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The Journal of Thoracic and Cardiovascular Surgery, Vol 94, 488-497, Copyright © 1987 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association

ARTICLES

Tricuspid regurgitation in patients with acquired, chronic, pure mitral regurgitation. II. Nonoperative management, tricuspid valve annuloplasty, and tricuspid valve replacement

SR Cohen, JE Sell, CL McIntosh and RE Clark
Department of Surgery, Dartmouth-Hitchock Medical Center, Hanover, N.H.

The incidence, preoperative and intraoperative diagnosis, methods, and the clinical and hemodynamic features of patients with and without tricuspid regurgitation associated with chronic mitral regurgitation were presented in Part I. This study (Part II) compares the early and late results in patients with chronic, pure mitral regurgitation undergoing isolated mitral valve replacement, mitral replacement and tricuspid valve annuloplasty, and mitral and tricuspid valve replacement. The mean follow-up interval was 6 years. Those with the longest duration of symptoms (18 years) required tricuspid and mitral valve replacement (11 patients), whereas those with the shortest duration (8.1 years) had only mitral replacement (22 patients). Eight patients had minimal tricuspid regurgitation by digital palpitation, with no procedure performed, and six had tricuspid valve annuloplasty, only one of whom received a ring support. Operative mortality rate was similar in all groups (13% to 18%). All but two of the surviving patients improved by at least one New York Heart Association functional class, and no statistically significant differences were found between preoperative and postoperative hemodynamic data. There were no statistically significant differences in survival at 1, 5, or 8 years (85%, 70%, and 60%, respectively) for patients with or without TR. Only two of the surviving five patients who underwent tricuspid valve annuloplasty were alive 3 years after operation, whereas 70% to 80% of those with mitral replacement or mitral and tricuspid replacement were alive after the same time interval. It is not clear whether or not the pathogenesis of tricuspid regurgitation resulting from mitral regurgitation is different from that of tricuspid regurgitation resulting from mitral stenosis. It is our contention that whether tricuspid regurgitation arises because of anatomic destruction of the tricuspid valve or because of right ventricular dilatation with tricuspid annular enlargement, the underlying mitral valve lesion may determine the preoperative and postoperative courses of these patients. Therefore, when tricuspid valve disease is being evaluated, we urge that patients be categorized by the nature of their underlying mitral or aortic valve lesions.

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