Infections are the most common inflammatory triggers and acute and chronic infections have been associated with the development
and progression of atherosclerotic disease raising interest in the infectious hypothesis of atherosclerosis. Pathogens have been
identified in atherosclerotic plaques and large epidemiological studies have documented conflicting associations between serological evidence
of infection and cardiovascular events. Influenza A was mostly studied as a trigger for cardiovascular events during winter months,
whilst cytomegalovirus, Chlamydia pneumoniae, helicobacter pylori and porphyromonas ginigivalis were the most studied chronic
pathogens which had been associated with the development and progression of cardiovascular disease.
Infectious agents can contribute to atherosclerosis by having a direct effect on the vascular wall or via indirect effects including inflammatory
responses and molecular mimicry. Efforts to prevent infection with vaccination or treat specific infectious agents with antibiotics
have provided mostly negative results, thereby challenging the validity of the infectious hypothesis of atherosclerosis.
Keywords: Chlamydia, viruses, bacteria, atherosclerosis, antibiotics, mechanisms, atherosclerotic disease, Influenza A, helicobacter pylori, porphyromonas ginigivalis
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