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Tricuspid valve dysfunction and surgery after orthotopic cardiac transplantation.
European Journal of Cardio-thoracic Surgery 2000 April
OBJECTIVE: The study examines the prevalence of tricuspid regurgitation and biopsy-induced flail tricuspid leaflets after orthotopic heart transplantation and evaluates the results of the tricuspid valve surgery.
METHODS: By a computerized search of the databases 647 of 889 patients who survived heart transplantation for more than 30 days were identified for this study. The primary tool for rejection monitoring in our institution is the daily observation of intramyocardial ECG (IMEG) based on day-by-day changes of the maximal QRS complex amplitude. Endomyocardial biopsy with 45-cm-long sheath bioptome was performed only in doubtful IMEG and echocardiographic data and at times of annual routine heart catheterization. Tricuspid regurgitation was diagnosed clinically and by echocardiography as mild, moderate and severe. Eleven patients received prosthetic valve replacements (four bioprostheses and seven mechanical valves) and six patients underwent valve reconstruction. The choice of xenograft valve was dictated by the condition of renal function. Patient survival and incidence of tricuspid regurgitation and freedom from operation for severe tricuspid regurgitation were analyzed with Kaplan-Meier method.
RESULTS: The prevalence of tricuspid regurgitation was 20.1%. Mild and moderate tricuspid regurgitation was seen in 14.5 and 3.1% of the patients, respectively, who were responsive to medical therapy and remained clinically stable in NYHA class I-II. Severe tricuspid regurgitation was seen in 16 (2.5%) patients who presented signs of an acute right heart dysfunction. Tricuspid valve pathology at operation revealed biopsy-induced rupture of the Chordae tendineae at various valve segments mostly the anterior and posterior leaflets. There was one hospital death (<30 day) and five late deaths due to infection, arrhythmia and trauma and no procedural-related or directly cardiac related death. Ten patients (62.5%) are alive at a mean follow-up time of 29.9 months (range 4-81 months) and nine survivors are in NYHA class I-II and one in class III.
CONCLUSIONS: Severe tricuspid regurgitation in transplanted hearts is associated mainly with biopsy-induced injury or endocarditis. Other regimes of rejection monitoring may help to eliminate this complication. Apart from our preference of valve repair, the choice of valve substitute may be influenced by the presence or the prospect of chronic renal failure. Heart transplant patients can safely undergo valve surgery with acceptable mortality, low morbidity and excellent intermediate-term clinical results. Mild to moderate functional tricuspid regurgitation is responsive to medical therapy and non-progressive and occur in 17.6% of orthotopic transplanted hearts without having a detrimental effect on the right ventricular performance.
METHODS: By a computerized search of the databases 647 of 889 patients who survived heart transplantation for more than 30 days were identified for this study. The primary tool for rejection monitoring in our institution is the daily observation of intramyocardial ECG (IMEG) based on day-by-day changes of the maximal QRS complex amplitude. Endomyocardial biopsy with 45-cm-long sheath bioptome was performed only in doubtful IMEG and echocardiographic data and at times of annual routine heart catheterization. Tricuspid regurgitation was diagnosed clinically and by echocardiography as mild, moderate and severe. Eleven patients received prosthetic valve replacements (four bioprostheses and seven mechanical valves) and six patients underwent valve reconstruction. The choice of xenograft valve was dictated by the condition of renal function. Patient survival and incidence of tricuspid regurgitation and freedom from operation for severe tricuspid regurgitation were analyzed with Kaplan-Meier method.
RESULTS: The prevalence of tricuspid regurgitation was 20.1%. Mild and moderate tricuspid regurgitation was seen in 14.5 and 3.1% of the patients, respectively, who were responsive to medical therapy and remained clinically stable in NYHA class I-II. Severe tricuspid regurgitation was seen in 16 (2.5%) patients who presented signs of an acute right heart dysfunction. Tricuspid valve pathology at operation revealed biopsy-induced rupture of the Chordae tendineae at various valve segments mostly the anterior and posterior leaflets. There was one hospital death (<30 day) and five late deaths due to infection, arrhythmia and trauma and no procedural-related or directly cardiac related death. Ten patients (62.5%) are alive at a mean follow-up time of 29.9 months (range 4-81 months) and nine survivors are in NYHA class I-II and one in class III.
CONCLUSIONS: Severe tricuspid regurgitation in transplanted hearts is associated mainly with biopsy-induced injury or endocarditis. Other regimes of rejection monitoring may help to eliminate this complication. Apart from our preference of valve repair, the choice of valve substitute may be influenced by the presence or the prospect of chronic renal failure. Heart transplant patients can safely undergo valve surgery with acceptable mortality, low morbidity and excellent intermediate-term clinical results. Mild to moderate functional tricuspid regurgitation is responsive to medical therapy and non-progressive and occur in 17.6% of orthotopic transplanted hearts without having a detrimental effect on the right ventricular performance.
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