Tricuspid Regurgitation

Background

Tricuspid regurgitation may result from structural alterations of any one or all of the components of the tricuspid valve apparatus. Components include the leaflets, chordae tendinea, annulus, and papillary muscles or adjacent right ventricular (RV) muscle. The lesion may be classified as primary when it is caused by an intrinsic abnormality of the valve apparatus or as secondary when it is caused by RV dilatation.

NextPathophysiology

The pathophysiology of tricuspid regurgitation focuses on the structural incompetence of the valve. The incompetent nature of the valve can result from primary structural abnormalities of the leaflets and chordae or from secondary myocardial dysfunction and dilatation.[1]

Tricuspid valve insufficiency due to leaflet abnormalities may be secondary to endocarditis or rheumatic heart disease. When due to the latter, it generally occurs in combination with tricuspid stenosis. Ebstein anomaly is the most common congenital form of tricuspid regurgitation.

In tricuspid regurgitation, chronic RV volume overload results in right-sided congestive heart failure (CHF) manifested by hepatic congestion, peripheral edema, and ascites.

With inspiration, the severity of tricuspid regurgitation increases, which is due to inspiratory-induced widening of the RV, which results in enlargement of the tricuspid valve annulus and an increase in the effective regurgitant orifice area.[2]

PreviousNextEpidemiologyFrequencyUnited States

Incidence of tricuspid regurgitation appears to be 0.9%.

International

Incidence of tricuspid regurgitation appears to be less than 1%.

Mortality/Morbidity

The morbidity and mortality of the disease process are secondary to the underlying cause. In rheumatic disease, mortality rates with treatment are less than 3%. In Ebstein anomaly, mortality depends upon the severity of the valvular deformity and the feasibility of correction. Mortality rates with correction are approximately 10%. Tricuspid regurgitation resulting from myocardial dysfunction or dilatation has a mortality of up to 50% at 5 years.

Race

No race predilection is apparent.

Sex

No sex predilection is apparent.

Age

Ebstein anomaly can be detected at birth and during early childhood. In patients older than 15 years, the most common form of tricuspid regurgitation is rheumatic valvular disease. In the adult population, other predisposing factors, including carcinoid, bacterial endocarditis, and CHF, takes precedence.

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