Tricuspid Regurgitation: Causes, Symptoms, Diagnosis, Management and Prevention

Tricuspid Regurgitation: An In-Depth Review

~Introduction

Tricuspid Regurgitation (TR) is a valvular heart disorder characterized by the backward flow of blood from the right ventricle into the right atrium during systole due to incompetence of the tricuspid valve. Although it is often secondary to other cardiac diseases, especially those affecting the left side of the heart or the pulmonary vasculature, it may also arise from primary pathology of the tricuspid valve itself. Once considered relatively benign, severe tricuspid regurgitation is now recognized as a significant cause of morbidity and mortality when left untreated.

~Anatomy and Physiology of the Tricuspid Valve

The tricuspid valve is one of the four cardiac valves and lies between the right atrium and right ventricle. It typically consists of three leaflets — anterior, posterior, and septal — attached to a fibrous annulus. The valve leaflets are anchored to the right ventricular papillary muscles via chordae tendineae, which maintain valve competence during systole.

Normal tricuspid valve function depends on the integrity and coordination of the following structures:

• Leaflets (provide the surface for closure)

• Chordae tendineae and papillary muscles (maintain tension)

• Annulus (supports leaflet coaptation)

• Right atrium and ventricle (provide appropriate geometry and contraction)

When any of these components is altered structurally or functionally, the valve may fail to close properly, leading to regurgitation.

~Etiology (Causes of Tricuspid Regurgitation)

Tricuspid regurgitation can be classified as primary (organic) or secondary (functional) depending on the underlying mechanism.

1. Primary (Organic) Tricuspid Regurgitation

Primary TR results from direct disease of the valve apparatus, including the leaflets, chordae, or papillary muscles. Common causes include:

• Rheumatic heart disease: Causes thickening, fusion, or deformity of the valve leaflets.

• Infective endocarditis: Particularly common among intravenous drug users, leading to leaflet destruction or perforation.

• Congenital anomalies: Such as Ebstein’s anomaly, where the tricuspid valve is displaced downward into the right ventricle.

• Trauma or iatrogenic causes: Resulting from endomyocardial biopsy, pacemaker lead insertion, or cardiac surgery.

• Carcinoid heart disease: Caused by serotonin-induced fibrosis of the valve leaflets.

• Myxomatous degeneration: Similar to mitral valve prolapse but involving the tricuspid valve.

• Radiation-induced valvular disease or drugs (e.g., fenfluramine, ergot derivatives).

2. Secondary (Functional) Tricuspid Regurgitation

Secondary TR is more common and results from annular dilation or right ventricular enlargement secondary to other diseases. Causes include:

• Left-sided heart diseases: Mitral valve stenosis or regurgitation leading to pulmonary hypertension.

• Pulmonary hypertension: From chronic lung disease or pulmonary embolism.

• Right ventricular dilation: Due to right heart failure, volume overload, or cardiomyopathy.

• Atrial fibrillation: Which causes right atrial enlargement and annular dilation.

• Left-to-right shunts: Such as atrial septal defect causing right heart volume overload.

~Pathophysiology

The degree of tricuspid regurgitation depends on both the size of the regurgitant orifice and the pressure gradient between the right ventricle and right atrium during systole. In TR, the incompetent valve allows systolic backflow of blood into the right atrium, leading to:

• Volume overload of the right atrium and ventricle

• Right atrial enlargement

• Right ventricular dilation and dysfunction

• Increased systemic venous pressure

In chronic cases, the body adapts to some extent by enlarging the right-sided chambers. However, progressive dilation eventually leads to worsening regurgitation — a vicious cycle that culminates in right-sided heart failure. Systemic congestion becomes evident as peripheral edema, ascites, hepatomegaly, and jugular venous distension.

~Clinical Features

1. Symptoms

Mild tricuspid regurgitation may remain asymptomatic for years. Symptoms typically appear as the regurgitation worsens and right heart failure develops. Common complaints include:

• Fatigue and weakness (due to reduced cardiac output)

• Abdominal discomfort and fullness (from hepatic congestion)

• Peripheral edema and weight gain

• Ascites

• Anorexia and nausea

• Palpitations (from atrial fibrillation)

• Dyspnea (in cases with associated pulmonary hypertension)

2. Signs

Physical findings are characteristic and help in bedside diagnosis:

• Jugular venous distension (JVD): Prominent ‘v’ waves and rapid ‘y’ descent.

• Hepatomegaly: Pulsatile liver due to regurgitant flow transmitted backward.

• Peripheral edema and ascites.

• Right ventricular heave: Felt at the lower left sternal border.

• Murmur:

  • Character: Holosystolic, blowing murmur.

  • Location: Best heard at the left lower sternal border.

  • Intensity: Increases with inspiration (Carvallo’s sign).

  • Radiation: May radiate to the epigastrium.

• Systolic pulsation of the liver may also be noted.

~Complications

If left untreated, severe tricuspid regurgitation can result in:

• Right-sided heart failure

• Hepatic congestion leading to cirrhosis (cardiac cirrhosis)

• Atrial fibrillation

• Thromboembolic events

• Progressive renal dysfunction

• Increased mortality

~Diagnosis

1. Clinical Evaluation

Diagnosis often begins with history and physical examination, revealing typical symptoms of venous congestion and the characteristic systolic murmur.

2. Electrocardiogram (ECG)

Findings may include:

• Right atrial enlargement: Peaked P waves in lead II.

• Atrial fibrillation

• Right ventricular hypertrophy in advanced cases.

