Endocarditis pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Maliha Shakil, M.D. [2]

Overview

The turbulent blood flow around the heart valves is a risk factor for the development of endocarditis. The valves may be damaged congenitally, from surgery, by auto-immune mechanisms, or simply as a consequence of old age. The damaged endothelium of these areas becomes a site for attachment of infectious agents in infectious endocarditis. Dental procedures, colorectal cancer, urinary tract infections and intravenous drug use are the most common routes of introducing the infectious agent into the bloodstream. In non-bacterial thrombotic endocarditis (NBTE), the damaged part of a heart valve becomes covered with a blood clot which organizes.

Pathophysiology

Pathogenesis

Infective Endocarditis

The pathogenesis of infective endocarditis includes:[1][2]

Pathogenic Factors Mechanism
Valvular Damage
  • Altered and turbulent flow
  • Catheters, electrodes, and other intracardiac devices
  • Solid particles from repeated intravenous injections
  • Chronic inflammation
Bacteremia
Lack of blood supply to valves
  • Blunted immune response
  • Therapeutic drugs have difficulty reaching infected valves

Nonbacterial thrombotic endocarditis

Nonbacterial thrombotic endocarditis (NBTE), also called marantic endocarditis is most commonly found on previously undamaged valves.[2] As opposed to infective endocarditis, the vegetations in NBTE are small, sterile, and tend to aggregate along the edges of the valve or the cusps.[2] Also unlike infective endocarditis, NBTE does not cause an inflammation response from the body.[2] NBTE usually occurs due to hypercoaguable states such as systemic bacterial infection or pregnancy.[2] NBTE may also occur in patients with cancer, particularly mucinous adenocarcinoma.[2] Libman-Sacks endocarditis is another form of sterile endocarditis; this form occurs more often in patients with lupus erythematosus and is thought to be due to the deposition of immune complexes. Libman-Sacks endocarditis involves small vegetations, while infective endocarditis is composed of large vegetations.[2] These immune complexes precipitate an inflammatory reaction, which helps to differentiate it from NBTE.[2] Also unlike NBTE, Libman-Sacks endocarditis does not seem to have a preferred location of deposition and may form on the undersurfaces of the valves or even on the endocardium.[2]

Gross and Microscopic Pathology

Characteristic features of endocarditis on gross pathology and histopathological analysis include:[3]

Endocarditis Subtype Features on Gross Pathology Features on Histopathological Microscopic Analysis
Infective Endocarditis
  • Left-sided valve involvement (mitral, aortic) more common generally
  • Right-sided valve involvement (pulmonic, tricuspid valve) more common in intravenous drug abusers
  • Valvular vegetations
  • Valvular destruction
  • Inflammatory infiltrate
  • Abundant neutrophils
  • Plasma cells may be present in subacute endocarditis
  • Microorganisms present
Nonbacterial Thrombotic Endocarditis
  • Round non-destructive vegetations, usually at the line of closure
  • Vegetations without inflammation and microorganisms

Pathology

Image courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology

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References

  1. Infective endocarditis. Wikipedia (2015). URL=https://en.wikipedia.org/wiki/Infective_endocarditis#Pathogenesis Accessed on September 21, 2015
  2. 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 2.8 Endocarditis. Wikipedia (2015). URL= https://en.wikipedia.org/wiki/Endocarditis Accessed on September 21, 2015
  3. Infective Endocarditis. Libre Pathology (2015). URL=http://librepathology.org/wiki/index.php/Infective_endocarditis Accessed on September 21, 2015

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