Endocarditis pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

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. The three most common pathogens are strepotococcus viridans, staphylococcus and enterococcus. 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
  • Dental procedures
  • Intravenous drug use
  • Complicated urinary tract infections
  • Colorectal cancer
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 Pathology

Microscopic Pathology

Pathology

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

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

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