Tricuspid stenosis pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Tricuspid stenosis is characterized by structural changes in the tricuspid valve. The pathophysiology of tricuspid valve depends on the underlying etiology. In rheumatic heart disease, the most common cause of tricuspid stenosis, there is diffuse thickening of the leaflets and chordae tendinae as well as fusion of the commissures.

Pathophysiology

The pathophysiology of tricuspid valve depends on the underlying etiology.

• Rheumatic tricuspid stenosis:
  • Diffuse thickening of the leaflets occur. Fusion of the commissures may or may not occur.
  • Chordae tendineae may become thickened and shortened.
  • As a result of the dense collagen and elastic fibers that make up leaflet tissue, the normal leaflet layers become significantly distorted.
• Carcinoid heart disease:
  • Fibrous white plaques located on the valvular and mural endocardium are characteristic presentations of carcinoid valve lesions.
  • Valve leaflets become thick, rigid and smaller in area.
  • Atrial and ventricular surfaces of the valve structure contain fibrous tissue proliferation.
• Congenital tricuspid stenosis:
  • More common in infants
  • Lesions may present in a number of different ways, either singularly or in any combination of the following:
    • Incompletely developed leaflets
    • Shortened or malformed chordae
    • Small annuli
    • Papillary muscles of abnormal size and number
• Infective endocarditis:
  • Stenosis may develop as a result of large infected vegetations obstructing the opening of the tricuspid valve.
• Other conditions may mimic tricuspid stenosis by the mechanical obstruction of flow through the tricuspid valve:
  • Supravalvular obstruction from congenital diaphragms
  • Intracardiac or extracardiac tumors
  • Thrombosis or emboli
  • Large endocarditis vegetations
  • Other conditions that impair right-sided filling
    • Constrictive pericarditis
    • Restrictive cardiomyopathy