OVERVIEW
Tricuspid valve insufficiency can be relative or organic. In the relative case, the valve itself is not diseased, but the right ventricle is hypertrophied and the atrioventricular annulus is dilated accordingly, causing poor alignment of the tricuspid valve leaflets and resulting in closure insufficiency. Patients with severe rheumatic heart disease with mitral stenosis or insufficiency are often associated with relative tricuspid insufficiency. Organic tricuspid insufficiency is a sequela of rheumatic fever and is rare clinically, mostly associated with both mitral and aortic valve pathology. Pathologic changes are thickening and coiling of valve fibers, shortening of the tendon cords, enlargement of the annulus, and failure of the valves to fully align during cardiac contraction. Often there is fusion of the valve junctions, resulting in both stenosis and stenosis.
Etiology
Acquired simple tricuspid insufficiency can occur in carcinoid syndrome, as carcinoid plaque often deposits on the ventricular surface of the tricuspid valve and adheres the valve cusp to the wall of the right ventricle, causing tricuspid insufficiency, and in most cases, this type of patient has concomitant pulmonary valvular disease. Tricuspid valve insufficiency is often accompanied by obvious enlargement of the right heart.
Symptoms
The pathophysiology of tricuspid valve insufficiency is the result of tricuspid regurgitation, i.e., systolic blood flow from the right ventricle back into the right atrium, resulting in a high degree of enlargement of the right atrium, elevated pressures, and impaired venous blood return. Due to the increased load on the right ventricle, compensated and hypertrophied, right heart failure is prone to occur.
Symptoms and signs of tricuspid valve insufficiency are related to the degree of valve closure insufficiency. Mild insufficiency is not easy to detect clinically. In more severe cases, there may be fatigue, poor appetite, liver distension, abdominal distension and lower limb edema.
Typical signs: jugular venous distention with pulsation; large and palpable liver; and a systolic wind-blowing murmur in the fourth intercostal space at the left sternal border, which increases at the end of deep inspiration. Typical signs can be absent in patients with severe tricuspid regurgitation. Carvallo’s sign may be negative if the liver is sclerotic due to prolonged bruising and is no longer pulsatile, and the murmur is no longer enhanced with inspiration after volume loading of the right heart has reached an extreme point.
Examination
There are the following examination methods for this disease:
1. X-ray examination
Photographs show hypertrophy of the right atrium and right ventricle, with bulging of the right edge of the heart, along with changes caused by other valvular lesions.
2. Electrocardiography
It shows atrial hypertrophy, high and wide P wave; and right bundle branch block or right ventricular hypertrophy, even myocardial strain. Atrial fibrillation is often present.
3. Echocardiography and Doppler examination
Cross-sectional ultrasound can detect the size of the tricuspid annulus, understand the thickening of the valve, and help to distinguish relative and organic lesions. In the case of tricuspid valve insufficiency, microbubbles can be seen traveling to and from the tricuspid valve by echocardiography; Doppler can directly monitor the abnormal signals from the right ventricle to the right atrium and can estimate the degree of regurgitation.
4. Cardiac catheterization
The right atrial pressure waveform is characterized by a prominent V wave and a steepening of the y descending branch, which is more pronounced during inspiration. The right atrial pressure waveform is similar to the right ventricular pressure waveform, only the amplitude is smaller, which is called right ventriculization of right atrial pressure, and is the manifestation of severe tricuspid regurgitation.
5. Cardiovascular angiography
Right ventriculography and right anterior oblique cinematography can show tricuspid regurgitation and its degree. However, there are potential false positives due to cardiac catheterization across the tricuspid valve.
Diagnosis
The diagnosis of tricuspid valve insufficiency should include knowledge of the degree of closure. Typical clinical signs are valuable in the diagnosis of severe tricuspid valve closure insufficiency. In the past, right ventriculography was used as a means of diagnosing suspicious cases and estimating the degree of regurgitation. In recent years, ultrasound and Doppler have gradually replaced invasive testing.
Treatment
In mild cases of relative tricuspid valve insufficiency, after correction of the primary other valvular lesions and after a period of recovery, the degree of insufficiency is mostly reduced or even disappears due to the decrease in right ventricular pressure and the shrinkage of the right heart. However, in some patients with severe rheumatic heart disease, hemodynamic disturbances caused by tricuspid regurgitation in the postoperative days are one of the factors contributing to low cardiac output and, consequently, to surgical death. Other patients with pulmonary arterial hypertension do not get the expected results and have prolonged postoperative right heart failure. Therefore, in recent years, it has been advocated that for tricuspid valve insufficiency of moderate degree or above, tricuspid annuloplasty should be performed at the same time after the completion of the other valve surgery, in order to obtain more satisfactory results.
Organic tricuspid valve insufficiency requires surgical treatment; for mild lesions, the fused junction can be incised under direct vision and then annuloplasty can be performed; for more severe lesions, valve replacement should be performed.