Tricuspid Regurgitation 

  • Author: Mary C Mancini, MD, PhD; Chief Editor: Richard A Lange, MD   more...
 
Updated: Sep 27, 2011
 

Background

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.

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Pathophysiology

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 RV volume overload results in right-sided congestive heart failure (CHF) manifested by hepatic congestion, peripheral edema, and ascites.

With inspiration, the severity of tricuspid regurgitation increases, which is due to inspiratory-induced widening of the RV, which results in enlargement of the tricuspid valve annulus and an increase in the effective regurgitant orifice area.[2]

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Epidemiology

Frequency

United States

Incidence of tricuspid regurgitation appears to be 0.9%.

International

Incidence of tricuspid regurgitation appears to be less than 1%.

Mortality/Morbidity

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.

Race

No race predilection is apparent.

Sex

No sex predilection is apparent.

Age

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.

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Contributor Information and Disclosures
Author

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

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

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Martin 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.

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

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; Encysive 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; LungRx Clinical Trials + honoraria; Bayer Grant/research funds Consulting

Amer Suleman, MD  Private Practice

Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions

Disclosure: Nothing to disclose.

Chief Editor

Richard A Lange, MD  Professor and Executive Vice Chairman, Department of Medicine, Director, Office of Educational Programs, University of Texas Health Science Center at San Antonio

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

Disclosure: Nothing to disclose.

Additional Contributors

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author Frank Sheridan, MD to the development and writing of this article.

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