Author + information
- Steven F. Bolling, MD∗ ()
- ↵∗Reprint requests and correspondence:
Dr. Steven F. Bolling, Cardiac Surgery, University of Michigan, 1500 East Medical Center Drive, 2120 TC/0348, Ann Arbor, Michigan 48109-0348.
In this issue of the Journal, Kammerlander et al. (1), from Austria, describe an observational study of 539 patients with previous left-sided heart valve surgery. The majority underwent aortic, not mitral, valve procedures and were followed for a mean of 53 months to assess the impact of tricuspid regurgitation (TR) on their outcome. Significant TR, defined as moderate or severe, was present in 17% of these patients post-operatively. As opposed to patients who did not have or develop TR, those who did presented an entirely different demographic; they had more mitral and tricuspid surgery, a greater likelihood of having symptomatic heart failure, worse kidney function, a higher rate of atrial fibrillation, and poor right ventricular (RV) systolic function. Overall Kaplan-Meier survival by univariate analysis was significantly worse (p < 0.001) in patients with TR; 36% of patients with TR died as opposed to only 19% of patients without TR.
However, by multivariable Cox analysis, only RV function, age, left atrial size, diabetes, and redo status were significantly associated with mortality, not TR. Tricuspid regurgitation, per se, was not an “independent” influence on late mortality. The authors conclude that RV dysfunction, not TR, is associated with worsened survival after left heart surgery. They also surmise that surgery for late TR following left heart surgery may not be beneficial and comment that studies are needed to define who would benefit from late redo surgery for TR.
There are significant limitations to this study. It was a single-center observational study, with no data on rehospitalization for heart failure and quality of life. Additionally, echo data appear to be incomplete as to the timing, appearance, and degree of TR, and echo determination of “right ventricular dysfunction” in the presence of significant TR is clearly difficult to assess. Furthermore, right heart catheterization and hemodynamic data were unavailable in these patients. Additionally, those who developed TR had very different underlying pathology (aortic vs. mitral), implying differing left ventricular geometry, size, etc. Finally, as with all statistical analyses, uncountable variables may exert great influence. Nevertheless, the authors concluded that TR is not “independently associated with survival late after left heart valve surgery” (1).
The finding that late TR may be independently innocuous or noninfluential appears somewhat contradictory to previous findings regarding TR. The seminal paper by Nath et al. (2), published in JACC in 2004, showed that both moderate and severe TR, at any time, increased mortality independent of pulmonary pressures or of left or right ventricular size and function. This study encompassed more than 5,200 patients followed for >5 years. Recently, researchers at the University of Pennsylvania again confirmed the adverse impact of late TR (3). Their 12-year follow-up study showed a 4-fold increase in late mortality when patients were left with significant TR following mitral surgery.
The clinical approach to TR has been influenced by numerous studies, notably from Dreyfus et al. (4). They randomized 311 patients undergoing left-sided mitral valve surgery to either tricuspid annuloplasty or no tricuspid annuloplasty based on a tricuspid valve annular diameter greater than twice the normal size (>70 mm) regardless of the grade of regurgitation. At 2 years following the surgery, return of significant “moderate-to-severe tricuspid regurgitation” was 2% in those who had tricuspid annuloplasty versus almost 50% for those who did not. There was an adverse mortality impact of late TR, which showed that despite a good mitral result, TR does not go away or get better over time. Other authors have reported that annuloplasty in the presence of tricuspid annular dilation can stabilize TR grade, prevent an increase in RV size, and favorably impact mortality (5–7). Conversely, Bernal et al. (8) showed 35% 30-day mortality for redo isolated tricuspid annuloplasty for late TR.
Additionally, the relationship between RVr function and TR is complex and intertwined. Yiu et al. (9) showed in TR patients, who subsequently underwent tricuspid valve annuloplasty during left heart valve surgery, RV geometry, RV size, and TR were independently associated with adverse events. Furthermore, Mukherjee and colleagues (10) demonstrated experimentally that the RV gets better when isolated RV is corrected. Recently, 2 large clinical reviews by Desai et al. (11) and by Betrand et al. (12) confirmed this and showed that RV geometry and function improve after tricuspid valve repair at the time of left-sided valve surgery. These findings provided the basis of the Class IIa recommendation in the most recent European Society of Cardiology/European Association of CardioThoracic Surgeons (13) and American College of Cardiology/American Heart Association (14) guidelines suggesting tricuspid annuloplasty at the time of left-sided surgery with any degree of TR or “prophylactically” with tricuspid annular diameter >40 mm.
So how does one interpret the conclusion, in this observational study, that TR is not an independent predictor of mortality? It may be that the interactions among TR, the RV, pulmonary hypertension, and the left ventricle is far too complex for this analysis. Furthermore, physiological and demographic differences between the TR and no TR groups may have been far too extensive to meaningfully “match” or overcome in any mathematical or statistical way.
Although statistically following a multivariable Cox analysis, TR was not “independently” shown to be a predictor of mortality, logically we should not conclude that late TR does not matter or has no influence on outcome after left-sided heart surgery. Significant TR does not appear to be benign at any time, and it probably does matter. Clearly a randomized, controlled trial of correction of TR/tricuspid annular dilation may be needed to definitively answer the question of whether TR is independently associated with late mortality after left heart surgery.
↵∗ Editorials published in the Journal of the American College of Cardiology reflect the views of the authors and do not necessarily represent the views of JACC or the American College of Cardiology.
Dr. Bolling has reported that he has no relationships relevant to the contents of this paper to disclose.
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