Tricuspid stenosis pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Pathophysiology
Tricuspid stenosis is a result of structural alterations of the tricuspid valve that accelerates inadequate excursion of the valve leaflets. Rheumatic fever is the most common etiology. Tricuspid valve involvement occurs universally with mitral and aortic valve involvement. Rheumatic tricuspid stenosis results in the tricuspid valve leaflets becoming thickened and slcerotic as the chordae tendineae become shortened. This restricted valve results in an obstructed blood flow into the right ventricle, and thus, to the pulmonary vasculature. Consequently, right atrial enlargement may be present. The obstructed venous return results in hepatic enlargement, decreased pulmonary blood flow, and peripheral edema. Rarely, tricuspid stenosis may be caused by carcinoid syndrome, endocarditis, endomyocardial fibrosis, systemic lupus erythematosus, and congenital tricuspid atresia.
In the case of congenital tricuspid stenosis, many forms of valve leaflet deformity may occur, including deformed leaflets, deformed chordae, and displacement of the entire valve apparatus. Other cardiac anomalies are usually present.