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 hypercoagulable states such as pregnancy or systemic bacterial infection. The characteristic lesion of endocarditis is vegetation. Vegetations are composed of fibrin, inflammatory cells, platelets, and microorganisms.

• The pathogenesis of infective endocarditis includes:

• The exact pathogenesis of nonbacterial thrombotic endocarditis is not completely understood.
• Nonbacterial thrombotic endocarditis (NBTE), also called marantic endocarditis is most commonly found on previously undamaged valves.
• The vegetations in nonbacterial thrombotic endocarditis are sterile and small.
• The vegetations mostly aggregate at the edges of the valve or the cusps.
• We can divide the pathogenesis pathway of nonbacterial endocarditis into to phase:
  • Initiating phase
    • Immune complexes:^[1][2]
      • Circulating immune complexes and complement deposition can initiate the process.
      • The example for this initiating factor in libman sacks endocarditis in lupus patients.
    • Hypoxia:^[3][4]
      • 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:^[5][6]
      • There is an association between hypercoagulable state and clotting factor abnormalities with initiation of nonbacterial thrombotic endocarditis.
    • Carcinomatosis:^[7]
      • 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

Genes involved in the pathogenesis of infective endocarditis include:^[8]

• Interleukin-6 c.471+870G>A
• Interleukin-1b c.315C>T
• Selectin-E c.-19 GT

Genes involved in the pathogenesis of nonbacterial thrombotic endocarditis include:^[9]

• Homozygous for the C677T mutation of the methylenetetrahydrofolate reductase gene which leads to hyperhomocysteinemia.

Conditions associated with endocarditis include:

• Prosthetic heart valves^[10]
• Valvular heart disease (mitral valve prolapse is the most common valvular lesion that predisposes to endocarditis)^[11][12]
• Intravenous drug abuse^[13]
• Intracardiac devices, such as implantable cardioverter-defibrillators^[14]
• Hemodialysis^[15]
• Congenital heart disease^[16]
• History of rheumatic heart disease^[17]
• Diabetes mellitus^[18][19]
• Colon cancer^[20]

• Hypercoagulable state such as pregnancy and systemic bacterial infection ^[21][22]
• Malignancy especially mucin-producing adenocarcinomas (most commonly associated with pancreatic adenocarcinomas)^[23]
• Systemic lupus erythematosus^[24]

On gross pathology, characteristic findings of endocarditis are:

On microscopic histopathological, characteristic findings of endocarditis are:

• Vegetation:
  • Vegetations are composed of fibrin, inflammatory cells, platelets, and microorganisms.^[25]

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

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