(See also Overview of Cardiac Valvular Disorders Overview of Cardiac Valvular Disorders Any heart valve can become stenotic or insufficient (also termed regurgitant or incompetent), causing hemodynamic changes long before symptoms. Most often, valvular stenosis or insufficiency... read more .)
Etiology of Tricuspid Regurgitation
Tricuspid regurgitation may be
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 Atrioventricular Septal Defect Atrioventricular (AV) septal defect consists of an ostium primum type atrial septal defect and a common AV valve, with or without an associated inlet (AV septal type) ventricular septal defect... read more )
Drugs (eg, ergotamine, fenfluramine, phentermine)
Ebstein anomaly Ebstein anomaly Other structural congenital cardiac anomalies include the following: Aortopulmonary window Congenitally corrected transposition Double outlet right ventricle Ebstein anomaly read more (downward displacement of a congenitally malformed tricuspid cusp into the right ventricle [RV])
Idiopathic myxomatous degeneration
Valvular abnormalities caused by infective endocarditis Infective Endocarditis Infective endocarditis is infection of the endocardium, usually with bacteria (commonly, streptococci or staphylococci) or fungi. It may cause fever, heart murmurs, petechiae, anemia, embolic... read more in users of illicit IV drugs
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 Atrial Fibrillation Atrial fibrillation is a rapid, irregularly irregular atrial rhythm. Symptoms include palpitations and sometimes weakness, effort intolerance, dyspnea, and presyncope. Atrial thrombi may form... read more ) and/or papillary muscle displacement (most commonly as a result of left heart disease causing pulmonary hypertension Pulmonary Hypertension Pulmonary hypertension is increased pressure in the pulmonary circulation. It has many secondary causes; some cases are idiopathic. In pulmonary hypertension, pulmonary vessels become constricted... read more and leading to RV dilation or geometric distortion).
Long-standing severe TR may lead to RV dysfunction–induced HF Classification Heart failure (HF) is a syndrome of ventricular dysfunction. Left ventricular failure causes shortness of breath and fatigue, and right ventricular failure causes peripheral and abdominal fluid... read more and atrial fibrillation Atrial Fibrillation Atrial fibrillation is a rapid, irregularly irregular atrial rhythm. Symptoms include palpitations and sometimes weakness, effort intolerance, dyspnea, and presyncope. Atrial thrombi may form... read more (AF).
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 AF or atrial flutter Atrial Flutter Atrial flutter is a rapid regular atrial rhythm due to an atrial macroreentrant circuit. Symptoms include palpitations and sometimes weakness, effort intolerance, dyspnea, and presyncope. Atrial... read more .
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.
Holosystolic murmur heard best at the left middle or lower sternal border (frequently not heard)
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).
Diagnosis of Tricuspid Regurgitation
Mild tricuspid regurgitation is most often detected on echocardiography Echocardiography This photo shows a patient having echocardiography. This image shows all 4 cardiac chambers and the tricupsid and mitral valves. Echocardiography uses ultrasound waves to produce an image of... read more 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
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 MRI Cardiac imaging tests can delineate cardiac structure and function. Standard imaging tests include Echocardiography Chest x-ray CT MRI read more is now the preferred method for evaluating RV size and function.
An ECG and chest x-ray are often done.
ECG Electrocardiography The standard electrocardiogram (ECG) provides 12 different vector views of the heart’s electrical activity as reflected by electrical potential differences between positive and negative electrodes... read more 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 Chest x-ray Chest imaging includes use of plain x-rays, computed tomography (CT) scanning, magnetic resonance imaging (MRI), nuclear scanning, including positron emission tomography (PET) scanning, and... read more 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 Cardiac Catheterization Cardiac catheterization is the passage of a catheter through peripheral arteries or veins into cardiac chambers, the pulmonary artery, and coronary arteries and veins. Cardiac catheterization... read more 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.
Prognosis for Tricuspid Regurgitation
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.
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, HF, 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. 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 (1 Treatment reference 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... read more ).
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 Anticoagulation for patients with a prosthetic cardiac valve Any heart valve can become stenotic or insufficient (also termed regurgitant or incompetent), causing hemodynamic changes long before symptoms. Most often, valvular stenosis or insufficiency... read more ).
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.
1. Otto CM, Nishimura RA, Bonow RO, et al: 2020 ACC/AHA Guideline for the Management of Patients With Valvular Heart Disease: Executive Summary: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation 143(5):e35–e71, 2021. doi: 10.1161/CIR.0000000000000932
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.