Tricuspid Valve Reconstructions

Abstract

The most common type of acquired tricuspid regurgitation (TR) is the so-called secondary type resulting form enlargement of the orifice, incident to congestive cardiac failure with right ventricular dilatation due to left ventricular disease. This type of TR is often functional and may vanish when the left ventricular failure and the pulmonary hypertension disappear or when the right heart failure is successfully treated [1]. It may, however, be permanent with long-standing dilatation of the right ventricle. Rheumatic disease can produce organic changes in the tricuspid valve characterized by fibrosis with contracture of the leaflets and commisural fusion; the former leads to TR, the latter to stenosis. Usually rheumatic tricuspid disease results in an incompetent valve with variable amounts of stenosis. The orifice size is larger than that in mitral stenosis, even when hemodynamically there is severe obstruction to flow, for the vis a tergo of blood reaching the right atrium is less than that of blood reaching the left atrium, and therefore the hemodynamic effects of moderate tricuspid stenosis are the equivalent of tight mitral stenosis [2].