Tricuspid stenosis is an unusual valvular abnormality that many typically occurs in association with several other valvular lesions. For several years, surgical commissurotomy and valvuloplasty were the only accessible techniques to correct tricuspid stenosis. The evolution of balloon valvotomy techniques has revolutionized the direction of mitral stenosis. Similar techniques may be used to deal with tricuspid stenosis.

TS is nearly always as a result of rheumatic fever; tricuspid regurgitation is typically also present, as is rheumatic mitral valvulopathy (typically mitral stenosis). Uncommonly, atrial fibrillation happens.

Tricuspid stenosis results from alterations in the construction of the tricuspid valve that precipitate substandard trip of the valve leaflets. The most frequent etiology is rheumatic fever, and tricuspid valve participation happens universally with aortic and mitral valve participation. The limited valve opening hampers the flow of blood to the right ventricle and, later, to the pulmonary vasculature.

Right atrial enlargement is found as a result. The venous return leads to hepatic enlargement, reduced pulmonary blood circulation, and peripheral edema. Other uncommon reasons for tricuspid stenosis contain endomyocardial fibrosis, endocarditis, carcinoid syndrome, systemic lupus erythematosus, and congenital tricuspid atresia.

In the infrequent cases of congenital tricuspid stenosis, the valve leaflets may show various types of deformity, which could contain deformed leaflets, deformed chordae, and displacement of the whole valve gear. Other cardiac anomalies usually are present.

Symptoms and Indications

The primary observable signal is a giant flickering a wave with sluggish y descent in the jugular veins. Jugular venous distention may happen, rising with inspiration (Kussmaul signal). The face could become dusky and scalp veins may dilate when the individual is recumbent (suffusion signal). Hepatic congestion and peripheral edema might occur.

On auscultation, TS may generate a soft opening snap plus a mid-diastolic rumble with presystolic accentuation.

Findings of TS frequently coexist with those of mitral stenosis and so are much less outstanding. The murmurs could be discerned clinically (see see Discerning Murmurs of Tricuspid and Mitral StenosisTables).

Diagnosis

Echocardiography

Investigation is guessed based on history as well as physical examination and supported by Doppler echocardiography revealing a pressure gradient throughout the tricuspid valve. Vital TS is signified with a mean forward gradient throughout the valve > 5 mm Hg. Two dimensional echocardiography reveals thickened motion and decreased leaflets with RA An ECG and chest x-ray are regularly got. Liver enzymes are elevated as a result of passive hepatic congestion.

Cardiac catheterization is seldom suggested for assessment of TS. When catheterization is suggested (eg, to assess coronary physiology), findings contain elevated RA pressure having a slow drop in early diastole as well as a diastolic pressure gradient over the tricuspid valve.

Treatment

  • Diuretics and aldosterone antagonists
  • Seldom valve repair or replacing

Signs to direct treatment is rare. Patients with hepatic blockage resulting in cirrhosis or acute systemic venous blockage and attempt restriction may reap the benefits of interventions like balloon valvotomy or valve repair or replacing. Relative results are unstudied.

Vital Points

Tricuspid stenosis is typically as a result of rheumatic fever; mitral stenosis and tricuspid regurgitation are frequently additionally present.