(See also Overview of Cardiac Valvular Disorders.)
Tricuspid regurgitation may be
Primary tricuspid regurgitation is less common. It can be 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 right ventricle [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.
Secondary tricuspid regurgitation is due to leaflet tethering, which is the result of reduced leaflet coaptation caused by annular dilation (typical of right atrial dilation caused by chronic atrial fibrillation) and/or papillary muscle displacement (most commonly as a result of left heart disease causing pulmonary hypertension and leading to RV dilation or geometric distortion).
Tricuspid regurgitation 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 tricuspid regurgitation 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 tricuspid regurgitation 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 tricuspid regurgitation 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 tricuspid regurgitation 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:
2-Dimensional failure of coaptation or flail
Large regurgitant jet on color Doppler
Large flow convergence zone proximal to the valve
Vena contracta width > 7 mm
Systolic flow reversal in the hepatic veins (specific for severe TR)
Transtricuspid E wave dominant > 1 cm/second
Dense, triangular, early peaking, continuous wave Doppler of TR jet
In secondary TR, a dilated annulus > 40 mm (measured in the apical 4-chamber view) predicts severe TR. 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, which typically should be done when echocardiographic image quality is inadequate.
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 tricuspid regurgitation 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. However, in contrast to left-sided valvular regurgitation, there is no robust way to discern when the RV is starting to decompensate. Given this, patients are commonly referred late for surgery. In the context of the significant risks of surgery the overall outcome is poor.
Very mild tricuspid regurgitation is a normal finding and requires no action. Medical treatment of causes (eg, HF, endocarditis) is indicated.
Patients with severe tricuspid regurgitation 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, 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 repair is generally preferred to replacement. 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 years. A bioprosthetic valve requires temporary anticoagulation (see also Anticoagulation for patients with a prosthetic cardiac valve).
Progress is being made toward a percutaneous valve repair procedure. This will fill an unmet need and allow a lower risk percutaneous repair much earlier in the natural history of severe TR.
Tricuspid regurgitation (TR) usually occurs in a normal valve affected by right ventricular dilation; less often there is an intrinsic valve disorder (eg, due to infective endocarditis, carcinoid syndrome, certain drugs).
Jugular venous distention may occur; severe TR may cause abdominal distension, hepatic enlargement, and peripheral edema.
Heart sounds include a holosystolic murmur heard best at the left middle or lower sternal border or at the epigastrium when the patient is sitting upright or standing; the murmur becomes louder with inspiration.
TR is usually well tolerated, but severe cases may require annuloplasty, valve repair, or valve replacement.