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Letters to the Editor |
Department of Cardiovascular Surgery, German Heart Center, Clinic at the Technical University, Munich, Germany
Received 16 October 2008; accepted 20 October 2008.
* Corresponding author. Address: Klinik für Herz- und Gefäßchirurgie, Deutsches Herzzentrum, Klinik an der Technischen Universität München, Lazarettstraße 36, D-80636 München, Germany. Tel.: +49 89 1218 4111; fax: +49 89 1218 4123. (Email: Guenther{at}dhm.mhn.de).
Key Words: Tricuspid valve • Etiology • Endocarditis • Outcome
We thank Elsayed and Poullis for their interest and comments [1] on our recently published study of early and late outcome after tricuspid valve surgery [2].
The authors stress the impact of etiology of tricuspid valve (TV) disease on outcome. We agree that etiology is one of the most important factors influencing operative results. For instance, Filsoufi and colleagues in a series of 81 patients who underwent TV replacement could identify organic etiology as the only predictor of late death [3]. Traditionally, tricuspid regurgitation is classified as being either functional or organic. Functional tricuspid regurgitation secondary to left heart pathology is the major cause of TV disease [4]. Patients with functional TV disease are good candidates for TV repair and thus the incidence of functional TV disease in large series of TV reconstruction is reported to be 75% [5]. Patients with organic TV disease more frequently require valve replacement and outcomes are worse than after repair of secondary TV regurgitation.
In our study patients with congenital anomalies (e.g. Ebstein's anomaly) were excluded. A total of 205/416 (49%) patients presented with a functional tricuspid regurgitation, 100 (24%) showed an organic (mainly rheumatic) TV disease, 5 (1.2%) patients presented with cardiomyopathy, in 5 patients TV regurgitation was caused by a trauma and 22 (5%) patients showed other disorders. Functional TV regurgitation was more prevalent in the repair group as compared to the replacement group (61% vs 16%). Organic tricuspid valve disease was more prevalent in the replacement group (50% vs 15%). Because of the retrospective nature of our study we had difficulties in determining the etiology of the TV disease. In 53/416 patients (13%) we could not determine the etiology and therefore we did not want to include this parameter in the multivariate analysis.
Infective endocarditis of the tricuspid valve has been on the rise over the last decades. An increase in chronic indwelling intravenous cannulae and intravenous drug abuse have contributed to this increase. The reported incidence ranges from 2% to 10%. In our study 26 (6%) patients had a history of endocarditis.
Twenty-three patients underwent TV repair. The other three patients underwent valve replacement, two with a mechanical and one with a biological prosthesis. Only 8 out of 26 patients presented with an acute endocarditis (diagnosed within 3 months prior to surgery). The predominant cause was infection of a pacing lead. Only one patient had a history of intravenous drug abuse. None of these patients with acute endocarditis died within 30 days postoperatively.
Tricuspid valve excision without insertion of prosthesis has been used to control infection. This technique has never been used in our hospital. Our preference has been to repair the valve whenever possible. If valve replacement is required we prefer a biological prosthesis.
References
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