Coronary artery disease, the leading cause of morbidity and mortality in developed countries, is a chronic inflammatory process that develops in response to a variety of
injuries. A number of microbial organisms have been implicated in its pathogenesis. The strongest evidence to date for an association between an infectious agent and
coronary heart disease is that for Chlamydia pneumoniae. Evidence implicating other microbial organisms is much less compelling. Sero-epidemiological and pathological data have linked
infection with C. pneumoniae to atherosclerotic
coronary artery disease. A possible mechanism by which C. pneumoniae may participate in the pathogenesis of
atherosclerosis is through immune activation and the initiation of a chronic inflammatory state in the infected arterial wall. Locally secreted inflammatory
cytokines trigger a cascade of secondary cellular processes that lead to characteristic structural changes. C. pneumoniae has been detected in
atherosclerotic plaques and in the serum of patients with
coronary artery disease. It induces foam cells (the hallmark of early
atherosclerosis) and it markedly accelerates this disease process in animal models. C. pneumoniae has been associated with elevated levels of inflammatory
cytokines and
acute phase reactants. Data from three interventional studies in humans have suggested that treatment with
antibiotics decreases inflammatory markers and perhaps influences the anti-C. pneumoniae antibody titers; however, adverse clinical events were not uniformly reduced in all trials. Two large prospective clinical trials, the WIZARD trial and
ACES, are underway to confirm these preliminary findings and test the hypothesis that
antibiotics may be beneficial in preventing or modifying the course of
coronary artery disease. At present, antimicrobial
therapy for
atherosclerosis is not advocated outside of well-controlled research settings.