Tricuspid Regurgitation Clinical Presentation

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

History

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.[3]

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.

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Physical

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
  • Ascites
  • Peripheral edema
  • 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.
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Causes

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.

Endocarditis

  • 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.

Ebstein anomaly

  • 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.[4]

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.

Carcinoid

  • 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.[5]

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

  • Trauma to the right ventricle may damage the structures of the tricuspid valve, resulting in insufficiency of the structure.[6]
  • More commonly it is associated with stab wounds or projectile destruction of the valve.

Connective-tissue diseases

  • 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

  • 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.
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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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