Tricuspid Regurgitation

Tricuspid regurgitation is a valvular heart disease characterized by the abnormal backflow of blood from the right ventricle to the right atrium during systole, due to inadequate coaptation of the tricuspid valve leaflets. This retrograde flow reduces the effectiveness of ventricular contraction and causes volume overload of the right heart chambers, with repercussions on systemic venous pressure.

Etiology, Pathogenesis and Pathophysiology

The causes of tricuspid regurgitation can be classified as primary (organic) or secondary (functional).

Primary forms result from structural damage to the tricuspid valve, as seen in rheumatic disease (fibrosis, calcification, and leaflet retraction), infective endocarditis (with leaflet destruction or perforation), congenital heart diseases (e.g., Ebstein’s anomaly), and myxomatous degenerative forms with leaflet prolapse.
Secondary forms are the most common and result from tricuspid annular dilation due to right ventricular remodeling in diseases causing pressure or volume overload, such as: pulmonary hypertension (primary or secondary); advanced left heart disease, especially with mitral regurgitation or stenosis; dilated cardiomyopathy and other cardiomyopathies; device-induced dysfunction (TRI: tricuspid regurgitation induced by leads); post-surgical dysfunction, for instance after left valve replacement or congenital heart surgery.

Tricuspid regurgitation leads to the backflow of blood into the right atrium during systole, causing:

• Atrial volume overload with right atrial dilation and increased right atrial pressure;
• Retrograde increase in systemic venous pressure, resulting in signs of venous congestion (jugular vein distension, hepatomegaly, ascites, edema);
• Reduced left ventricular filling due to decreased pulmonary flow, leading to reduced systemic cardiac output and hypoperfusion symptoms.

In chronic forms, a state of partial hemodynamic compensation develops due to the high compliance of the right chambers, delaying symptom onset. In acute forms, however, the sudden onset of regurgitation causes a rapid increase in right atrial and systemic venous pressures, potentially evolving into right-sided cardiogenic shock.

Clinical Manifestations

The clinical presentation of chronic tricuspid regurgitation is primarily marked by signs and symptoms of systemic venous congestion and, to a lesser extent, by symptoms due to reduced cardiac output. Symptoms are often masked by those of associated left heart disease, making early recognition of tricuspid involvement challenging.

The most frequent symptoms include:

• Peripheral edema (ankles, sacrum), abdominal distension, ascites;
• Jugular vein distension with prominent V wave;
• Epigastric fullness and congestive hepatomegaly with possible tenderness on palpation;
• Fatigue, exercise intolerance, mild exertional dyspnea due to reduced systemic output.

On physical examination, the following signs may be present:

• Slight jaundice of the cheeks due to hepatic congestion;
• Pulsatile liver synchronous with the cardiac cycle;
• Hyperdynamic apical impulse, displaced downward;
• Low-pitched holosystolic murmur, best heard along the lower left sternal border and accentuated with deep inspiration (Carvallo’s sign).

A right-sided third heart sound and systolic thrill over the xiphoid may be found in advanced stages.

Diagnosis and Investigations

The diagnosis of tricuspid regurgitation requires appropriate integration of clinical data, physical signs, and imaging studies. Due to its frequent association with left-sided heart disease, a systematic approach is essential to recognize the specific features of tricuspid regurgitation and distinguish it from other conditions.

ECG is the initial test and may reveal signs of right atrial overload (tall, peaked P waves—"P pulmonale") and right ventricular overload (right axis deviation, prominent R waves in V1). These findings may be obscured by atrial fibrillation, a common arrhythmia in tricuspid regurgitation, especially in the setting of mitral disease.

Chest X-ray may show right-sided cardiomegaly with enlargement of the right atrium and ventricle and a prominent right heart border. Signs of systemic venous congestion may be present, such as diaphragmatic elevation due to hepatomegaly or pleural effusions. The cardiac axis may appear vertical, with downward and medial displacement of the apex.

Transthoracic echocardiography, and transesophageal echo if needed for preoperative evaluation or in inconclusive cases, is the reference diagnostic tool. It allows assessment of:

• Dilation of the right atrium and/or ventricle, with hyperkinesis or systolic dysfunction in advanced cases;
• Structural valvular abnormalities such as leaflet thickening, retraction, or displacement, and chordal anomalies;
• Vena contracta width and regurgitant jet area as semi-quantitative indicators of severity.

Doppler studies are essential for regurgitation quantification. Key parameters include:

• Vena contracta ≥ 0.7 cm and large systolic regurgitant jet suggest severe regurgitation;
• Diastolic flow reversal in hepatic veins, a pathognomonic sign of severe regurgitation;
• EROA (Effective Regurgitant Orifice Area) > 0.4 cm² and regurgitant volume > 45 mL per current guidelines.

In selected cases, especially in surgical candidates, right heart catheterization is indicated. It allows direct measurement of right-sided pressures, assessment of a pathological systolic atrioventricular gradient, and evaluation of cardiac output and pulmonary/hepatic venous pressures.

Treatment and Prognosis

Therapeutic management of tricuspid regurgitation depends mainly on:

• Severity of regurgitation
• Right ventricular function
• Presence of associated valvular disease
• Systemic congestion signs and NYHA class

In mild and asymptomatic isolated forms, clinical and echocardiographic monitoring may suffice. Endocarditis prophylaxis is recommended in at-risk contexts. If symptoms or systemic congestion occur, medical therapy aims to improve right ventricular function and reduce congestion:

• Loop diuretics (e.g., furosemide) to reduce fluid retention;
• Aldosterone antagonists (e.g., spironolactone) for anasarca and ascites management;
• Vasodilators in cases with high right ventricular afterload.

Surgical therapy is indicated for symptomatic severe regurgitation or in asymptomatic patients undergoing surgery for other valves (e.g., mitral or aortic), especially with right ventricular dilation. Surgical options include:

• Annuloplasty, when the valve is morphologically preserved;
• Valve replacement, required in cases of severe structural damage or annuloplasty failure.

Recently, transcatheter tricuspid valve repair techniques (TTVR) are under development, showing promise in high-risk surgical candidates.

Prognosis in tricuspid regurgitation is strongly linked to right ventricular function and the presence of severe pulmonary hypertension. Isolated, well-compensated forms may remain stable for years, whereas the onset of systemic symptoms or right heart failure significantly worsens long-term outcomes.

References
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