Tricuspid insufficiency (TI), more commonly called tricuspid regurgitation (TR), 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.
|Other names||Tricuspid regurgitation|
|Echocardiogram showing typical findings in severe tricuspid regurgitation|
|Causes||Abnormally high blood pressure , other heart problem|
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
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.
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.
- Primary causes
- Secondary causes
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,
The diagnosis of TR may be suspected if the typical murmur of TR is heard. Severe TR may be suspected if right ventricular enlargement is seen on chest x-ray, and other causes of this enlargement are ruled out.
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.
Tricuspid valve replacement using either a mechanical prosthesis or a bioprosthesis may be indicated. (Mechanical prostheses may cause thrombo‐embolic phenomena, bioprostheses may have a degeneration problem). Some evidence suggests that there are no significant differences between a mechanical or biological tricuspid valve in a recipient.
Surgery vs. no surgery for TR has been statistically assessed by looking back on consecutive series of hospital cases, mainly of secondary causes. In these cases, one finds that surgery predicts outliving non-surgery cases initially matched in health ~60% of the time (HR = .74).
The prognosis of TR is less favorable for males than females. Survival rates are proportional to TR severity; but even mild TR reduces survival compared to those with no TR. If the TR is due to left heart failure or pulmonary hypertension, prognosis is usually dictated by these conditions, not the TR.
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