Tricuspid valve dysfunction can result from morphological alterations in the valve or from functional aberrations of the myocardium. Tricuspid stenosis is almost always rheumatic in origin and is generally accompanied by mitral and aortic valve involvement. 
Most stenotic tricuspid valves are associated with clinical evidence of regurgitation that can be documented by performing a physical examination (murmur), echocardiography, or angiography. Stenotic tricuspid valves are always anatomically abnormal, and the cause is limited to a few conditions. With the exceptions of congenital causes or active infective endocarditis, tricuspid stenosis takes years to develop. [2, 3]
Tricuspid stenosis results from alterations in the structure of the tricuspid valve that precipitate inadequate excursion of the valve leaflets. The most common etiology is rheumatic fever, and tricuspid valve involvement occurs universally with mitral and aortic valve involvement. With rheumatic tricuspid stenosis, the valve leaflets become thickened and sclerotic as the chordae tendineae become shortened. The restricted valve opening hampers blood flow into the right ventricle and, subsequently, to the pulmonary vasculature. Right atrial enlargement is observed as a consequence. The obstructed venous return results in hepatic enlargement, decreased pulmonary blood flow, and peripheral edema. Other rare causes of tricuspid stenosis include carcinoid syndrome, endocarditis, endomyocardial fibrosis, systemic lupus erythematosus, and congenital tricuspid atresia. [2, 3, 4]
In the rare instances of congenital tricuspid stenosis, the valve leaflets may manifest various forms of deformity, which can include deformed leaflets, deformed chordae, and displacement of the entire valve apparatus. Other cardiac anomalies are usually present. 
United States data
Tricuspid stenosis is rare, occurring in less than 1% of the population. While found in approximately 15% of patients with rheumatic heart disease at autopsy, it is estimated to be clinically significant in only 5% of these patients. The incidence of the congenital form of the disease is less than 1%.
Tricuspid stenosis is found in approximately 3% of the international population. It is more prevalent in areas with a high incidence of rheumatic fever. The congenital form of the disease is rare and true incidence is not available.
Race-, sex-, and age-related demographics
No racial predisposition is apparent.
Tricuspid stenosis is observed more commonly in women than in men, similar to mitral stenosis of rheumatic origin. The congenital form of the disease has a slightly higher male predominance.
Tricuspid stenosis can present as a congenital lesion or later in life when it is due to some other condition. The congenital form accounts for approximately 0.3% of all congenital heart disease cases. The frequency of tricuspid stenosis in the older population, due to secondary causes, ranges from 0.3-3.2%.
The mortality associated with tricuspid stenosis depends on the precipitating cause. The general mortality rate is approximately 5%.
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Mary C Mancini, MD, PhD, MMM Surgeon-in-Chief and Director of Cardiothoracic Surgery, Christus Highland
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, Phi Beta Kappa, Society of Thoracic Surgeons
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: Received salary from Medscape for employment. for: Medscape.
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 Thoracic Society, American College of Physicians, American Heart Association
Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: Actelion, Bayer, Gilead, Lung Biotechnology, United Therapeutics<br/>Received research grant from: Actelion, Bayer, Gilead, Ikaria, Lung Biotechnology, Pfizer, Reata, United Therapeutics<br/>Received income in an amount equal to or greater than $250 from: Actelion, Bayer, Gilead, Lung Biotechnology, Medtronic, Reata, United Therapeutics.
Richard A Lange, MD, MBA President, Texas Tech University Health Sciences Center, Dean, Paul L Foster School of Medicine
Disclosure: Nothing to disclose.
Park W Willis IV, MD Sarah Graham Distinguished Professor of Medicine and Pediatrics, University of North Carolina at Chapel Hill School of Medicine
Park W Willis IV, MD is a member of the following medical societies: American Society of Echocardiography
Disclosure: Nothing to disclose.
The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author Frank M Sheridan, MD to the development and writing of this article.
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