Tricuspid regurgitation may result from structural alterations of any one or all of the components of the tricuspid valve apparatus. Components include the leaflets, chordae tendinea, annulus, and papillary muscles or adjacent right ventricular (RV) muscle. The lesion may be classified as primary when it is caused by an intrinsic abnormality of the valve apparatus or as secondary when it is caused by RV dilatation.
The pathophysiology of tricuspid regurgitation focuses on the structural incompetence of the valve. The incompetent nature of the valve can result from primary structural abnormalities of the leaflets and chordae or from secondary myocardial dysfunction and dilatation.1
Tricuspid valve insufficiency due to leaflet abnormalities may be secondary to endocarditis or rheumatic heart disease. When due to the latter, it generally occurs in combination with tricuspid stenosis. Ebstein anomaly is the most common congenital form of tricuspid regurgitation.
In tricuspid regurgitation, chronic right ventricular volume overload results in right-sided congestive heart failure (CHF) manifested by hepatic congestion, peripheral edema, and ascites. For more on heart failure, see Medscape’s Heart Failure Resource Center.
Incidence of tricuspid regurgitation appears to be 0.9%.
Incidence of tricuspid regurgitation appears to be less than 1%.
The morbidity and mortality of the disease process are secondary to the underlying cause. In rheumatic disease, mortality rates with treatment are less than 3%. In Ebstein anomaly, mortality depends upon the severity of the valvular deformity and the feasibility of correction. Mortality rates with correction are approximately 10%. Tricuspid regurgitation resulting from myocardial dysfunction or dilatation has a mortality of up to 50% at 5 years.
No race predilection is apparent.
No sex predilection is apparent.
Ebstein anomaly can be detected at birth and during early childhood. In patients older than 15 years, the most common form of tricuspid regurgitation is rheumatic valvular disease. In the adult population, other predisposing factors, including carcinoid, bacterial endocarditis, and CHF, takes precedence.
The patient with tricuspid regurgitation presents with the signs and symptoms of right-sided heart failure. The spectrum of presenting symptoms is dependent upon whether the condition is secondary to left ventricular (LV) dysfunction. If it is, dyspnea on exertion, orthopnea, and paroxysmal nocturnal dyspnea accompany ascites and peripheral edema as common presenting complaints. Exercise intolerance may also be observed. The patient rarely reports angina, which may be present in the absence of coronary artery disease secondary to RV overload and strain.2
These patients must be questioned regarding intravenous drug use, history of rheumatic fever, and febrile episodes because bacterial endocarditis is a common cause of tricuspid valvular disease.
S3 gallop is present, and the following physical findings may be found:
Jugular venous distention with a prominent V wave: When present, a pansystolic murmur is heard along the lower left sternal border with inspiratory accentuation.
Diminished peripheral pulse volume secondary to impaired forward blood flow: Patients with this sign may have relative hypotension secondary to therapeutic interventions used to decrease volume overload.
Pulmonary rales if the tricuspid regurgitation is associated with LV dysfunction or mitral stenosis
RV heave and S 4 gallop that increases with inspiration
Cachexia and jaundice
Atrial fibrillation (For more information on atrial fibrillation, see Medscape’s Atrial Fibrillation Resource Center.)
A high-pitched pansystolic murmur (loudest in the fourth intercostal space in the parasternal region). The murmur is usually augmented during inspiration and is reduced in intensity and duration in the standing position and during a Valsalva maneuver. A short, early diastolic flow rumble may be present due to increased flow across the tricuspid valve.
Pure tricuspid regurgitation can be caused by at least 10 conditions.
Rheumatic heart disease
Tricuspid regurgitation secondary to rheumatic involvement is usually associated with mitral and aortic valve pathology.1
The valve develops diffuse fibrous thickening without commisural fusion, fused chordae, or calcific deposits. Occasionally, the chordae may be mildly thickened by fibrous tissue.
Rheumatic disease is the most common cause of pure tricuspid regurgitation due to deformation of the leaflets.
This is an important cause of tricuspid regurgitation. Precipitating factors that can contribute to infection of the valve include alcoholism, intravenous drug use, neoplasms, infected indwelling catheters, extensive burns, and immune deficiency disease.
The clinical presentation is often that of pneumonia from septic pulmonary emboli rather than CHF. Heart murmurs are frequently absent and blood cultures may be negative. Annular abscesses are not uncommon.
This entity is a congenital malformation of the tricuspid valve characterized by apical displacement of the annular insertion of the septal and posterior leaflets and atrialization of a portion of the ventricular myocardium.
Prognosis for these patients depends upon the degree of apical displacement of the tricuspid annulus and the severity of the regurgitation.3
Prolapse (floppy, redundant)
The incidence of floppy tricuspid valve varies from 0.3-3.2%.
The lesion appears to be associated with prolapse of the mitral valve and uncommonly occurs in an isolated fashion.
Histological examination of the floppy tricuspid valve shows alterations on the valve spongiosa.
Pure tricuspid regurgitation can occur as part of the carcinoid heart syndrome.
Fibrous white plaques form on the ventricular aspect of the tricuspid valve and endocardium, causing the valve to adhere to the RV wall.
Proper coaptation of the leaflets does not occur during systole, resulting in tricuspid regurgitation.4
Papillary muscle dysfunction
Papillary muscle dysfunction may result from necrosis (secondary to myocardial infarction), fibrosis, or infiltrative processes.
Although dysfunction secondary to myocardial infarction is less common than occurs with the mitral valve, the underlying cause must be determined in order to plan treatment.
Trauma to the right ventricle may damage the structures of the tricuspid valve, resulting in insufficiency of the structure.5
More commonly it is associated with stab wounds or projectile destruction of the valve.
Patients with Marfan syndrome or other connective-tissue diseases (eg, osteogenesis imperfecta, Ehlers-Danlos syndrome) may have tricuspid regurgitation.
Typically, dysfunction of other valves is also observed in the same patient.
The etiology of the regurgitation can be attributed to a floppy tricuspid valve and a mildly dilated tricuspid valve annulus.
Medications that act via serotoninergic pathways may cause valvular lesions similar to those observed with carcinoid.
Medications used to treat migraine (eg, methysergide), Parkinson disease (eg, pergolide), and obesity (eg, fenfluramine) have been associated with tricuspid regurgitation.
Anatomically normal tricuspid valve
A common etiology of tricuspid regurgitation is dilatation of the RV cavity.
The valve structures are normal; however, because of enlargement of the cavity and dilatation of the annulus, proper coaptation of the leaflets is not possible.
Causes of the dilatation include mitral stenosis, pulmonic stenosis or regurgitation, pulmonary hypertension, dilated cardiomyopathy, and RV failure.