Ann Thorac Surg 2003;75:1826-1828
© 2003 The Society of Thoracic Surgeons
Original article: cardiovascular
Predictors of residual tricuspid regurgitation after mitral valve surgery
Katsuhiko Matsuyama, MDa*,
Masahiko Matsumoto, MDa,
Takaaki Sugita, MDa,
Junichiro Nishizawa, MDa,
Yoshiyuki Tokuda, MDa,
Takehiko Matsuo, MDa
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
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Abstract
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BACKGROUND: Whether preoperative tricuspid regurgitation (TR) will regress or progress late after surgery is unknown. The aim of this study was to evaluate predictors of significant TR late after mitral valve surgery.
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+.
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Introduction
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Tricuspid regurgitation (TR) often accompanies mitral or aortic valve disease. This condition is functional rather than organic, and is associated with pulmonary hypertension or right ventricular dilatation [1]. Significant TR can contribute to increased morbidity and mortality, despite adequate left-sided valve correction [2]. TR may decrease gradually after surgery because repair of the left-sided valve lesions can decrease the right ventricular pressure or reduce volume overload [3]. However, in some cases, TR does not necessarily regress spontaneously after repair of the cardiac lesions [4–6]. Whether preoperative TR will regress or progress late after surgery is unknown. The fate of TR in patients undergoing mitral valve replacement (MVR) has been published previously [6]. However, the report lacked detail regarding preoperative TR, and the study population was composed of only late survivors. We retrospectively studied 174 patients to evaluate predictors of significant late TR after mitral valve surgery without tricuspid valve surgery.
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Material and methods
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Between March 1988 and September 2001, 274 patients had mitral valve surgery at our institution. Of these patients, 175 consecutive patients underwent mitral valve surgery without tricuspid valve surgery, and their records were retrospectively reviewed. Patients with concomitant procedures, such as coronary artery bypass grafting or aortic valve replacement, were excluded form this study. All patients had complete physical examinations preoperatively, with echocardiographic studies and cardiac catheterization. The preoperative and intraoperative patient characteristics are summarized in Table 1.
The amount of TR was graded conventionally 1 through 4+ as determined by echocardiography before and after operation as previously reported [7]. Preoperatively, 46 patients (26%) had 2+ TR, and 128 patients (74%) had 1+ or less TR. The decision of concomitant tricuspid valve repair in patients with 2+ TR was based on the surgeon’s inspection or direct digital exploration of the valve during surgery, whereas all patients with 3+ or more TR had tricuspid valve surgery. Three surgeons were involved during the study period. Significant postoperative TR was defined as 3+ or more TR. Preoperative pulmonary artery pressure (PAP) was measured by cardiac catheterization. Pulmonary hypertension was defined as a systolic PAP of more than 40 mm Hg. After discharge from our hospital, all echocardiographic studies were carried out every 6 months or every year by a skilled echocardiography technician. The latest echocardiographic examination was regarded as the end of the follow-up period.
The results were expressed as means ± standard deviation unless otherwise indicated. All of risk factors were analyzed using the X2 or Fischer’s exact test. Multiple analysis by forward stepwise logistic regression was used to identify predictors of TR development. A p value of less than 0.05 was considered significant.
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Results
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There was one operative death. A total of 174 patients were included in this study. MVR was undergone in 76 patients, (44%) and mitral valve repair was 92 patients (56%). MVR was performed using a St. Jude Medical prosthesis (St. Paul, MN) in all patients. The mean follow-up was 8.2 ± 3.6 years (range 1.0 to 14.5 years) after surgery. There were 14 late deaths (8%). The cause of death was sudden death in 2 patients, cardiac failure in 1 patient, brain infarction or bleeding in 3 patients, respiratory failure in 2 patients, hepatic failure in 2 patients, renal failure in 1 patient, and cancer in 3 patients. Valve-related complication included brain infarction in 4 patients (1 death), intracranial bleeding in 3 patients (1 death), and gastrointestinal bleeding in 1 patient. There were no patients requiring reoperation for significant TR during the follow-up period. Data were available for all 174 patients on both preoperative and postoperative echocardiography. Immediately after surgery there was significant TR (3+ or more) in only 4 patients (2%). However, there was significant TR in 28 patients (16%) during the follow-up period (Table 2).
Of the 46 patients with preoperative 2+ TR, TR progressed in 17 patients (37%). 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 (Table 3).
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Comment
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The surgical management of secondary TR due to left-sided heart valve lesions remains controversial. In this series, significant TR was present in 16% of patients late after MVR without tricuspid valve surgery.
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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References
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Abstract
Introduction
