Tricuspid Stenosis
Etiology-
Generally rheumatic in origin
Females more than in males
Usually associated with Mitral Stenosis
Clinicallly evident Tricuspid Stenosis occurs in 5-10% of cases
Rheumatic Tricuspid Stenosis is commonly associated with some degree of Tricuspid Regurgitation
Nonrheumatic causes of TS are rare.
Pathophysiology
A diastolic pressure gradient between the Right Atrium and Right Ventricle defines Tricuspid Stenosis.
A mean diastolic pressure gradient of 4 mmHg is usually sufficient to elevate the mean RA pressure to levels that result in systemic venous congestion.
This results in a reduced cardiac output, which is restored towards normal when the right atrial pressure increases.
The elevated Right Atrial preassure and Systemic venous congestion gives the clinical features of Tricuspid Stenosis
Clinical Features
Symptoms-
Since the development of MS generally precedes that of TS, many patients initially have symptoms of pulmonary congestion.
Spontaneous improvement of these symptoms should raise the possibility that TS may be developing.
Fatigue secondary to low cardiac output.
Discomfort due to edema, ascitis and hepatomegaly.
Signs-
The jugular veins are ditended. In cases of sinus rhythm (i.e. in absence of atrial fibrillation and other arrhythmias) there is prominent a wave and a slow y descent.
Mid-diastolic murmur- usually best heard at the lower left sternal border. Augmented during inspiration and reduced during expiration.
Features of right heart failure- hepatic congestion (hepatomegaly), ascitis and bilateral pitting edema.
Investigations
The ECG features of RA enlargement include tall, peaked P waves in lead II, as well as prominent, upright P waves in lead V1.
The chest x-ray in patients with combined TS and MS shows particular prominence of the RA and superior vena cava without much enlargement of the PA and with less evidence of pulmonary vascular congestion than occurs in patients with isolated MS.
On echocardiographic examination, the tricuspid valve is usually thickened and domes in diastole.
The transvalvular gradient can be estimated by Doppler echocardiography.
Management
Medical management consists of diuretic therapy and salt restriction. Specially during preoperative period.
Tricuspid valvotomy is occasionally possible, but tricuspid valve replacement is often necessary.
Other valves usually also need replacement because tricuspid valve stenosis is rarely an isolated lesion.
Tricuspid Regurgitation
Etiology-
Primary- Rheumatic heart disease
Endocarditis, particularly in IV drug abusers
Ebstein’s congenital anomaly
Secondary- Right ventricular dilatation due to chronic heart failure.
Right ventricular infraction
Pulmonary Hypertension (eg. Cor pulmonale)
Clinical Features
Symptoms-
Nonspecific related to reduced forward flow like tiredness.
Signs-
Features of systemic venous congestion. Ascitis, bilateral pitting edema, hepatic enlargement and raised JVP.
JVP- systolic wave a cv wave replacing normal x descent.
A pansystolic murmur at the left sternal edge.
Investigations
ECG- right axis deviation
Chest X-ray- right ventricular enlargement
Echo- reveals dilated right ventricles, thickened tricuspid valve of Rheumatic origin, Endocarditis vegetation and Ebstein anomaly.
Management
Often improves when the cause of right ventricular overload is corrected. Eg. Diuretics and vasodilator treatment of CCF.
Patient with normal pulmonary artery pressure tolerate isolated tricuspid reflux well so the valve replavement is not always necessary.
Annuloplasty ring- with marked dilatation of tricuspid annulus
Tricuspid valve replacement in rheumatic damage.
