Tricuspid Regurgitation
Backward flow of blood from the right ventricle into the right atrium during systole. Most commonly secondary (functional) due to RV dilatation from pulmonary hypertension or left-sided heart disease.
Key Facts
Most commonly functional/secondary (~85%): RV dilatation from pulmonary hypertension, left-sided heart disease, or RV infarction Primary causes: infective endocarditis (IV drug use), rheumatic disease, carcinoid syndrome, Ebstein anomaly, radiation Murmur: pansystolic at left lower sternal edge, increases with inspiration (Carvallo sign) Signs of right heart failure: elevated JVP with prominent CV waves, hepatomegaly (pulsatile), peripheral oedema, ascites Treatment: primarily directed at the underlying cause; diuretics for congestion Surgery: tricuspid annuloplasty at time of left-sided valve surgery if significant TR; isolated TV surgery less common
Overview
Key Facts
Tricuspid regurgitation (TR) is the backward flow of blood from the right ventricle to the right atrium during systole. Mild TR is extremely common and often physiological. Significant TR is most often secondary to right ventricular dilatation.
Epidemiology
- Mild/trace TR: detected in up to 70-80% of normal echocardiograms
- Clinically significant TR: prevalence ~0.5-1%
- Functional TR accounts for ~85% of significant cases
- Increasing prevalence with age and in patients with left-sided heart disease
Aetiology
Secondary (functional) — most common:
- Pulmonary hypertension (any cause)
- Left-sided heart disease (mitral valve disease, LV failure)
- RV infarction
- Atrial fibrillation (annular dilatation from RA enlargement)
- Pulmonary embolism, cor pulmonale
Primary:
- Infective endocarditis (especially IV drug users — right-sided)
- Rheumatic heart disease (usually with mitral involvement)
- Carcinoid syndrome (plaque deposits on valve)
- Ebstein anomaly (apical displacement of tricuspid valve)
- Radiation, drugs (ergotamine, fenfluramine)
- Pacemaker/ICD lead impingement
- Myxomatous degeneration, trauma
Pathophysiology
- RV dilatation stretches the tricuspid annulus → leaflet coaptation failure → regurgitation
- Volume overload of RA and RV → further dilatation → worsening TR (vicious cycle)
- Elevated RA pressure transmitted to systemic veins → hepatic congestion, peripheral oedema, ascites
- In severe TR, reversal of flow in hepatic veins during systole
Clinical Presentation
Typical Presentation
- Often overshadowed by symptoms of the underlying left-sided heart disease
- Right heart failure symptoms: peripheral oedema, abdominal distension (ascites), hepatomegaly
- Fatigue, exercise intolerance (low cardiac output)
- Dyspnoea (from associated pulmonary hypertension or left-sided disease)
Examination Findings
- Pansystolic murmur at left lower sternal edge, increases with inspiration (Carvallo sign)
- Elevated JVP with prominent CV waves (systolic waves from regurgitant flow)
- Pulsatile hepatomegaly
- Peripheral oedema, ascites
- RV heave (parasternal lift)
- In severe TR with low cardiac output: murmur may be soft or absent
Red Flags
- Progressive right heart failure despite treatment of left-sided disease
- Severe TR with RV dysfunction
- TR with IV drug use (suspect endocarditis)
- Carcinoid features: flushing, diarrhoea, wheezing
Differential Diagnosis
| Diagnosis | Key Features | Investigation |
|---|---|---|
| Mitral regurgitation | Pansystolic at apex, radiates to axilla, does not increase with inspiration | Echocardiography |
| VSD | Pansystolic at LLSE, thrill, does not increase with inspiration | Echocardiography |
| Pulmonary regurgitation | Early diastolic murmur at LUSE | Echocardiography |
| Constrictive pericarditis | Elevated JVP (Kussmaul sign), pericardial knock | Echo, CT, MRI |
| Hepatic cirrhosis | Ascites, jaundice, spider naevi — may coexist | LFTs, USS liver |
| Budd-Chiari syndrome | Hepatomegaly, ascites, abdominal pain | Hepatic vein Doppler |
Diagnosis / Investigation
Bedside
- ECG: AF, RA enlargement (tall P waves in II — P pulmonale), RVH, RBBB
- JVP assessment: CV waves
Bloods
- BNP/NT-proBNP: heart failure severity
- LFTs: congestive hepatopathy (elevated bilirubin, transaminases)
- FBC: polycythaemia in chronic hypoxia
- Blood cultures: if endocarditis suspected
- 5-HIAA (24h urine): if carcinoid suspected
Imaging
- Echocardiography: TR severity (vena contracta, EROA, jet area), RV size and function (TAPSE, FAC), RA size, PA pressure estimation, valve morphology
- Cardiac MRI: RV volumes and function (gold standard for RV assessment)
- CT chest: pulmonary hypertension assessment
Special Tests
- Right heart catheterisation: definitive haemodynamic assessment, PA pressures
- Exercise echo: assess functional significance of TR
Management
Non-pharmacological
- Sodium and fluid restriction for right heart failure
- Treat underlying cause (left-sided heart disease, pulmonary hypertension)
Pharmacological
- Diuretics: loop diuretics (furosemide 40-120mg OD) ± spironolactone 25-50mg OD for right heart congestion
- Treat underlying cause: optimise LV function, control AF, manage pulmonary hypertension
- Anticoagulation for AF if indicated
Surgical/Interventional
- Tricuspid annuloplasty: performed at time of left-sided valve surgery if moderate or severe TR (NICE NG208)
- Tricuspid valve replacement: if severe primary TR with valve destruction (e.g., endocarditis)
- Transcatheter tricuspid valve repair (e.g., TriClip): emerging therapy for inoperable patients
- Isolated TV surgery: higher operative mortality (~5-10%); reserved for severe symptomatic TR
Referral Criteria
- Severe TR with right heart failure: cardiology assessment
- TR associated with left-sided valve surgery: consider concurrent annuloplasty
- Suspected endocarditis: urgent referral
Prognosis
- Severe TR is associated with increased mortality regardless of LV function or PA pressures
- Functional TR may improve with treatment of underlying cause (e.g., after mitral valve surgery, AF treatment)
- Isolated severe TR: 5-year mortality ~25-40%
- Post-tricuspid annuloplasty: good outcomes if performed at time of left-sided surgery
- Isolated tricuspid surgery: operative mortality ~5-10%
- Progressive RV dysfunction with severe TR carries poor prognosis
Other Relevant Information
Causes of Tricuspid Regurgitation by Category
| Category | Examples |
|---|---|
| Functional | LV failure, pulmonary HTN, AF, RV infarct |
| Infective | Endocarditis (IVDU) |
| Congenital | Ebstein anomaly |
| Rheumatic | Usually with mitral disease |
| Carcinoid | Serotonin-mediated plaque deposition |
| Iatrogenic | Pacemaker/ICD leads, radiation |
JVP Waveform in TR
| Wave | Normal | In TR |
|---|---|---|
| a wave | Atrial contraction | May be absent in AF |
| c wave | Tricuspid closure | Merged into v wave |
| v wave | Passive atrial filling | Giant CV wave (regurgitant systolic wave) |