Tricuspid stenosis

Tricuspid stenosis. (O Tricuspid stenosis) It is the reduction of the valve orifice, generally secondary to rheumatic fever, in this case generally accompanied by involvement of other valves (especially the mitral valve); an inflammatory process that can also affect the valve’s supporting apparatus. It can be congenital (rarely) and is not inherited (accompanying interatrial or ventricular septal defect), carcinoid syndrome, etc. It is a rare valve disease, and is more frequent in women than in men.


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  • 1 Etiology
  • 2 Pathophysiology
  • 3 Clinical picture
  • 4 Physical examination
  • 5 Complementary explorations
  • 6 Treatment
  • 7 Sources


It is a rare valve disease. In general, it is of rheumatic origin and is almost always associated with mitral stenosis . Other causes of tricuspid stenosis are carcinoid syndrome and endomyocardial fibrosis .


As in mitral stenosis , a transvalvular gradient occurs during diastole. Its magnitude is low, since cardiac output is reduced, but increases on inspiration.

Elevation of atrial pressure determines systemic venous congestion. When the patient maintains sinus rhythm, he presents giant waves in the pressure plot of the right atrium.

Although a mitral stenosis coexists, the elevation of the pulmonary pressures is slight, as a consequence of the reduction of the cardiac output, that is, there is an obstacle to the filling of the right ventricle, appearing a diastolic gradient between AD and RV that increases with inspiration .

The result is an elevation of the pressure in the AD with elevation of the wave “a” and consequently clinical symptoms of right heart failure with an increase in jugular pressure, congestive hepatomegaly, ascites, malleolar edema, etc.

Cardiac output is low at rest and does not rise with exercise, and therefore pressures in the RV, pulmonary vessels, and left chambers do not increase.

Clinical picture

In most cases, there are previous clinical signs of pulmonary congestion (due to associated mitral injury), although when tricuspid stenosis is significant, there is a discordance between the degree of dyspnea and the magnitude of the right failure: jugular engorgement, hepatomegaly, edema and ascites. Some patients also have splenomegaly and jaundice and develop a cachectic picture. The clinical manifestations of low expenditure, fatigue and muscle weakness are practically constant.

The diagnosis can be easily omitted, since auscultatory signs are attributed to associated mitral stenosis. Above all, it is necessary to look for the presence of two opening clicks, the first tricuspid (0.06 sec from the second noise) and the second mitral click, and a diastolic murmur that increases in inspiration in the xiphoid area.

Signs of pulmonary hypertension may be missing, as can the right ventricular beat. Radiologically, the dilatation of the right atrium and the superior vena cava can be seen. In patients with sinus rhythm, the ECG shows pointy P waves in leads DII and V1; in most cases, however, the underlying rhythm is atrial fibrillation.

The echocardiogram of the stenotic tricuspid valve is analogous to that of mitral stenosis and the contribution of the Doppler examination is similar. Catheterization reveals the transtricuspid diastolic gradient; above 5 mm Hg the stenosis is usually severe, corresponding to a valve area of ​​1.5 cm2 or less.

Physical exploration

There may be hepatomegaly and even splenomegaly, increased pressure of the jugular veins with a prominent “a” wave (before a prominent “a” wave in distended jugular veins, without other signs of pulmonary hypertension such as an enlarged right ventricle or 2R enhancement, think about the possibility of tricuspid stenosis) and a decreased “y” collapse, and a diastolic murmur similar to that of mitral stenosis located in the lower part of the left sternal border and in the xiphoid appendix, which increases with inspiration (sign de Rivero Carvallo) and decreases with expiration and with Valsalva; the diastolic murmur is accompanied by a 1R boost.

Complementary explorations

  • Accumulated “P” waves (pulmonary P morphology), but without RV overload data.
  • Chest x- ray . The right atrium appears enlarged, which is difficult to assess on the anteroposterior X-ray, but on the lateral it is seen occupying the retrosternal space.
  • Echocardiography . Evaluates the thickening of the tricuspid, and quantifies the gradient between AD and RV.

These are the data derived from tricuspid stenosis, but we must add the data corresponding to mitral and / or aortic valve disease that generally coexist with tricuspid valve disease.


Treatment of severe tricuspid stenosis is surgical. Open commissurotomy is usually followed by a satisfactory functional result and is always preferable to valve replacement. It is practiced in the course of the same intervention in which the mitral lesion repair is performed.

Medical treatment consists of low sodium diet and diuretics. In moderate and severe tricuspid stenosis, when a coexisting mitral valve disease is necessary, surgery is also performed on the tricuspid, generally by commissurotomy.

The time of the ET intervention is usually made to coincide with that of the MS treatment, almost always coexisting. ETs with valves less than 2 cm2 or those in which the gradient between AD and RV is greater than 5 mmHg are considered severe.

When it is necessary to implant a tricuspid valve prosthesis, it is better that it be biological, due to the high risk of thrombosis that tricuspid prostheses have. Another action on the tricuspid may be percutaneous balloon valvuloplasty.


by Abdullah Sam
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