Tricuspid regurgitation

Overview

•Tricuspid valve fails to close during systole → blood leaks from RV into RA

•Secondary (functional) TR accounts for ~80% of significant cases - structurally normal valve fails to coapt due to RV dilation and annular dilatation

•Primary TR - structural valve disease (infective endocarditis, rheumatic, carcinoid)

•Mild TR detectable in up to 65-85% of normal individuals on echo - often a normal variant

Aetiology

Primary vs secondary TR

Feature	Primary TR	Secondary TR
Valve structure	Structurally abnormal	Structurally normal
Mechanism	Leaflet/chordal destruction or thickening	RV dilation → annular dilatation → malcoaptation
Key causes	IE (PWID - S. aureus), rheumatic disease, carcinoid (TR + stenosis)	Left heart disease, pulmonary hypertension, heart failure

Presentation

•Mild/moderate TR often asymptomatic - incidental echo finding

•Peripheral oedema, ascites, abdominal discomfort - raised RA pressure → systemic venous congestion

•Pulsatile hepatomegaly - systolic pulsation from transmitted regurgitant wave; highly specific sign

•Raised JVP with prominent cv wave - regurgitant jet merges c and v waves into large systolic rise

•Pan-systolic murmur - left lower sternal edge (4th intercostal space); louder on inspiration (Carvallo's sign)

•RV heave - sustained left parasternal lift from RV enlargement

•Fatigue, exercise intolerance - reduced RV forward output

💡

Carvallo's sign: TR murmur becomes louder on inspiration (increased venous return augments regurgitant volume). Key bedside discriminator from mitral regurgitation, which does not increase with inspiration.

Investigations

🥇 First-line

•TTE - confirms TR, grades severity, assesses RV size and function, estimates PA pressure, evaluates valve morphology

•ECG - RA enlargement (peaked P waves 'P pulmonale'), RBBB, AF

•Chest X-ray - cardiomegaly, right heart border prominence, pleural effusions

•Bloods - FBC, U&Es, LFTs (hepatic congestion), BNP/NT-proBNP

🥈 Second-line

•TOE - better leaflet visualisation before surgery; when TTE suboptimal

•Gold standard RV assessment: cardiac MRI - volumetric assessment when echo technically limited

•Right heart catheterisation - invasive; measures PA pressures and cardiac output before surgical planning

Severity	Vena contracta	EROA
Mild	<0.3 cm	<20 mm²
Moderate	0.3-0.69 cm	20-39 mm²
Severe	≥0.7 cm	≥40 mm²; systolic hepatic vein flow reversal

Differential diagnosis

•Mitral regurgitation - pan-systolic murmur at apex, radiates to axilla, louder on expiration, does NOT increase with inspiration

•VSD - harsh pan-systolic murmur at left lower sternal edge; distinguished by echo

•Tricuspid stenosis - mid-diastolic murmur at left lower sternal edge; prominent a wave (not cv wave) in JVP

•Pulmonary regurgitation - early diastolic murmur (Graham Steell) at left upper sternal edge

Management

•Treat the underlying cause first - optimise left heart failure, repair mitral valve disease, treat pulmonary hypertension; functional TR may improve or resolve

•Diuretics: furosemide ± spironolactone (for ascites) - reduces venous congestion; does not address TR itself

•Rate control in AF: bisoprolol or digoxin - reduces AF-driven annular dilatation

🥈 Second-line

•surgical tricuspid valve repair (annuloplasty) - indicated for severe TR at time of left-sided valve surgery, or isolated severe symptomatic TR with preserved RV function; repair preferred over replacement

•Transcatheter edge-to-edge repair (TEER - TriClip/PASCAL) - emerging option for high-surgical-risk patients with severe TR

🥉 Third-line

•tricuspid valve replacement - when repair not feasible (carcinoid, heavily calcified/destructed valve); bioprosthetic valves preferred due to thrombosis risk with mechanical valves at low-flow pressures

⚠️

For mechanical tricuspid valves: warfarin is preferred over DOACs - DOACs are not approved for this indication and carry higher thrombosis risk in the right heart low-flow environment.

Complications

•Progressive right heart failure - RV dilation perpetuates a self-worsening cycle of TR and further RV impairment

•Cardiac cirrhosis - chronic raised RA pressure → centrilobular fibrosis, coagulopathy, jaundice

•Cardiorenal syndrome - venous hypertension reduces renal perfusion; common in advanced TR

•Atrial fibrillation - RA dilatation predisposes to AF, which worsens TR (bidirectional relationship)

•Infective endocarditis in PWID - septic pulmonary emboli → multiple cavitating lung lesions

Prognosis

•Prognosis tied to underlying cause and degree of RV dysfunction - not TR severity alone

•Severe TR with RV dysfunction = high-risk surgical population; operative mortality rises sharply with impaired RV function

•Earlier intervention (before irreversible RV dilation) increasingly advocated; cardiac cachexia, renal impairment, and hepatic dysfunction are markers of poor prognosis