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Tricuspid Regurgitation

  • Author: Mary C Mancini, MD, PhD, MMM; Chief Editor: Richard A Lange, MD, MBA  more...
 
Updated: Jun 02, 2014
 

Background

Tricuspid regurgitation may result from structural alterations of any or all of the components of the tricuspid valve apparatus (see Anatomy). 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 right ventricular (RV) dilatation.

Common presenting complaints in patients with LV dysfunction include the following (see Presentation):

  • Dyspnea on exertion
  • Orthopnea
  • Paroxysmal nocturnal dyspnea
  • Ascites
  • Peripheral edema

Color flow Doppler echocardiography is a mainstay for evaluating tricuspid regurgitation (see Workup). Depending on the etiology and severity of tricuspid regurgitation, treatment may involve medication or surgical repair or replacement of the valve. (See Treatment and Medication.)

See also Tricuspid Atresia and Tricuspid Stenosis.

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Anatomy

The right atrioventricular valve complex (the tricuspid valve) comprises the following:

  • Three valve leaflets (although as few as two and as many as six leaflets have been described)
  • Annulus
  • Supporting chordae tendineae
  • Papillary muscles

The coordinated actions of the tricuspid valve are made possible by the atrial and ventricular masses, conduction system tissue, and support structure of the fibroelastic cardiac skeleton.

Pathophysiologic variants include the following:

See Tricuspid Valve Anatomy for further details.

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Pathophysiology

The pathophysiology of tricuspid regurgitation focuses on the structural incompetence of the valve. The incompetence can result from primary structural abnormalities of the leaflets and chordae or, more often, be secondary to 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.

Inspiration increases the severity of tricuspid regurgitation. Inspiration induces widening of the RV, which enlarges the tricuspid valve annulus and thus increases the effective regurgitant orifice area.[2]

Chronically, tricuspid regurgitation leads to RV volume overload, which results in right-sided congestive heart failure (CHF). This manifests as hepatic congestion, peripheral edema, and ascites.

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Etiology

Pure tricuspid regurgitation can be caused by at least 10 conditions, as follows:

  • Rheumatic heart disease
  • Endocarditis
  • Ebstein anomaly
  • Tricuspid valve prolapse
  • Carcinoid
  • Papillary muscle dysfunction
  • Trauma
  • Connective-tissue diseases
  • Medications
  • RV dilatation

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.

Endocarditis is an important cause of tricuspid regurgitation. Factors that can contribute to infection of the valve include alcoholism, intravenous drug use, neoplasms, infected indwelling catheters, extensive burns, and immune deficiency. 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.

Ebstein anomaly 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]

The incidence of tricuspid valve prolapse (floppy tricuspid valve) varies from 0.3-3.2%. The lesion appears to be associated with prolapse of the mitral valve; uncommonly, it 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 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 RV may damage the structures of the tricuspid valve, resulting in insufficiency of the structure.[5] Stab wounds and projectiles are the most common sources of trauma in these cases.

Marfan syndrome or other connective-tissue diseases (eg, osteogenesis imperfecta, Ehlers-Danlos syndrome) may cause tricuspid regurgitation. Dysfunction of other heart valves is typically present, as well. The tricuspid 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.

In persons with an 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, the leaflets cannot coapt properly. The following disorders can cause RV dilatation:

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Epidemiology

The incidence of tricuspid regurgitation in the United States appears to be 0.9%. Internationally, the incidence of tricuspid regurgitation also appears to be less than 1%. No racial or sexual differences in incidence are apparent.

Age at presentation varies with the etiology of tricuspid regurgitation. 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 take precedence; these include carcinoid, bacterial endocarditis, and heart failure.

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Prognosis

The prognosis in patients with tricuspid regurgitation is generally good. If the cause of the regurgitation is infection, removal of the valve generally cures the problem, provided that the source of the infection (eg, poor dentition, illicit drug use) is eliminated. For patients with accompanying pulmonary hypertension or cardiac dilatation, the prognosis is directly related to the prognosis for those conditions.

Complications of tricuspid regurgitation include cardiac cirrhosis, ascites, thrombus formation, and embolization. Possible complications of operative intervention include heart block, arrhythmias, thrombosis of the prosthetic valve, and infection.

Mortality/morbidity

The morbidity and mortality associated with tricuspid regurgitation vary with 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. Tricuspid regurgitation resulting from myocardial dysfunction or dilatation has a mortality of up to 50% at 5 years.

Mortality rates with correction are approximately 10%. Tricuspid valve replacement for severe tricuspid regurgitation can be performed with an acceptable operative mortality if patients undergo surgery before the onset of advanced heart failure symptoms.[6]

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Contributor Information and Disclosures
Author

Mary C Mancini, MD, PhD, MMM Professor and Chief of Cardiothoracic Surgery, Department of Surgery, Louisiana State University School of Medicine in Shreveport

Mary C Mancini, MD, PhD, MMM is a member of the following medical societies: American Association for Thoracic Surgery, American College of Surgeons, American Surgical Association, Society of Thoracic Surgeons, Phi Beta Kappa

Disclosure: Nothing to disclose.

Chief Editor

Richard A Lange, MD, MBA President, Texas Tech University Health Sciences Center, Dean, Paul L Foster School of Medicine

Richard A Lange, MD, MBA is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American Heart Association, Association of Subspecialty Professors

Disclosure: Nothing to disclose.

Acknowledgements

Martin Gerard Keane, MD, FACC, FAHA Associate Professor, Cardiovascular Medicine Division, Department of Medicine, University of Pennsylvania School of Medicine

Martin Gerard Keane, MD, FACC, FAHA is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Heart Association, American Society of Echocardiography, Pennsylvania Medical Society, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Ronald J Oudiz, MD, FACP, FACC, FCCP Professor of Medicine, University of California, Los Angeles, David Geffen School of Medicine; Director, Liu Center for Pulmonary Hypertension, Division of Cardiology, LA Biomedical Research Institute at Harbor-UCLA Medical Center

Ronald J Oudiz, MD, FACP, FACC, FCCP is a member of the following medical societies: American College of Cardiology, American College of Chest Physicians, American College of Physicians, American Heart Association, and American Thoracic Society

Disclosure: Actelion Grant/research funds Clinical Trials + honoraria; Ikaria Grant/research funds Clinical Trials + honoraria; Gilead Grant/research funds Clinical Trials + honoraria; Pfizer Grant/research funds Clinical Trials + honoraria; United Therapeutics Grant/research funds Clinical Trials + honoraria; Lilly Grant/research funds Clinical Trials + honoraria; Lung LLC Clinical Trials + honoraria; Bayer Grant/research funds Consulting; Medtronic Consulting fee Consulting; Novartis Consulting fee Consulting

Frank M Sheridan, MD Cardiologist, Providence Everett Medical Center

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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