Surgical assessment of tricuspid valve replacement for severe tricuspid regurgitation without stenosis

Ann Thorac Cardiovasc Surg. 1999 Oct;5(5):300-3.

Abstract

Eight patients undergoing tricuspid valve replacement (TVR) for severe tricuspid regurgitation (TR) without stenosis were subjected to the study. Four patients had primary TR due to trauma, infective endocarditis, or Ebstein's anomaly, and the other 4 had secondary TR associated with mitral valve lesions. The right heart pressure as well as clinical manifestations due to right heart failure showed deteriorated values in both the primary and secondary TR groups, though pulmonary arterial pressure was higher in the latter group. In 2 patients, initial annuloplasty procedures could not reduce TR sufficiently and were instantly abandoned for TVR. These 2 patients, one with congenital and one with secondary TR, died of intractable right heart failure early postoperatively, while the remaining 6 patients are alive to date, in the New York Heart Association (NYHA) functional class I, during the follow-up period of 6-192 (mean, 104) months. The 2 patients who died had shown a longer morbid duration and a lower preoperative right ventricular systolic function indicated by stroke work to pulmonary artery resistance. This paper might suggest that an earlier surgical intervention in severe TR is recommended before the right ventricular function deteriorates.

Publication types

  • Clinical Trial

MeSH terms

  • Adolescent
  • Adult
  • Aged
  • Echocardiography
  • Evaluation Studies as Topic
  • Female
  • Follow-Up Studies
  • Heart Valve Prosthesis*
  • Humans
  • Male
  • Middle Aged
  • Severity of Illness Index
  • Survival Rate
  • Time Factors
  • Treatment Outcome
  • Tricuspid Valve / diagnostic imaging
  • Tricuspid Valve / surgery
  • Tricuspid Valve Insufficiency / diagnostic imaging
  • Tricuspid Valve Insufficiency / mortality
  • Tricuspid Valve Insufficiency / surgery*
  • Ventricular Dysfunction, Right / etiology
  • Ventricular Dysfunction, Right / physiopathology*