Ann Thorac Surg 2004;78:1642-1643
© 2004 The Society of Thoracic Surgeons
INVITED COMMENTARY
Francis D. Pagani, MD, PhD
Section of Cardiac Surgery University of Michigan Health System 2120 Taubman Center Box 0348 1500 East Medical Center Dr Ann Arbor, MI 48109 USA
fpagani{at}umich.edu
Anderson and colleagues have provided us with a thoughtful retrospective study describing the significance of tricuspid regurgitation (TR) detected by intraoperative transesophageal echocardiography at the time of orthotopic heart transplantation in 130 patients over a 10-year period. The authors have demonstrated that mild or greater (
2+) degrees of TR were associated with poor posttransplant survival.
Obviously there are significant limitations in any retrospective study, and the authors have clearly recognized and acknowledged the areas of greatest concern. In particular, it is well known that the use of transesophageal echocardiography has limitations in accurately assessing the degree of TR and degree of right ventricular (RV) dysfunction. The ability to quantify TR is albeit, better than the ability to quantify RV dysfunction. The method of quantification of TR utilized by Anderson and colleagues is somewhat simplistic. Using the instantaneous appearance of the area of the regurgitant tricuspid valve (TV) jet can sometimes overestimate the degree of TR when the jet is not holosystolic. Conversely, when the TV jet impinges on the wall of the right atrium, a smaller jet area may be visualized, underestimating the degree of the regurgitant jet. Also, it is important to take into consideration the size of the convergence zone when quantifying TR. These limitations become most important in the group of patients with mild (2+) or moderate (3+) degrees of TR and with no evidence of RV dysfunction. Intuitively for this group, it is difficult to imagine that TR of only a mild degree (2+) in the absence of RV dysfunction would have such a profound impact on early survival. Unfortunately the number of patients in this study with isolated significant TR and no RV dysfunction was small (n = 7); therefore it is difficult to draw major assumptions from these data for this subgroup. One must speculate whether significant underestimation of the degree of TR or RV dysfunction may have occurred with this group. Thus the overall inability to accurately assess the degree of RV dysfunction may have been the reason for both TR and RV dysfunction being observed as independent predictors of mortality in the proportional hazards model, and not just RV dysfunction alone. The second, somewhat puzzling observation is the absence of an effect of mild to moderate TR on late survival (> 6 months). If this degree of TR had such a profound adverse effect on early survival, why would this adverse effect not continue into late follow-up? Again, the numbers remain small, but if this observation is accurate, one can postulate that the cause of early mortality may not have been entirely attributable to TR alone, or alternatively, the dynamics of favorable pulmonary remodeling and reduction in pulmonary resistance occurred differently in the group of survivors making the continued presence of TR less significant.
Doctor Anderson and colleagues have thoughtfully raised issues to debate regarding the importance of managing RV dysfunction and TR. That concomitant TV repair at the time of orthotopic heart transplantation may benefit and improve posttransplant RV dysfunction and survival is both intriguing and intuitive, but remains speculative on the basis of the data presented in this article. Importantly, because the overall incidence of significant TR is low in this setting, I would hope that the surgical community waits for additional future studies to determine whether the use of TV repair is appropriate to affect the natural history of TR, nicely brought to light by Anderson and colleagues.
