Tricuspid regurgitation (TR) is insufficiency of the tricuspid valve causing blood flow from the right ventricle to the right atrium during systole. The most common cause is dilation of the right ventricle. Symptoms and signs are usually absent, but severe TR can cause neck pulsations, a holosystolic murmur, and right ventricular–induced heart failure or atrial fibrillation. Diagnosis is by physical examination and echocardiography. TR is usually benign and does not require treatment, but some patients require annuloplasty or valve repair or replacement.
TR is most commonly secondary, caused by dilation of the right ventricle (RV) with malfunction of a normal valve, as occurs in pulmonary hypertension, RV dysfunction–induced heart failure (HF), and pulmonary outflow tract obstruction.
TR is less commonly primary, due to valvular abnormalities caused by infective endocarditis in users of illicit IV drugs, carcinoid syndrome, blunt chest trauma, rheumatic fever, idiopathic myxomatous degeneration, congenital defects (eg, cleft tricuspid valve, endocardial cushion defects), Ebstein anomaly (downward displacement of a congenitally malformed tricuspid cusp into the RV), Marfan syndrome, and use of certain drugs (eg, ergotamine, fenfluramine, phentermine). Iatrogenic causes include pacemaker leads that cross the tricuspid valve and valve damage sustained during RV endomyocardial biopsy.
Long-standing severe TR may lead to RV dysfunction–induced HF and atrial fibrillation (AF).
Symptoms and Signs
TR usually causes no symptoms, but some patients experience neck pulsations due to elevated jugular pressures. Symptoms of severe TR include fatigue, abdominal bloating, and anorexia. Patients may also develop symptoms of AF or atrial flutter.
Signs of moderate to severe TR include jugular venous distention, with a prominent merged c-v wave and a steep y descent, and sometimes enlarged liver and peripheral edema. In severe TR, a right jugular venous thrill may be palpable, as may systolic hepatic pulsation and an RV impulse at the left lower sternal border.
On auscultation, the 1st heart sound (S1) may be normal or barely audible if a TR murmur is present; the 2nd heart sound (S2) may be split (with a loud pulmonic component [P2] in pulmonary hypertension) or single because of prompt pulmonic valve closing with merger of P2and the aortic component (A2). An RV 3rd heart sound (S3) may be audible near the sternum with RV dysfunction–induced HF.
The murmur of TR is frequently not heard. When evident, it is a holosystolic murmur heard best at the left middle or lower sternal border or at the epigastrium with the bell of the stethoscope when the patient is sitting upright or standing. The murmur may be high-pitched if TR is trivial and due to pulmonary hypertension, or it may be medium-pitched if TR is severe and has other causes. When the murmur is not present at all, the diagnosis is best made by the appearance of the jugular venous wave pattern and the presence of hepatic systolic pulsations. The murmur varies with respiration, becoming louder with inspiration (Carvallo sign).
Mild TR is most often detected on echocardiography done for other reasons. More moderate or severe TR may be suggested by history and physical examination. Confirmation is by echocardiography.
Severe TR is characterized echocardiographically by ≥ 1 of the following:
When TR is moderate or severe, the peak regurgitant velocity will underestimate pulmonary pressure. Two-dimensional echocardiography detects the structural abnormalities present in primary TR.
Cardiac MRI is now the preferred method for evaluating RV size and function.
An ECG and chest x-ray are often done. ECG is usually normal but, in advanced cases, may show tall peaked P waves caused by right atrial enlargement, a tall R or QR wave in V1 characteristic of RV hypertrophy, or AF. Chest x-ray is usually normal but, in advanced cases with RV hypertrophy or RV dysfunction–induced HF, may show an enlarged superior vena cava, an enlarged right atrial or RV silhouette (behind the upper sternum in the lateral projection), or pleural effusion.
Laboratory testing is not needed but if done may show hepatic dysfunction in patients with severe TR.
Cardiac catheterization is indicated for accurate measurement of pulmonary pressure when TR is severe and to evaluate coronary anatomy when surgery is planned. Catheterization findings include a prominent right atrial c-v pressure wave during ventricular systole.
Severe TR ultimately has a poor prognosis, even if it is initially well-tolerated for years. As with left-sided valvular regurgitation, the volume-overloaded ventricle eventually decompensates irreversibly.
Very mild TR is a normal finding and requires no action. Medical treatment of causes (eg, HF, endocarditis) is indicated. Patients with severe TR should undergo operation as soon as symptoms are present despite medical treatment or when there is moderate, progressive RV enlargement or dysfunction. During surgery for left-sided heart lesions, moderate or mild TR with dilated annulus > 40 mm should also undergo repair.
Surgical options include annuloplasty, valve repair, and valve replacement. Annuloplasty, in which the tricuspid valve annulus is sutured to a prosthetic ring or a tailored reduction in annulus circumferential size is done, is indicated when TR is due to annular dilation. Valve repair or replacement is indicated when TR is due to primary valve abnormalities or when annuloplasty is not technically feasible. Tricuspid valve replacement is indicated when TR is due to carcinoid syndrome or Ebstein anomaly. A bioprosthetic valve is used to reduce the risk of thromboembolism associated with the low pressures of the right heart; in the right heart, unlike the left heart, bioprosthetic valves last > 10 yr.
Last full review/revision July 2014 by Guy P. Armstrong, MD
Content last modified July 2014