The infectious burden in atherothrombosis

Antonella Tufano1, Mirko Di Capua, Antonio Coppola

  • 1Department of Clinical and Experimental Medicine, Federico II University Hospital, Naples, Italy. atufano@unina.it

Insights

Infections may contribute to atherosclerosis, a complex inflammatory artery disease. The cumulative burden of chronic infections, not just single pathogens, might increase vascular disease and thrombotic risk.

Area of Science:

  • Cardiovascular Science
  • Infectious Disease Epidemiology
  • Immunology

Background:

  • Atherosclerosis pathogenesis involves lipid metabolism, immune response, and chronic inflammation.
  • Infectious diseases are linked to atherosclerosis risk, with pathogens like Chlamydia pneumoniae, Porphyromonas gingivalis, and Helicobacter pylori implicated.
  • The aggregate burden of chronic infections, termed 'infectious burden,' is increasingly recognized as a potential contributor to atherothrombosis.

Purpose of the Study:

  • To review evidence linking various infectious pathogens to atherothrombosis.
  • To explore hypothesized mechanisms by which infections contribute to atherosclerosis.
  • To discuss the potential role of antimicrobial treatments in managing infection-related vascular disease.

Main Methods:

  • Literature review of studies investigating the relationship between infections and atherosclerosis.
  • Analysis of proposed direct and indirect mechanisms of pathogen involvement in vascular disease.
  • Evaluation of data on the impact of infectious burden on atherothrombosis.

Main Results:

  • Multiple infectious agents beyond Chlamydia pneumoniae are associated with increased vascular disease risk.
  • Infections can promote atherosclerosis via direct vascular cell infection or indirect inflammatory responses.
  • The cumulative effect of multiple chronic infections may be more significant than single infections in atherothrombosis.

Conclusions:

  • A growing body of evidence suggests a link between infectious agents and atherothrombosis.
  • The precise role of infection as a proinflammatory cause of atherosclerosis requires further investigation.
  • Antimicrobial strategies may hold potential for managing infection-associated vascular complications.

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