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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.
Abstract:
Pathogenesis of atherosclerosis involves multiple mechanisms, including imbalanced lipid metabolism, disturbed equilibrium of the immune response, and chronic inflammation of the artery wall. Several reports have shown a relationship between the development of atherosclerosis and the presence of infectious diseases, widely occurring in the general population, often chronic and/or asymptomatic. Beyond Chlamydia pneumoniae, a large number of infectious agents have been linked with an increased risk of vascular disease, with variable strength of supporting data: Porphyromonas gingivalis, Helicobacter pylori, influenza A virus, herpes virus, hepatitis C virus, cytomegalovirus, and human immunodeficiency virus. Infections may contribute to atherosclerosis either via direct infection of vascular cells or via the indirect effects of cytokines or acute phase proteins induced by infection at "nonvascular" sites. More recently, investigators reported that the aggregate burden ("infectious burden") of these chronic infections, rather than the effects of a single organism, might contribute to atherosclerosis and its thrombotic complications. However, the role of infection, as a proinflammatory cause of atherosclerosis, is still debated in the literature. This article will review available data suggesting a relationship between different infective pathogens and atherothrombosis, the hypothesized mechanisms, and the potential role for antimicrobial treatment.
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