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Tricuspid Stenosis

It is rare disease, with rheumatic etiology seen in 90 per cent of cases. In patients with rheumatic mitral stenosis only 3-5 per cent have concomitant tricuspid stenosis. Milder degrees of organic tricuspid valve involvement, up to 15-30 per cent are noted in autopsy series and in echocardiogram. Also tricuspid stenosis progresses much more slowly and develops clinical features on an average a decade later than mitral stenosis.Unusual causes of tricuspid stenosis include carcinoid disease, congenital anomalies, infective endocarditis, Whipple’s Disease and right atrial myxoma.

Pathophysiology
Obstruction to the tricuspid valve results in increased right atrial pressures, systemic venous congestion with right heart failure and low cardiac output state.

Clinical Findings
Since tricuspid stenosis, which is most often rheumatic, coexist with mitral stenosis, it is difficult to differentiate symptoms of one disease from other. In general, patient will have complaints of dyspnoea, fatigue and peripheral edema. Jugular venous pressure is characterized by prominent “a” wave and slow “y” descent in sinus rhythm. Absence of ‘y’ trough is noted in atrial fibrillation. Diastolic murmur generated across tricuspid valve has a distinct crescendo-decrescendo shape–a finding accentuated in 1 o heart block. It is typically located at lower left sternal border and increases with inspiration. Tricuspid opening snap is difficult to appreciate.

ECG

AF is seen 50 per cent of cases. Right Atrial enlargement is obvious in those with sinus rhythm.Conduction abnormalities like 1 0 heart block may be obvious.

Chest X-ray

Chest X-ray shows prominent right atrium and inconspicuous pulmonary artery.Echocardiography Findings are subtle. One should carefully search for organic tricuspid valve involvement in all rheumatic heart disease patients. Findings include thickened tricuspid valve leaflets with doming motion, commissural fusion and chordal thickening.2D echo helps in determining the etiology and nature of tricuspid valve involvement. Doppler findings are very helpful. Normal velocities across tricuspid valve are less than 1m/sec with a
mean gradient of less than 2 mmHg. Tricuspid stenosis is considered significant when mean  gradient is > 7 mmHg or PHT is > 190 ms. It is better to measure at held expiration to avoid respiratory variation. Accurate Doppler evaluation excludes the need for cardiac catheterization.

Hemodynamic Measurements
Unless one suspects it clinically and echocardiographically, and plans the hemodynamic study—diagnosis of tricuspid stenosis is easily missed at routine catheterization. Prominent ‘a’ wave in right atrial pressure trace in a patient with sinus rhythm should make one suspect tricuspid stenosis. Pull back gradient especially in a patient with atrial fibrillation can easily miss the gradient. One should place two catheters simultaneously in RA and RV and measure the diastolic gradient. These small gradients can be exaggerated by exercise.

Management

Medical therapy is ineffective. With diuretics, symptoms of congestion are replaced by that of low cardiac output state. Occasional cases of balloon tricuspid valvuloplasty are reported. Since tricuspid stenosis is often accompanied by regurgitation and mitral valve disease simultaneous surgical correction with comissurotomy and tricuspid annuloplasty is performed. When tricuspid valve is destroyed badly, tricuspid valve replacement may be needed. In general it is avoided in view of poor long term results. Unrecognized and uncorrected rheumatic tricuspid stenosis can have deleterious effects on the results of mitral and aortic surgery. It is worth repeating that 10 per cent of patients with mitral valve disease and up to 50 per cent of patients with combined mitral and aortic valve disease have associated organic tricuspid valve disease. A diligent echocardiography examination avoids major post operative embarrassment.

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