Antibiotic therapy for coronary heart disease: the myth and the reality.

Abstract

Atherosclerosis is acknowledged as an active inflammatory and thrombotic disease, as opposed to simple degeneration. Infection with microorganisms may contribute to this inflammation and hence the atherosclerotic process. The "infective" hypothesis - first proposed more than a century ago by Virchow - has been revisited in recent years and has implicated numerous microorganisms as potential stimuli. The greatest body of evidence points to Chlamydia pneumoniae, a respiratory pathogen, as the "culprit" microorganism. Consistent finding of bacterial antigens, DNA and occasionally live "viable" organisms within human atherosclerotic plaque support the evidence for the concept linking C. pneumoniae to atherosclerosis. Although original seroepidemiological studies indicated an association, more recent prospective and larger studies suggest that there may be only a weak link between elevated antibodies and immune complexes to C. pneumoniae and coronary heart disease (CHD). Animal models have shown how atherogenesis can be induced by endovascular infection with C. pneumoniae; in vitro studies have explored various immunological and inflammatory pathways linking infection and atherothrombosis. On the basis of this, antibiotic trials have been explored to assess whether there is any role for antichlamydial agents in the treatment of cardiovascular events. Here, we focus on the main antibiotic studies and explores patient criteria and choice, duration of therapy, and whether effects on clinical events could be reduced.