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Coagulation and thrombosis in cardiovascular disease: plausible contributions of infectious agents

M C Herzberg1

  • 1School of Dentistry, University of Minnesota, Minneapolis, Minnesota, USA.

Annals of Periodontology
|March 13, 2002
PubMed

Insights

Infectious agents can trigger blood clots (thrombosis) by activating coagulation or platelets, increasing the risk of atherosclerosis and cardiovascular disease. This highlights a potential link between chronic infections and heart health.

Area of Science:

  • Cardiovascular Science
  • Infectious Disease
  • Pathology

Background:

  • Occlusive thrombus in coronary arteries is a primary cause of myocardial infarction.
  • Atheroma formation and fissuring can lead to thrombosis.
  • Chronic infections may contribute to atherosclerosis and thrombosis.

Purpose of the Study:

  • To explore the prothrombotic potential of infectious agents.
  • To investigate the mechanisms by which infections may influence cardiovascular disease pathogenesis.
  • To assess the cumulative risk of chronic pathogens on atherosclerosis and thrombosis.

Main Methods:

  • Review of in vitro and animal model evidence on microbial activation of coagulation.
  • Analysis of mechanisms for infectious agent-induced platelet aggregation.
  • Examination of pathological responses in disseminated intravascular coagulation and infective endocarditis.

Main Results:

  • Infectious agents can activate coagulation via enzymatic pathways or tissue factor up-regulation.
  • Some microbes directly induce platelet aggregation in vitro and in animal models.
  • Infections are linked to procoagulant responses in human conditions like DIC and endocarditis.

Conclusions:

  • Infectious agents possess direct and indirect prothrombotic potential.
  • Chronic pathogen burden may increase the lifetime risk of atherosclerosis and thrombosis.
  • Understanding these links is crucial for cardiovascular disease prevention and management.

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