Pathophysiology of Infective Endocarditis

  • Franck Thuny


Infective endocarditis is a life-threatening disease whose pathophysiology is based on unique host-pathogen interaction. Pathogenesis includes pre-existing endocardial lesions or inflammation that leads to endothelial cells and platelets activation, coagulation and thrombus formation. When bacteraemia occur and are repeated, pathogens can adhere to endocardial thrombus thanks to adhesins. After adhesion, the subsequent colonization and invasion of the endocardium maintain both the inflammation and the coagulation processes, resulting in a vicious circle with the formation of infective vegetation in which the pathogens persist, multiply and escape from the host defenses. Consequently, the vegetation will grow and the valve tissue will be destroyed, resulting ultimately in embolic events, abscess formation and valve dysfunction. Moreover, the excessive host response can be responsible to the aggravation of the lesions by secondary autoimmune effects.


Vegetation Bacteraemia Host-pathogen interaction Coagulation Thrombosis Inflammation Vasculitis 


  1. 1.
    Que YA, Moreillon P. Infective endocarditis. Nat Rev Cardiol. 2011;8:322–36.CrossRefPubMedGoogle Scholar
  2. 2.
    Benoit M, Thuny F, Le Priol Y, et al. The transcriptional programme of human heart valves reveals the natural history of infective endocarditis. PLoS One. 2010;5:e8939.CrossRefPubMedPubMedCentralGoogle Scholar
  3. 3.
    Kupferwasser LI, Hafner G, Mohr-Kahaly S, et al. The presence of infection-related antiphospholipid antibodies in infective endocarditis determines a major risk factor for embolic events. J Am Coll Cardiol. 1999;33:1365–71.CrossRefPubMedGoogle Scholar
  4. 4.
    Que YA, Haefliger JA, Piroth L, et al. Fibrinogen and fibronectin binding cooperate for valve infection and invasion in staphylococcus aureus experimental endocarditis. J Exp Med. 2005;201:1627–35.CrossRefPubMedPubMedCentralGoogle Scholar
  5. 5.
    Cabell CH, Jollis JG, Peterson GE, et al. Changing patient characteristics and the effect on mortality in endocarditis. Arch Intern Med. 2002;162:90–4.CrossRefPubMedGoogle Scholar
  6. 6.
    Fowler Jr VG, Miro JM, Hoen B, et al. Staphylococcus aureus endocarditis: a consequence of medical progress. JAMA. 2005;293:3012–21.CrossRefPubMedGoogle Scholar
  7. 7.
    Sy RW, Kritharides L. Health care exposure and age in infective endocarditis: results of a contemporary population-based profile of 1536 patients in Australia. Eur Heart J. 2010;31:1890–7.CrossRefPubMedGoogle Scholar
  8. 8.
    Thuny F, Avierinos JF, Habib G. Changing patterns in epidemiological profiles and prevention strategies in infective endocarditis: from teeth to healthcare-related infection. Eur Heart J. 2010;31:1826–7.CrossRefPubMedGoogle Scholar
  9. 9.
    Moreillon P, Que YA. Infective endocarditis. Lancet. 2004;363:139–49.CrossRefPubMedGoogle Scholar
  10. 10.
    Thuny F, Habib G, Le Dolley Y, et al. Circulating matrix metalloproteinases in infective endocarditis: a possible marker of the embolic risk. PLoS One. 2011;6:e18830. 2007;154:923–8.CrossRefPubMedPubMedCentralGoogle Scholar

Copyright information

© Springer International Publishing Switzerland 2016

Authors and Affiliations

  1. 1.Unit of Heart Failure and Valve Heart DiseaseNord HospitalMarseilleFrance

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