Management of tricuspid valve regurgitation

anagement of tricuspid regurgitation (TR) is becoming an increasingly difficult decisionmaking 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 al 3 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 degree of right ventricular dysfunction indicated by annular dilatation.In their experience with patients who were subjected to valvuloplasty for mitral valve regurgitation, Dreyfus et al 4 found that the tricuspid annulus was abnormally dilated in about 50% of the patients, even in the absence of TR. PHYSIOPATHOLOGY c6]7 We have shown that the initial and principal pathological process affecting the mitral valve in acute rheumatic carditis is dilatation of the annulus.In other words, the mitral annulus is abnormally weak due to rheumatic involvement. 6 8-11 It is therefore not surprising that the tricuspid annulus is similarly affected in some instances.Others have demonstrated that loss of contraction of the myocardium surrounding the annulus is the leading mechanism of TR. 12 We learnt, in fact, that so-called ''functional'' TR occurs in rheumatic heart disease only where there is severe pulmonary hypertension and the amount of regurgitation is relatively small. 3 10''Functional'' is a misleading term when used in the context of tricuspid valve disease.As with the mitral valve, annular pathology plays as important a role in causing valve malfunction as do leaflet, chordal or papillary muscle disease.Haemodynamically significant TR before rheumatic mitral valve surgery should not be regarded as functional, nor should it be anticipated that the TR will resolve after successful mitral surgery.Immediately after such surgery, the TR may appear relatively mild and easily controlled with diuretics.After months or years, however, forceful systolic waves and a pulsatile liver supervene. 6 13 TR is often a progressive condition.With the increased volume of TR, the right ventricle, as well as of course the right atrium, dilate.Eventually the right ventricular systolic function ''fails'', the diastolic pressure rises and the interventricular septum moves towards the left ventricle during diastole.This is an important example of cardiac chamber inter-relationships in which elevated pressure and expanding volume of one chamber compress, or constrain, the adjacent chamber and