6th May 2025

Tricuspid valve disease

Tricuspid regurgitation

Pathology and Epidemiology

Tricuspid regurgitation (TR) is a common finding in the general population, while at least moderate regurgitation is present in 0.55% of the general population, with prevalence increasing with age.

It is overwhelmingly secondary in nature, with >90% of cases due to either pressure or volume loading of the right ventricle or atrial dilation. In the context of HFrEF, tricuspid regurgitation is a very common finding due to elevated pulmonary pressures.

Primary valve disease aetiology is similar in nature to mitral disease, with infective endocarditis and degenerative valve disease common causes, though rarer disease such as carcinoid syndrome, iatrogenic damage secondary to pacing devices or congenital abnormalities such as Ebstein’s anomaly are other recognised causes.

Presentation – Symptoms

TR can be well tolerated for long periods of time. When more severe it can be associated with signs of right heart failure, including:

• Dyspnoea
• Fatigue
• Cyanosis
• Peripheral oedema
• Right upper quadrant pain due to hepatic congestion

As with other valve diseases, if there is a specific underlying cause then there may be symptoms specific to that disease ie splinter haemorrhages in infective endocarditis, flushing and diarrhoea in carcinoid syndrome or symptoms of heart failure in secondary regurgitation due to HFrEF.

Presentation – Signs

Signs of TR are typically those of right sided heart failure, including peripheral oedema, ascites, raised jugular venous pressure and right upper quadrant tenderness.

Signs specific to TR will include:

• High pitched systolic murmur in the tricuspid region, louder on inspiration
• Loud P2 (in absence of pulmonary hypertension)

Diagnosis and Investigations

Significant TR is often found incidentally due to a clinical diagnosis of heart failure. Typical workup will include standard investigations mentioned above, ECG, chest Xray, echocardiogram and blood tests.

ECG will likely be non-specific, though there may be evidence of P pulmonale with peaked P waves, there may be complete or incomplete right bundle branch block. Chest Xray may show cardiomegaly, pleural effusions and pulmonary congestion.

Routine blood tests may demonstrate obstructive liver function tests due to the congestion alongside elevated NT pro BNP due to increased cardiac wall stress.

Echocardiography will demonstrate evidence of regurgitation on colour flow and spectral doppler, while 2d may suggest the aetiology, be it RV dilation, valve leaflet perforation or displaced tricuspid leaflet in Ebstein’s anomaly.

Grading Severity 

Severity is typically graded using a range of echocardiographic parameters including spectral doppler profile, vena contracta width, systolic flow reversal in the hepatic veins and regurgitant volume. The knowledge of these values is beyond requirements at MRCP. 

Alongside echo, cardiac MRI is often used to help evaluate the right ventricle morphology and function, as direct morphological and functional assessment is challenging with echo.

Treatment options

Medical therapy of TR is typically limited to diuretics to help offload the right ventricle.

Surgical tricuspid valve replacement is possible in both primary and secondary TR. In secondary regurgitation annuloplasty with prosthetic rings is preferable to replacement where technically feasible.

Like transcatheter mitral edge to edge repair, similar technologies are being developed for the tricuspid valve, though these remain in their infancy and are not commonly performed outside of research setting.

Criteria for interventional treatment 

In primary TR, surgery is recommended for severe disease if either the patient is undergoing left sided valve surgery, or there is evidence of isolated severe primary TR. The strength of both these recommendations however is low.

In secondary TR, surgery is recommended in severe disease for patients undergoing left sided valve surgery, or in those with significant symptoms or RV dilation in the absence of severe RV dysfunction, severe LV dysfunction or severe pulmonary hypertension.