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Tricuspid Stenosis Clinical Presentation

  • Author: Mary C Mancini, MD, PhD, MMM; Chief Editor: Richard A Lange, MD, MBA  more...
 
Updated: Dec 18, 2014
 

History

See the list below:

  • Fatigue, due to limited cardiac output, may be present.
  • Systemic venous congestion leads to abdominal discomfort and swelling. The onset is usually gradual, but it may be rapid if atrial fibrillation or flutter develops. (For related information, see Medscape's Atrial Fibrillation Resource Center).
  • Dyspnea may be present but is not severe unless concomitant mitral valve disease is present.
  • Patients may complain about prominent pulsations in the neck.
  • When tricuspid stenosis occurs concomitantly with mitral stenosis, the decrement of cardiac output to the pulmonary bed may paradoxically diminish the dyspnea, hemoptysis, and orthopnea typically seen with mitral stenosis.
  • Obtain information regarding preceding rheumatic fever, symptoms of the carcinoid syndrome, and possible congenital abnormalities.
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Physical

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  • With sinus rhythm (more common with tricuspid stenosis than with mitral stenosis), the jugular venous pulse increases and the A wave is prominent (may be confused with an arterial pulse).
  • If atrial fibrillation occurs, the A wave is lost.
  • Peripheral edema and ascites are frequent.
  • Without significant mitral pathology, the patient should not be dyspneic and can probably lie flat without symptoms.
  • A prominent right atrium may be palpable to the right of the sternum. If not obscured by mitral stenosis sounds, a tricuspid opening snap may be heard. A diastolic murmur is audible along the left sternal border or at the xiphoid, which increases with inspiration. Often, tricuspid regurgitation is also present, represented by a holosystolic murmur in a similar location.
  • The first heart sound may be split widely. The second heart sound may be single. This single sound is due to the inaudible closure of the pulmonary valve from the decrease in blood flow through the stenotic tricuspid valve.
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Causes

At least 4 conditions can cause obstruction of the native tricuspid valve. These include (1) rheumatic heart disease, (2) congenital abnormalities, (3) metabolic or enzymatic abnormalities, and (4) active infective endocarditis.

  • Rheumatic tricuspid stenosis: In this entity, diffuse thickening of the leaflets occurs, with or without fusion of the commissures. The chordae tendineae may be thickened and shortened. Calcification of the valve rarely occurs. The leaflet tissue is composed of dense collagen and elastic fibers that produce a major distortion of the normal leaflet layers.
  • Carcinoid heart disease: Carcinoid valve lesions characteristically manifest as fibrous white plaques located on the valvular and mural endocardium. The valve leaflets are thickened, rigid, and reduced in area. Fibrous tissue proliferation is present on the atrial and ventricular surfaces of the valve structure.
  • Congenital tricuspid stenosis: These lesions are observed more commonly in infants. They may manifest as incompletely developed leaflets, shortened or malformed chordae, small annuli, abnormal size and number of the papillary muscles, or any combination of these defects.
  • Infective endocarditis: Large infected vegetations obstructing the orifice of the tricuspid valve may produce stenosis. This condition is relatively uncommon, even in those who abuse intravenous drugs.
  • Unusual causes: Rare causes of tricuspid stenosis include Fabry disease and giant blood cysts.
  • Mimickers of tricuspid stenosis: Several conditions may mimic tricuspid stenosis by obstructing flow through the valve. These conditions include supravalvular obstruction from congenital diaphragms, intracardiac or extracardiac tumors, thrombosis or emboli, or large endocarditis vegetations. In addition, conditions that impair right-sided filling can produce similar symptoms and physical findings. These conditions include constrictive pericarditis and restrictive cardiomyopathy.
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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.

Specialty Editor Board

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.

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.

Additional Contributors

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.

Acknowledgements

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.

References
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  5. Faletra F, La Marchesina U, Bragato R, De Chiara F. Three dimensional transthoracic echocardiography images of tricuspid stenosis. Heart. 2005 Apr. 91(4):499. [Medline].

  6. [Guideline] Nishimura RA, Otto CM, Bonow RO, Carabello BA, Erwin JP 3rd, Guyton RA, et al. 2014 AHA/ACC guideline for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2014 Jun 10. 63(22):e57-185. [Medline].

  7. [Guideline] Vahanian A, Alfieri O, Andreotti F, Antunes MJ, Barón-Esquivias G, Baumgartner H, et al. Guidelines on the management of valvular heart disease (version 2012). Eur Heart J. 2012 Oct. 33(19):2451-96. [Medline].

  8. Badheka AO, Shah N, Ghatak A, Patel NJ, Chothani A, Mehta K, et al. Balloon Mitral Valvuloplasty in United States: A 13 year perspective. Am J Med. 2014 May 20. [Medline].

  9. Roberts PA, Boudjemline Y, Cheatham JP, et al. Percutaneous Tricuspid Valve Replacement in Congenital and Acquired Heart Disease. JACC. 2011. 58:117-22.

  10. Godart F, Baruteau AE, Petit J, et al. Transcatheter tricuspid valve implantation: A multicentre French study. Arch Cardiovasc Dis. 2014 Nov. 107(11):583-91. [Medline].

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A representation of a stenotic tricuspid valve. This image demonstrates fusion of the commissures (shown as dotted lines).
 
 
 
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