Tricuspid regurgitation and tricuspid valve disease !

The valve between the right atrium and right ventricle leaks, so blood flows backwards. It often follows lung or left-heart disease.

Updated 2026-11-01

Structures involved

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Why it happens

What it is

Tricuspid regurgitation (TR) is backflow of blood from the right ventricle into the right atrium during systole because the tricuspid valve does not close properly. Most cases are secondary (functional): the leaflets are normal but the annulus and right ventricle are dilated by pressure or volume overload. Primary TR comes from disease of the leaflets or chordae themselves. Tricuspid stenosis is rare and is almost always rheumatic, usually together with mitral disease.

Who gets it

Trivial TR is found on echocardiography in most healthy people and is not a disease. Clinically significant TR becomes more frequent with age, in women and in people with atrial fibrillation, pulmonary hypertension or left-sided valve disease. In Colombia and Latin America, rheumatic heart disease and Chagas cardiomyopathy remain relevant causes of right-heart dilation, alongside chronic lung disease.

Causes

Secondary (about 80–90%): pulmonary hypertension from left-heart disease (mitral valve disease, left ventricular failure), chronic lung disease or pulmonary embolism; right ventricular infarction or cardiomyopathy; atrial fibrillation with annular dilation
Primary: infective endocarditis (classically Staphylococcus aureus in people who inject drugs), rheumatic heart disease, carcinoid heart disease, myxomatous degeneration or prolapse
Congenital: Ebstein anomaly, tricuspid valve dysplasia
Device- and injury-related: pacemaker or defibrillator leads crossing the valve, chest trauma, damage during endomyocardial biopsy
Drugs: ergot-derived dopamine agonists and some serotonergic appetite suppressants (valvulopathy)

Risk factors

Pulmonary hypertension of any cause
Left-sided valve disease, especially mitral stenosis or regurgitation
Atrial fibrillation and older age
Injection drug use (endocarditis)
Transvenous pacemaker or defibrillator leads

Pathophysiology

With each ventricular contraction part of the right ventricular stroke volume returns to the right atrium. Right atrial pressure rises and is transmitted to the venae cavae, liver and peripheral veins, producing raised jugular pressure with large systolic v waves, hepatic congestion, ascites and oedema. The extra volume dilates the right ventricle and annulus further, which worsens the leak (TR begets TR). Forward flow to the lungs falls, so fatigue and low output appear late. Chronic hepatic congestion can lead to cardiac (congestive) cirrhosis, and low renal perfusion with venous congestion causes cardiorenal dysfunction.

Classification

Primary (organic, leaflet disease) vs secondary (functional, annular and ventricular dilation); atrial functional TR in atrial fibrillation
Severity on echocardiography: mild, moderate, severe (some systems add massive and torrential)
Stages A–D (at risk, progressive, asymptomatic severe, symptomatic severe)
Tricuspid stenosis: usually rheumatic and combined with mitral disease

Symptoms and signs

Often silent when mild; symptoms reflect the cause (for example dyspnoea from pulmonary hypertension or left-heart disease)
Fatigue and reduced exercise tolerance
Leg and ankle oedema, abdominal swelling (ascites) and right upper quadrant discomfort from liver congestion
Pulsations felt in the neck
Loss of appetite, early satiety and weight loss in advanced disease

Diagnosis

Clinical: Holosystolic murmur at the left lower sternal border that increases with inspiration (Carvallo sign); raised jugular venous pressure with prominent systolic v waves; pulsatile, enlarged liver; ascites and peripheral oedema; right ventricular heave. The murmur may be soft or absent when the leak is massive.
Tests: ECG: right atrial enlargement, right ventricular hypertrophy or right bundle branch block, often atrial fibrillation. Natriuretic peptides, renal and liver function (congestion), blood cultures when endocarditis is suspected.
Imaging: Transthoracic echocardiography is the key test: leaflet anatomy, mechanism, severity by colour and Doppler (vena contracta, systolic hepatic vein flow reversal), annular and right ventricular size and function, and an estimate of pulmonary artery pressure. Cardiac MRI quantifies right ventricular volumes; right heart catheterisation clarifies pulmonary vascular resistance before surgery.

Differential diagnosis

Mitral regurgitation (apical murmur radiating to the axilla, does not increase with inspiration)
Ventricular septal defect
Constrictive pericarditis or restrictive cardiomyopathy (raised jugular pressure, ascites)
Cirrhosis of primary liver origin
Nephrotic syndrome and other causes of generalised oedema

Goal of treatment

Treat the underlying cause, relieve venous congestion and repair or replace the valve before irreversible right ventricular dysfunction develops.

Treatment

Medical: Loop diuretics (sometimes with aldosterone antagonists) to relieve oedema, ascites and liver congestion.
Medical: Treat the cause: left-sided heart failure and valve disease, pulmonary hypertension, rate or rhythm control of atrial fibrillation, antibiotics for endocarditis.
Surgical: Tricuspid annuloplasty or repair, most often during left-sided valve surgery when TR is severe or the annulus is dilated; isolated repair or replacement for severe symptomatic TR before the right ventricle fails.
Procedure: Transcatheter tricuspid repair (edge-to-edge) or replacement in selected patients at high surgical risk.
Follow-up: Nursing: daily weight, fluid balance and oedema, abdominal girth, renal function and electrolytes on diuretics, signs of infection in people who inject drugs; periodic echocardiography.

Complications

Right-sided heart failure
Congestive hepatopathy and cardiac cirrhosis
Cardiorenal syndrome
Atrial fibrillation and flutter
Septic pulmonary emboli in tricuspid endocarditis
Protein-calorie malnutrition (cardiac cachexia)

Prognosis

Mild TR is benign. Severe TR is independently associated with higher mortality, and outcomes depend on the cause and on right ventricular function. Results of surgery are best when it is done before the right ventricle and liver are irreversibly damaged.

Prevention

Prevention and treatment of streptococcal pharyngitis and rheumatic fever
Early treatment of left-sided valve disease and pulmonary hypertension
Harm-reduction programmes for people who inject drugs
Careful lead placement and follow-up in people with intracardiac devices

Test yourself

Think of the answer, then tap the question to see it.

What happens to the TR murmur with inspiration, and what is this sign called?

It becomes louder (Carvallo sign), because venous return to the right heart increases.

What is the most common mechanism of tricuspid regurgitation?

Secondary (functional) TR from right ventricular and annular dilation, usually due to pulmonary hypertension or left-heart disease.

Which organism classically causes tricuspid endocarditis in people who inject drugs?

Staphylococcus aureus.

Which jugular venous waveform finding is typical of severe TR?

Large systolic (c-v) waves.

Which tumour syndrome causes right-sided valve fibrosis with TR and pulmonary stenosis?

Carcinoid syndrome with liver metastases (carcinoid heart disease).

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Educational information, not medical advice. For any symptom, see a health professional.

Sources: Tricuspid regurgitation (MedlinePlus, US National Library of Medicine, 2026).

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Representative model, for educational purposes only.

Tricuspid anterior leaflet highlighted on the Durgical 3D model