Tricuspid Stenosis Clinical Presentation

Updated: Sep 25, 2016
  • Author: Mary C Mancini, MD, PhD, MMM; Chief Editor: Richard A Lange, MD, MBA  more...
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Presentation

History

Fatigue, due to limited cardiac output, may be present.

Systemic venous congestion leads to abdominal discomfort and swelling. The onset is usually gradual, but it may be rapid if atrial fibrillation or flutter develops. (For related information, see Medscape's Atrial Fibrillation Resource Center).

Dyspnea may be present but is not severe unless concomitant mitral valve disease is present.

Patients may complain about prominent pulsations in the neck.

When tricuspid stenosis occurs concomitantly with mitral stenosis, the decrement of cardiac output to the pulmonary bed may paradoxically diminish the dyspnea, hemoptysis, and orthopnea typically seen with mitral stenosis.

Obtain information regarding preceding rheumatic fever, symptoms of the carcinoid syndrome, and possible congenital abnormalities.

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Physical

With sinus rhythm (more common with tricuspid stenosis than with mitral stenosis), the jugular venous pulse increases and the A wave is prominent (may be confused with an arterial pulse).

If atrial fibrillation occurs, the A wave is lost.

Peripheral edema and ascites are frequent.

Without significant mitral pathology, the patient should not be dyspneic and can probably lie flat without symptoms.

A prominent right atrium may be palpable to the right of the sternum. If not obscured by mitral stenosis sounds, a tricuspid opening snap may be heard. A diastolic murmur is audible along the left sternal border or at the xiphoid, which increases with inspiration. Often, tricuspid regurgitation is also present, represented by a holosystolic murmur in a similar location.

The first heart sound may be split widely. The second heart sound may be single. This single sound is due to the inaudible closure of the pulmonary valve from the decrease in blood flow through the stenotic tricuspid valve.

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Causes

At least 4 conditions can cause obstruction of the native tricuspid valve. These include (1) rheumatic heart disease, (2) congenital abnormalities, (3) metabolic or enzymatic abnormalities, and (4) active infective endocarditis. Note the following:

  • Rheumatic tricuspid stenosis: In this entity, diffuse thickening of the leaflets occurs, with or without fusion of the commissures. The chordae tendineae may be thickened and shortened. Calcification of the valve rarely occurs. The leaflet tissue is composed of dense collagen and elastic fibers that produce a major distortion of the normal leaflet layers.

  • Carcinoid heart disease: Carcinoid valve lesions characteristically manifest as fibrous white plaques located on the valvular and mural endocardium. The valve leaflets are thickened, rigid, and reduced in area. Fibrous tissue proliferation is present on the atrial and ventricular surfaces of the valve structure.

  • Congenital tricuspid stenosis: These lesions are observed more commonly in infants. They may manifest as incompletely developed leaflets, shortened or malformed chordae, small annuli, abnormal size and number of the papillary muscles, or any combination of these defects.

  • Infective endocarditis: Large infected vegetations obstructing the orifice of the tricuspid valve may produce stenosis. This condition is relatively uncommon, even in those who abuse intravenous drugs.

  • Unusual causes: Rare causes of tricuspid stenosis include Fabry disease and giant blood cysts.

  • Mimickers of tricuspid stenosis: Several conditions may mimic tricuspid stenosis by obstructing flow through the valve. These conditions include supravalvular obstruction from congenital diaphragms, intracardiac or extracardiac tumors, thrombosis or emboli, or large endocarditis vegetations. In addition, conditions that impair right-sided filling can produce similar symptoms and physical findings. These conditions include constrictive pericarditis and restrictive cardiomyopathy.

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