Tricuspid regurgitation occurs when the tricuspid valve allows retrograde flow of blood from the right ventricle into the right atrium during systole.
A small, clinically insignificant amount of tricuspid regurgitation is present in about 70% of adults and can be considered a variant of normal anatomy.
Most clinically significant tricuspid regurgitation is functional; elevation of right ventricular end-systolic pressure (RVESP) causes progressive dilatation of the right atrium and ventricle thereby causing distortion of the annulus. This leads to valvular insufficiency, despite otherwise_anatomically normal_leaflets and chordae. This may be due to right ventricular pathology, pulmonary hypertension, or left heart failure.
Intrinsic valvular damage can be caused by infective endocarditis and rheumatic fever, but are a much less common cause of tricuspid regurgitation than dilation of the annulus.
Tricuspid regurgitation is also associated with Ebstein’s cardiac anomaly, a birth defect associated with lithium exposure in utero.
Tricuspid regurgitation is usually asymptomatic.
Some patients with more severe tricuspid regurgitation may present with a pulsating sensation in the neckfrom distended jugular veins and signs of right heart failure, such as peripheral edema, ascites, and painful hepatosplenomegaly.
Tricuspid regurgitation causes a holosystolic murmur heard best at the right or left mid-sternal borderthat becomes louder with maneuvers that increase venous return (e.g. inspiration). An extremely dilated right ventricle may have an associated right-sided S3.
Occasionally the systolic murmur is transmitted through the portal veins to the liver.
A pulsatile liver is virtually pathognomonic of tricuspid regurgitation. This is due to pulsatile flow through the portal vein, which may also be detected ultrasonographically.
Echocardiographyis the gold standard for diagnosing tricuspid regurgitation and may reveal valvular abnormalities, regurgitant flow, and associated right and/or left heart pathology.
Chest X-ray is_usually normal_, but may show an enlarged superior vena cava, right atrium, or right ventricle.
Electrocardiogram (ECG) may demonstrate nonspecific ST segment and T wave abnormalities over the precordial leads, consistent with right ventricular dysfunction.
The retrograde pressure wave from flow of blood back into the right atrium during systole may be transmitted to the jugular veins, leading to giant “v” or “cv” waves on jugular venous pulse tracing.
Prominent “cv” waves on jugular venous pulse tracing are pathognomonic of tricuspid regurgitation.
Medical therapy is the first-line management for symptomatic tricuspid regurgitation. Appropriate agents include:
Tricuspid regurgitation in the setting of infective endocarditis requires treatment with an appropriate antibiotic.
Tricuspid regurgitation secondary to pulmonary arterial hypertension (PAH) may improve with reduction of the pulmonary arterial pressure. This may be achieved through agents like phosphodiesterase inhibitors (sildenafil, tadalafil) or endothelin receptor antagonists (bosentan) in the setting of primary PAH, or mitral balloon valvuloplasty in the setting of mitral stenosis.
Valve repair or replacement surgery is indicated for tricuspid regurgitation in patients with:
Annuloplasty is indicated when dilatation of the valve annulus is the underlying cause of the regurgitation, and symptoms are severe.