Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Maliha Shakil, M.D. [2]
Overview
The pathogenesis of infective endocarditis includes valvular damage, altered and turbulent flow, bacteremia, and lack of blood supply to the valves.[1] Damaged endothelium becomes a site for attachment of infectious agents in infectious endocarditis. Nonbacterial thrombotic endocarditis is related to hypercoaguable states such as pregnancy or systemic bacterial infection.[2] The characteristic lesion of endocarditis is a vegetation. Vegetations are composed of fibrin, inflammatory cells, platelets, and microorganisms.[3]
Pathophysiology
Pathogenesis
Infective Endocarditis
The pathogenesis of infective endocarditis includes:[1][2]
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Pathogenic Factors
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Mechanism
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- Valvular Damage
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- Altered and turbulent flow
- Catheters, electrodes, and other intracardiac devices
- Solid particles from repeated intravenous injections
- Chronic inflammation
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- Bacteremia
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- Lack of blood supply to valves
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- Blunted immune response
- Therapeutic drugs have difficulty reaching infected valves
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Nonbacterial thrombotic endocarditis
- Nonbacterial thrombotic endocarditis (NBTE), also called marantic endocarditis is most commonly found on previously undamaged valves.
- The vegetations in NBTE are small, sterile, and tend to aggregate along the edges of the valve or the cusps.
- 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.
- 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
The characteristic lesion of endocarditis is a vegetation. Vegetations are composed of fibrin, inflammatory cells, platelets, and microorganisms.[3] Characteristic features of endocarditis on gross pathology and histopathological analysis include:[4]
Endocarditis Subtype
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Features on Gross Pathology
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Features on Histopathological Microscopic Analysis
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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
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- Inflammatory infiltrate
- Abundant neutrophils
- Plasma cells may be present in subacute endocarditis
- Microorganisms present
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Nonbacterial Thrombotic Endocarditis |
- Round non-destructive vegetations, usually at the line of closure
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- Vegetations without inflammation and microorganisms
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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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Nonbacterial Thrombotic 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.
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References
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