplanted heart has recently been reported as occurring rarely [9, 10]. We have presented 5 patients in whom severe, symptomatic tricuspid regurgitation developed secondary to biopsy-induced trauma after orthotopic cardiac transplantation. Alterations in endomyocardial biopsy techniques, such as the use of a long biopsy sheath as advocated by Huddleston and colleagues [10], may help prevent biopsy-induced tricuspid regurgitation.

	Addendum

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Since the submission of this article, a sixth patient with biopsy-induced severe tricuspid valve regurgitation resulting in immediate congestive heart failure required tricuspid valve replacement with a 29-mm Carpentier-Edwards valve.

	Footnotes

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Address reprint requests to Dr Karwande, Division of Cardiothoracic Surgery, University of Utah Medical Center, 50 N Medical Dr, Salt Lake City, UT 84132.

	References

Top Footnotes Abstract Introduction Case Reports Comment Addendum References

 

1. Ingermann CE, Spes CH, Tammen A, et al. Anatomic characteristics and valvular function of the transplanted heart: transthoracic versus transesophageal echocardiographic findings. J Heart Transplant 1990;9:331–8.[Medline]
2. Sarsam RA, Campbell CS, Yonan NA, et al. An alternative surgical technique in orthotopic cardiac transplantation. J Cardiovasc Surg 1993;8:344–9.
3. Cladellas M, Abadal ML, Pons-Llado G, et al. Early transient multivalvular regurgitation detected by pulsed Doppler in cardiac transplantation. Am J Cardiol 1986;58:1122–4.[Medline]
4. Choong CY, Abascal VM, Weyman J, et al. Prevalence of valvular regurgitation by Doppler echocardiology in patients with structurally normal hearts by two-dimensional echocardiography. Am Heart J 1989;117:636–42.[Medline]
5. Yoshida K, Yoshikawa J, Shakudo M, et al. Color Doppler evaluation of valvular regurgitation in normal subjects. Circulation 1988;78:840–7.[Abstract/Free Full Text]
6. Rees AP, Milani RV, Larie CJ, Smart FW, Ventura HO. Valvular regurgitation and right-sided cardiac pressures in heart transplant recipients by complete Doppler and color flow evaluation. Chest 1993;104:82–7.[Abstract/Free Full Text]
7. Johnson MR. Echocardiographic evaluation of the cardiac transplant recipient. Chest 1993;104:3–5.[Free Full Text]
8. Caves PK, Stinson EB, Billingham ME, Shumway NE. Percutaneous transvenous endomyocardial biopsy in human heart recipients: experience with a new technique. Ann Thorac Surg 1973;16:325–36.[Medline]
9. Votapka TV, Appleton RS, Pennington DG. Tricuspid valve replacement after orthotopic heart transplantation. Ann Thorac Surg 1994;57:752–4.[Abstract]
10. Huddleston CB, Rosenbloom M, Goldstein JA, Pasque MK. Biopsy-induced tricuspid regurgitation after cardiac transplantation. Ann Thorac Surg 1994;57:832–7.[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): Richard D. Stahl Shreekanth V. Karwande John A. Hawkins Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Stahl, R. D. Articles by Renlund, D. G. Search for Related Content PubMed PubMed Citation Articles by Stahl, R. D. Articles by Renlund, D. G. Related Collections Related Article