Functional Tricuspid Regurgitation

Functional (secondary) tricuspid regurgitation is regurgitation through structurally normal leaflets, caused by right ventricular or right atrial remodelling and annular dilatation. It accounts for 80 to 90% of significant tricuspid regurgitation.

Moderate or severe regurgitation rises with age, to about 4% over age 75, and is a strong independent predictor of death and heart failure admission. Common settings are left sided valve disease and left heart failure, pulmonary arterial hypertension, chronic thromboembolic disease, atrial fibrillation and cardiomyopathy.

Two forms exist. Ventricular functional regurgitation arises from right ventricular dilatation with leaflet tethering. Atrial functional regurgitation arises from right atrial and annular dilatation in long standing atrial fibrillation with preserved ventricular function.

Severity: severe is vena contracta 7 mm or more, effective regurgitant orifice area 40 mm2 or more, regurgitant volume 45 mL or more. Massive is vena contracta 14 to 20 mm, orifice area 60 to 79 mm2; torrential is vena contracta 21 mm or more, orifice area 80 mm2 or more.

Pathophysiology.

Annular dilatation (anteroposterior and septolateral, with a flat, circular annulus) and right ventricular enlargement displace the papillary muscles and tether the leaflets, so they fail to coapt.

Regurgitation adds volume load, which promotes further dilatation and a cycle of progression. Raised right atrial pressure causes hepatic congestion, cardiorenal syndrome, protein losing enteropathy and ascites.

Septal flattening reduces left ventricular filling. Late disease carries irreversible right ventricular failure and organ dysfunction, so timing of intervention matters.

Fatigue, exertional dyspnoea, abdominal distension, ascites, peripheral oedema, early satiety and right upper quadrant discomfort. Examination: raised jugular venous pressure with prominent v waves, a pulsatile liver, a parasternal heave, a holosystolic murmur at the left lower sternal edge that increases on inspiration (it may be absent when regurgitation is torrential), a third heart sound and ascites. Atrial fibrillation is common.

• Echocardiography: quantify regurgitation (vena contracta 7 mm or more, effective regurgitant orifice area 40 mm2 or more, regurgitant volume 45 mL or more indicate severe disease), with hepatic vein systolic flow reversal and a dense triangular continuous wave jet.
• Measure annular diameter (over 40 mm, or over 21 mm/m2, is dilated), leaflet tenting, and right atrial and ventricular size.
• Also measure TAPSE (under 17 mm abnormal), tricuspid annular S' (under 9.5 cm/s), fractional area change (under 35%), inferior vena cava size and pulmonary pressure.
• Cardiac CT or MRI: right ventricular volumes and ejection fraction (under 45% abnormal), annulus and anatomy for intervention.
• Right heart catheterisation for pulmonary vascular resistance (over 5 Wood units raises risk of isolated surgery) and wedge pressure.
• NT-proBNP, creatinine, liver tests and albumin (bilirubin and renal function predict surgical risk).
• Look for the cause: left sided valve disease, pulmonary hypertension, atrial fibrillation, cardiomyopathy and device leads.

Differential diagnosis.

• Primary tricuspid disease: Ebstein anomaly, flail leaflet, rheumatic, carcinoid and endocarditic regurgitation.
• Pacemaker or defibrillator lead related regurgitation.
• Constrictive pericarditis and restrictive cardiomyopathy.
• Liver disease or nephrotic syndrome with ascites and oedema.

Treat the cause. Correct left sided valve disease (mitral intervention first when significant), treat pulmonary hypertension (left heart disease optimisation, pulmonary vasodilators only in group 1 disease and under specialist direction), restore sinus rhythm in atrial fibrillation, and treat sleep apnoea and lung disease.

Decongestion.

• Furosemide 40 to 160 mg orally once or twice daily, or torsemide 20 to 100 mg daily, or bumetanide 1 to 5 mg daily (more reliable absorption in gut oedema).
• In decompensation, intravenous furosemide 40 to 80 mg bolus, then 5 to 20 mg/h infusion. Titrate to dry weight and weight loss of 0.5 to 1 kg daily.
• Add spironolactone 25 to 100 mg daily (potassium under 5.0 mmol/L, eGFR over 30; check at 1 and 4 weeks).
• Alternatively add acetazolamide 250 to 500 mg daily for 1 to 3 days, or metolazone 2.5 to 5 mg daily in short courses with daily electrolytes and creatinine.
• SGLT2 inhibitor when there is heart failure: dapagliflozin 10 mg daily (eGFR 25 or over), empagliflozin 10 mg daily (eGFR 20 or over).
• Sodium restriction to about 2 g daily; large volume paracentesis with albumin 6 to 8 g for each litre removed when tense. Avoid over diuresis.

Atrial fibrillation. Early rhythm control, catheter ablation, and anticoagulation.

• Apixaban 5 mg twice daily (2.5 mg twice daily when two of age 80 or over, weight 60 kg or under, creatinine 133 micromol/L or over).
• Or rivaroxaban 20 mg once daily with food (15 mg when creatinine clearance is 15 to 49 mL/min).

Intervention (before irreversible right ventricular and organ dysfunction).

• Surgical annuloplasty (ring) at the time of left sided surgery for severe regurgitation, moderate regurgitation, or mild regurgitation with annular diameter over 40 mm.
• Isolated surgery for symptomatic severe regurgitation (or progressive right ventricular dilatation) without severe right ventricular dysfunction, high pulmonary vascular resistance or advanced liver and kidney failure. Operative mortality is higher with advanced disease.
• Transcatheter edge-to-edge repair, annuloplasty or valve replacement for symptomatic severe regurgitation at high surgical risk: improves symptoms and quality of life. Caval valve implantation is used in selected patients.
• Antithrombotic therapy after surgical annuloplasty or bioprosthesis: warfarin to INR 2.0 to 3.0 for 3 months, then aspirin 75 to 100 mg daily.
• After transcatheter replacement: warfarin to INR 2.0 to 3.0 for 3 to 6 months.
• After edge-to-edge repair: antiplatelet therapy for 3 to 6 months, or anticoagulation when already indicated.

Monitoring. Clinical review and echocardiography every 6 to 12 months (every 3 to 6 months when severe), NT-proBNP, creatinine, electrolytes and liver tests with every diuretic change and at least every 3 months.

Referral and escalation. Refer symptomatic severe regurgitation early to a heart team and a tricuspid valve service. Urgent referral for refractory congestion, rising bilirubin or creatinine, or falling right ventricular function.

Special groups.

• Pregnancy: tolerated with preserved right ventricular function; limit diuretics; stop spironolactone and SGLT2 inhibitors.
• Older adults: low starting diuretic doses, watch for hyponatraemia and falls; transcatheter options are favoured.
• Kidney or liver impairment: diuretic resistance is common; combine loop diuretics with thiazide type agents carefully and adjust warfarin to INR.