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Ann Thorac Surg 2003;75:1826-1828
© 2003 The Society of Thoracic Surgeons
a Department of Cardiovascular Surgery, Tenri Hospital, Tenri, Nara, Japan
Accepted for publication December 31, 2002.
* Address reprint requests to Dr Matsuyama, Department of Cardiovascular Surgery, Tenri Hospital, 200 Mishima, Tenri, Nara, 632-8552 Japan
e-mail: k-matsuy{at}f3.dion.ne.jp
| Abstract |
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METHODS: A retrospective analysis was performed on a total of 174 patients who underwent mitral valve surgery without tricuspid valve surgery. Preoperatively, 46 patients (26%) had 2+ TR, and 128 patients (74%) had 1+ or less TR. Postoperative 3+ TR was considered significant TR. Variables were used to evaluate predictors of TR development by univariate or multivariate analysis.
RESULTS: The mean follow-up was 8.2 years (range 1.0 to 14.5 years) after surgery. There was progressive TR (3+ or more) in 28 patients (16%) during the follow-up period. In univariate analysis, atrial fibrillation, rheumatic etiology, huge left atrium, left ventricular dysfunction, and preoperative 2+ TR were significant risk factors for TR development. Multivariate analysis identified preoperative 2+ TR, atrial fibrillation, and huge left atrium as statistically significant predictors for late TR after surgery.
CONCLUSIONS: Aggressive repair of accompanying TR should be undertaken at the time of initial surgery in patients with huge left atrium or atrial fibrillation, even if preoperative TR is 2+.
| Introduction |
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| Material and methods |
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| Results |
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| Comment |
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Several mechanisms may be responsible for the high prevalence of late TR. First, persistent pressure overload due to pulmonary hypertension may contribute to TR progression [8]. However, a recent report demonstrated that preoperative pulmonary hypertension was not a risk factor for residual TR [6]. In this study, 17% patients without preoperative pulmonary hypertension had progressive TR, whereas TR developed in 13% patients with pulmonary hypertension. Preoperative pulmonary hypertension failed to be a significant risk factor for late TR. Second, TR may be caused by right ventricular dysfunction and tricuspid annular dilatation [9], although these factors were not assessed in the present study. Right ventricular dysfunction and tricuspid annular dilatation are irreversible and do not regress despite successful MVR [10]. A recent report has indicated that an enlarged tricuspid annulus with decreased systolic reduction in annular size is associated with a poor prognosis [9]. Although intraoperative inspection or palpation of the tricuspid valve by surgeons has been the most widely used methods to assess the need for tricuspid repair, tricuspid annulus function or annulus diameter could be important as an indication for tricuspid valve repair [9, 11].
Atrial fibrillation has been reported to be associated with right atrial size [12]. In this series, atrial fibrillation was a risk factor for late TR, which was probably caused by tricuspid annulus dilatation. Another possible mechanism of late TR includes the postoperative increase in cardiac output, which may stop the regression of tricuspid annular dilatation [6]. A huge left atrium, which was probably associated with atrial fibrillation, was an independent predictor for TR development in this study. Long-standing volume or pressure overload to the left ventricle may contribute to the enlarged left atrium, although left ventricular dysfunction failed to be a risk factor for late TR by multivariate analysis.
Preoperative 2+ TR was the most significant risk factor. As our policy, if tricuspid annulus dilatation was judged intraoperatively to be mild, even with 2+ TR, the tricuspid lesion was left alone with the expectation of a reduction in right ventricular overload after surgery. However, preoperative 2+ TR progressed in 37% patients late after surgery. This TR progression may be strongly associated with irreversible right ventricular dysfunction, which was present before surgery.
There are several limitations of this retrospective study. First, the function of the right ventricle and tricuspid annular size were not assessed. Further studies should be carried out regarding the relationship between the occurrence of late TR and right ventricular dysfunction or tricuspid annulus dilatation. Second, the present study had a relatively small number of patients to accurately evaluate predictors. Third, preoperative mitral valve lesions were variable including nonrheumatic disease, although mitral valve etiology failed to be a significant risk factor by multivariate analysis. Rheumatic disease may have relatively long duration effects on the volume or pressure overload to the right ventricle. Fourth, the follow-up period ranged from 1.0 to 14.5 years. For patients with short follow-up period, the study duration can be too short to find TR regression or progression.
In conclusion, the development of late TR is an important complication of MVR. Tricuspid valve repair itself, described by De Vega [13] or by using a ring, is a simple, short, and relatively inexpensive procedure with few complications. Aggressive repair of accompanying TR should be undertaken at the time of initial surgery in patients with a huge left atrium or atrial fibrillation, even if preoperative TR is 2+.
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