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 from infective endocarditis in IV drug abusers, carcinoid syndrome, chest or abdominal injury, rheumatic fever, idiopathic myxomatous degeneration, ischemic papillary muscle dysfunction, congenital defects (eg, cleft tricuspid valve, endocardial cushion defects), Ebstein anomaly (downward displacement of a distorted tricuspid cusp into the RV), Marfan syndrome, and use of certain drugs (eg, ergotamine, fenfluramine, phentermine).
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. Acute or severe TR may cause symptoms of RV dysfunction–induced HF. Patients may also develop symptoms of AF or atrial flutter.
Pedal edema or ascites can occur in severe TR.
The only visible sign of moderate to severe TR is jugular venous distention, with a prominent merged c-v wave and a steep y descent. 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 P2 and 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 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. Sometimes the murmur is not present at all and 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).
Very mild TR is a normal finding and requires no action. 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 in which the findings of severe TR may include: 2-dimensional failure of coaptation or flail, large regurgitant jet on color Doppler echocardiography, large flow convergence zone proximal to the valve, vena contracta width > 7 mm, systolic flow reversal in the hepatic veins, transtricuspid E wave dominant > 1 cm/sec, dense triangular early peaking continuous wave Doppler of TR jet. 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 also often obtained. 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.
Cardiac catheterization is rarely indicated for evaluation of TR. When catheterization is indicated (eg, to evaluate coronary anatomy), findings include a prominent right atrial c-v wave during ventricular systole.
Limited data suggest that 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.
Medical treatment of causes (eg, HF, endocarditis) is indicated. Patients with severe TR should undergo operation as soon as RV enlargement or dysfunction is apparent. During surgery for left-sided heart lesions, moderate TR 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.
If endocarditis has damaged the tricuspid valve and cannot be cured with antibiotics, the valve may be totally excised and not replaced until 6 to 9 mo later; this procedure is well tolerated.
Last full review/revision November 2012 by Guy P. Armstrong
Content last modified September 2013