Pathophysiology and natural history of TR
The tricuspid valve apparatus consists of the annulus, the anterior (largest), septal, and posterior (or inferior) leaflets, chordae, and papillary muscles. Most of the TV annulus lies on the atrioventricular junction; thus its size depends on RV volume. Tricuspid annular dilatation and reduced coaptation of the anterior (mainly) leaflet or right ventricular (RV) dilatation and papillary muscle displacement are the main mechanisms of functional TR.
When TR develops, there is a prolonged period of progressive RV and RA volume overload that engenders additional TR until right heart failure develops. PA pressure in functional TR is >55 mmHg. RV failure with severe TR or constrictive pericarditis are possible causes of cardiac cirrhosis due to ischaemic hepatopathy.
The 1-year survival of patients with severe, moderate, or no TR is 64%, 79%, and 92%, respectively.
Moderate and severe TR increase mortality independently of PV pressure or RV function, but in a recent study RV dysfunction, but not significant TR, was independently associated with survival late after left heart valve procedure.