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 usually benign; however, it is increasingly implicated as a risk factor for heart failure. Selected symptomatic patients require annuloplasty or valve repair or replacement.
(See also Overview of Cardiac Valvular Disorders.)
Etiology of Tricuspid Regurgitation
Tricuspid regurgitation may be
Primary
Secondary (most common)
Primary tricuspid regurgitation is less common. It can be due to
Blunt chest trauma
Congenital defects (eg, cleft tricuspid valve, endocardial cushion defects)
Ebstein anomaly (downward displacement of a congenitally malformed tricuspid cusp into the right ventricle [RV])
Idiopathic myxomatous degeneration
Valvular abnormalities caused by infective endocarditis
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).
Long-standing severe TR may lead to RV dysfunction–induced heart failure and atrial fibrillation.
Symptoms and Signs of Tricuspid Regurgitation
Tricuspid regurgitation usually causes no symptoms, but some patients experience neck pulsations due to elevated jugular pressures. Symptoms of severe TR include peripheral edema, fatigue, abdominal bloating, ascites, and anorexia. Patients may also develop symptoms of atrial fibrillation 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.
Auscultation
Holosystolic murmur heard best at the left middle or lower sternal border (frequently not heard)
On auscultation, the first heart sound (S1) may be normal or barely audible if a tricuspid regurgitation murmur is present; the second 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 third heart sound (S3) may be audible near the sternum with RV dysfunction–induced heart failure.
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. The murmur varies with respiration, becoming louder with inspiration (Carvallo sign).
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.
Diagnosis of Tricuspid Regurgitation
Echocardiography
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
Dense, triangular, early peaking, continuous wave Doppler of TR jet
Large flow convergence zone proximal to the valve
Large regurgitant jet on color Doppler (≥ 50% of right atrial area)
Systolic flow reversal in the hepatic veins (specific for severe TR)
Vena contracta width > 7 mm
The vena contracta is the narrowest diameter of the fluid stream downstream of an abnormal valve orifice; it is slightly smaller than the anatomic valve orifice.
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. Assessing RV systolic dysfunction is challenging and is suggested on echocardiography by tricuspid annular plane systolic excursion (TAPSE) < 16 mm or tricuspid annular systolic velocity < 10 cm/second.
Cardiac MRI is 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 atrial fibrillation.
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.
Treatment of Tricuspid Regurgitation
Treatment of cause
Sometimes annuloplasty or valve repair or replacement
Very mild tricuspid regurgitation is a normal finding and requires no action. Medical treatment of causes (eg, heart failure, endocarditis) is indicated.
Medical therapy with loop diuretics can relieve congestion. Aldosterone antagonists may be of additive benefit as they counter secondary hyperaldosteronism due to hepatic congestion. Treating the etiology is important in secondary TR.
Timing of intervention for tricuspid regurgitation depends on the patient's symptoms and RV function. 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. Severe LV dysfunction or severe pulmonary hypertension may make the surgical risk prohibitive.
During surgery for left-sided heart lesions, patients with moderate or mild TR with dilated annulus > 40 mm can undergo tricuspid annuloplasty, slowing progression to severe TR. However, tricuspid annuloplasty increases risk of the need for permanent pacing five-fold. The net clinical benefit is not certain and awaits long-term follow up of the randomized trial addressing this issue (1).
Surgical options include
Annuloplasty
Valve repair
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 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. Early studies have shown improvement in the degree of regurgitation and in right-sided hemodynamics. Development of a percutaneous repair procedure will allow lower risk repair much earlier in the natural history of severe TR.
Treatment reference
1. Gammie JS, Chu MWA, Falk V, et al: Concomitant tricuspid repair in patients with degenerative mitral regurgitation. N Engl J Med 386(4):327–339, 2022. doi: 10.1056/NEJMoa2115961
Prognosis for Tricuspid Regurgitation
Severe tricuspid regurgitation ultimately has a poor prognosis, even if it is initially well-tolerated for years. Less severe TR also affects prognosis, though no study has conclusively shown that early intervention reduces mortality.
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.
Key Points
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 medications).
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.
