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Management of tricuspid regurgitation (TR) is becoming an increasingly difficult decision-making problem. TR occurs in 8–35% of patients, especially in association with acquired left heart valve disease of rheumatic origin, primary isolated TR being very rare. It is more frequently found in association with mitral rather than with aortic valve disease, and is much rarer in degenerative disease. In the majority of patients (70–85%), the TR is said to be “functional”, caused by dilatation of the annulus as a result of increased pulmonary and right ventricular pressure; in the remaining 15–30% of the cases it may be organic and related to direct involvement of the tricuspid valve by the rheumatic disease.1,2 Whichever type, TR has a significant impact on the clinical condition and the medium and long-term prognosis of the patients. Hence, it requires special consideration during mitral and/or aortic valve surgery and thereafter.
In 1967, Brawnwald et al3 advised a conservative (no touch) approach to TR. Indeed, it was thought that appropriate correction of the left-sided valve disease would most probably result in a decrease or even abolition of the so-called functional TR. However, experience has shown that TR does not always disappear, and may increase, especially when the mitral and/or aortic valve disease is not completely or adequately resolved during surgery, as happens sometimes in cases with less than perfect correction of mitral regurgitation or stenosis. Furthermore, isolated severe TR is now increasingly observed in patients with normal left heart valve function after either mitral valve annuloplasty or replacement. The true incidence of secondary TR is not well known, but it has led some to question the functional nature of TR, accompanying left-sided valve disease.
Even moderate TR observed during surgery of left heart valves may not regress spontaneously, especially when there is already a …
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