3. Chest X-Ray

May show:

• Right atrial and ventricular enlargement

• Prominent superior vena cava or azygos vein

• Enlarged pulmonary arteries if pulmonary hypertension is present.

4. Echocardiography (Key Diagnostic Tool)

Echocardiography is the gold standard for assessing tricuspid regurgitation:

• Transthoracic echocardiography (TTE):

  • Direct visualization of tricuspid valve structure and motion.

  • Color Doppler shows the regurgitant jet.

  • Estimation of regurgitant volume, vena contracta, and effective regurgitant orifice area.

  • Assessment of right atrial and ventricular size and function.

  • Estimation of pulmonary artery pressure.

• Transesophageal echocardiography (TEE): Offers higher resolution images when needed.

• 3D Echocardiography: Provides detailed annular geometry for surgical planning.

5. Cardiac MRI

Useful for accurate quantification of right ventricular volume and regurgitant fraction, especially when echocardiographic data are suboptimal.

6. Cardiac Catheterization

Performed to assess hemodynamics, measure right atrial pressure, and evaluate pulmonary hypertension prior to surgical intervention.

~Grading of Severity

Tricuspid regurgitation is typically graded as mild, moderate, or severe based on:

• Vena contracta width: >0.7 cm suggests severe TR.

• Regurgitant jet area: >10 cm² on color Doppler indicates severe TR.

• Regurgitant volume and effective regurgitant orifice area (EROA):

  • Severe TR: EROA ≥ 40 mm² or regurgitant volume ≥ 45 mL/beat.

• Right atrial and ventricular enlargement and hepatic vein systolic flow reversal support severe disease.

~Management

Management of tricuspid regurgitation depends on its cause, severity, and associated conditions.

1. Medical Therapy

Primarily aimed at controlling symptoms of right heart failure and managing underlying causes.

• Diuretics (loop diuretics such as furosemide): Reduce systemic venous congestion and edema.

• Aldosterone antagonists (spironolactone): Help in resistant edema and ascites.

• Treat underlying diseases:

  • Manage left-sided heart disease and pulmonary hypertension.

  • Control atrial fibrillation and restore sinus rhythm if possible.

  • Antibiotics for infective endocarditis.

• Avoid excessive preload reduction to maintain adequate cardiac output.

Medical management is palliative and does not halt disease progression.

2. Surgical and Interventional Treatment

Surgical correction is considered in severe TR or when another cardiac surgery is planned (e.g., mitral valve repair).

A. Tricuspid Valve Repair

Preferred whenever feasible because it preserves native anatomy and ventricular function.

• Annuloplasty: Most common; involves reduction of the dilated annulus using a prosthetic ring (e.g., De Vega, Carpentier ring).

• Leaflet augmentation or chordal repair may be performed if needed.

B. Tricuspid Valve Replacement

Indicated when repair is not possible, such as in severe structural damage.

• Prosthetic options:

  • Bioprosthetic valves are preferred to avoid long-term anticoagulation.

  • Mechanical valves may be used in younger patients.

• Long-term complications include valve degeneration or thrombosis.

C. Transcatheter Therapies

Emerging minimally invasive options for high-risk patients:

• Transcatheter tricuspid valve repair (e.g., edge-to-edge repair with devices like TriClip or PASCAL).

• Valve replacement using percutaneous approaches (in development).

3. Indications for Surgery

• Severe primary TR with symptoms of right heart failure.

• Severe secondary TR during left-sided valve surgery.

• Moderate TR with annular dilation (>40 mm or >21 mm/m² on echo).

• Progressive right ventricular enlargement or dysfunction.

~Prognosis

The prognosis of tricuspid regurgitation depends on the etiology, severity, and timing of intervention.

• Mild TR has a favorable outcome and may remain stable.

• Severe untreated TR leads to progressive right heart failure, hepatic dysfunction, and reduced survival.

• Post-surgical outcomes are excellent when intervention occurs before irreversible right ventricular damage.

• In patients with functional TR, prognosis improves significantly if underlying left heart or pulmonary disease is managed effectively.

~Prevention

While primary prevention is often not possible, secondary TR can be minimized by:

• Early and effective management of left-sided valve disease.

• Control of pulmonary hypertension.

• Preventing rheumatic fever and infective endocarditis.

• Careful handling during pacemaker lead insertion to prevent leaflet injury.

~Recent Advances

Recent years have witnessed significant progress in the understanding and treatment of TR:

• 3D echocardiography and cardiac MRI allow more accurate assessment of valve geometry.

• Transcatheter tricuspid interventions (TTVI) have emerged as promising alternatives to open surgery, especially for high-risk patients.

• Development of dedicated tricuspid repair and replacement devices such as:

  • TriClip (Abbott)

  • PASCAL (Edwards Lifesciences)

  • EVOQUE and Cardioband systems
    These innovations are transforming TR management from neglected surgery to a focus of modern structural heart disease programs.

~Conclusion

Tricuspid regurgitation, once deemed a benign bystander in cardiac disease, is now recognized as a serious condition with significant clinical implications. Secondary TR remains far more prevalent and often arises as a sequela of left-sided heart disease or pulmonary hypertension. While medical therapy provides symptomatic relief, timely surgical or transcatheter intervention is crucial to prevent irreversible right ventricular failure and improve survival outcomes.

With advancing imaging, earlier recognition, and newer interventional technologies, the future outlook for patients with tricuspid regurgitation is becoming increasingly optimistic.