Tricuspid regurgitation (TR), also called tricuspid insufficiency, is a type of valvular heart disease in which the tricuspid valve of the heart, located between the right atrium and right ventricle, does not close completely when the right ventricle contracts (systole). TR allows the blood to flow backwards from the right ventricle to the right atrium, which increases the volume and pressure of the blood both in the right atrium and the right ventricle, which may increase central venous volume and pressure if the backward flow is sufficiently severe. The causes of TR are divided into hereditary and acquired; and also primary and secondary. Primary TR refers to a defect solely in the tricuspid valve, such as infective endocarditis; secondary TR refers to a defect in the valve as a consequence of some other pathology, such as left ventricular failure or pulmonary hypertension. The mechanism of TR is either a dilatation of the base (annulus) of the valve due to right ventricular dilatation, which results in the three leaflets being too far apart to reach one another; or an abnormality of one or more of the three leaflets.
Signs and symptoms The symptoms of TR depend on its severity. Severe TR causes right-sided heart failure, with the development of ascites and peripheral edema. In severe cases of right heart failure due to TR, venous congestion of the kidneys and liver may lead to cardiorenal syndrome (kidney failure secondary to heart failure) and cardiohepatic syndromes (liver failure secondary to heart failure) respectively. Venous congestion from TR and right heart failure may also lead to anasarca (diffuse swelling) and decreased intestinal absorption due to the swelling surrounding the intestines, in severe cases this may lead to cachexia and malnutrition. A pansystolic heart murmur may be heard on auscultation of the chest. The murmur is usually of low frequency and best heard on the lower left sternal border. It increases with inspiration, and decreases with expiration: this is known as Carvallo's sign. However, the murmur may be inaudible due to the relatively low pressures in the right side of the heart. A third heart sound may also be present, also heard at the lower sternal border, and increasing in intensity with inspiration. On examination of the neck, there may be giant C-V waves in the jugular pulse. With severe TR, there may be an enlarged liver detected on palpation of the right upper quadrant of the abdomen; the liver may be pulsatile on palpation and even on inspection.
Causes The causes of TR may be classified as congenital or acquired; another classification divides the causes into primary or secondary. Congenital abnormalities are much less common than acquired. The most common acquired TR is due to right ventricular dilatation. Such dilatation is most often due left heart failure or pulmonary hypertension. Other causes of right ventricular dilatation include right ventricular infarction, inferior myocardial infarction, and cor pulmonale. In regards to primary and secondary causes they are:
Mechanism In terms of the mechanism of tricuspid insufficiency, it involves the expansion of the tricuspid annulus (fibrous rings of heart). Tricuspid insufficiency is linked to geometric changes of the tricuspid annulus (decreased tricuspid annular release). The leaflets shape are normal but prevented from normal working mechanism due to a distortion of spatial relationships of leaflets and chords. It is also contemplated that the process via which tricuspid regurgitation emerges, is a decrease of contraction of the myocardium around the annulus.
Diagnosis The diagnosis of TR may be suspected if the typical murmur of TR is heard or other signs suggestive of right heart failure. Definitive diagnosis is made by echocardiogram, which is capable of measuring both the presence and the severity of the TR, as well as right ventricular dimensions and systolic pressures. Cardiac MRI or CT scan may also aid in the diagnosis of TR. On imaging studies, a regurgitant volume greater than 45 milliliters or greater than 50% regurgitation across the tricuspid valve is associated with poor outcomes.
Management
Medical Medical therapy for tricuspid regurgitation consists of diuretics (loop diuretics as the first line therapy with mineralocorticoid receptor antagonists added on for worsening or refractory cases). However, as the disease progresses, diuretics may become inefficient. Diuretic resistance in TR and right heart failure is thought to develop due to a variety of mechanisms working synergistically to lead to decreased effectiveness of diuretics. Decreased effective circulating volume, ie. decreased blood perfusing the kidneys, leads to activation of the renin–angiotensin–aldosterone system, which leads to the kidneys reabsorbing salt and water and vasoconstriction of the arterioles. Intestinal edema may also lead to decreased gut absorption of the diuretics and increased fluid retention may lead to an increased volume of distribution of the diuretic. All of the preceding mechanisms in TR with right heart failure (and sometimes secondary left heart failure) lead to diuretic resistance. Diuretic resistance is associated with a poor prognosis.
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