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:

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. 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. Also unlike infective endocarditis, NBTE does not cause an inflammation response from the body. NBTE usually occurs due to hypercoaguable states such as systemic bacterial infection or pregnancy. NBTE may also occur in patients with cancer, particularly mucinous adenocarcinoma. 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. These immune complexes precipitate an inflammatory reaction, which helps to differentiate it from NBTE. 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.

Gross and Microscopic Pathology

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

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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  Heart; Breast intraductal papilloma metastasis. Thrombotic Nonbacterial Endocarditis (Infected): Gross mitral valve natural color vegetations well illustrated these were secondarily infected with staphylococcus case of 8 year survival breast intraductal papillary adenocarcinoma with extensive metastases. Aortic valve also involved
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  Thrombotic Nonbacterial Endocarditis Infected: Micro low mag H&E fibrin vegetation with masses of staphylococci and inflammatory cells in valve secondarily infected case 8 year survival breast papillary intraductal adenocarcinoma with extensive metastases gross is aortic valve lesions.

Videos

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