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 pathogenesis of infective endocarditis includes valvular damage, altered and turbulent flow, bacteremia, and lack of blood supply to the valves. 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. The characteristic lesion of endocarditis is a vegetation. Vegetations are composed of fibrin, inflammatory cells, platelets, and microorganisms.

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

• The exact pathogenesis of nonbacterial thrombotic endocarditis is not completely understood.
• We can divide the pathogenesis pathway of nonbacterial endocarditis into to phase:
  • Initiating phase
    • Immune complexes
      • circulating immune complexes and complement deposition can initiate the process.
      • The example for this initiating factor in libman sacks endocarditis in lupus patients.
    • Hypoxia
      • Some studies demonstrated that hypoxia may lead to tissue factor activation.
      • Higher tissue factor level has an association with higher rate of endocarditis.
      • Other studies implies that the rate of endocarditis is higher in smokers and patients with chronic lung disease and possibly hypoxia.
    • Hypercoagulability
      • There is an association between hypercoagulable state and clotting factor abnormalities with initiation of nonbacterial thrombotic endocarditis.
    • Carcinomatosis
      • The association between cancer and nonbacterial thrombotic endocarditis is well established.
      • In most of the cases of cancer related endocarditis we have abnormal activity of tissue factor.
      • Tissue factor may be secreted from promyelocytic leukaemia cells.
      • Tissue factor may be expressed on the surface of adenocarcinoma cells which leads to increased expression of tissue factor by endothelial cells.
  • Verrucae formation

• 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.

Genetics

Associated Conditions

Gross Pathology

Microscopic Pathology

Gross and Microscopic Pathology

The characteristic lesion of endocarditis is a vegetation. Vegetations are composed of fibrin, inflammatory cells, platelets, and microorganisms. 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

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.

Videos

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References