A review of Chlamydia pneumoniae and atherosclerosis.

Chlamydia pneumoniae is a Gram-negative obligate intracellular bacterium that causes acute upper and lower respiratory infections. Its distribution is worldwide. Seroepidemiological studies have shown an association between C. pneumoniae and atherosclerosis, and the risk of acute myocardial infarction. Several studies had detected C. pneumoniae in atherosclerotic lesions from coronary and carotid arteries, in abdominal aortic aneurysms (AAA), and in sclerotic aortic valves. One study consistently succeeded in culturing C. pneumoniae from an atherosclerotic lesion, indicating the presence of viable organisms. However, the pathogenicity is unknown, and the significance of detecting the organism is unresolved. In two minor controlled clinical trials, patients with ischaemic heart disease were randomised into antibiotic-treated and placebo groups. Both trials showed a significant reduction in serious endpoints in patients receiving macrolide. Macrolide therapy thus seems to improve the outcome of severe ischaemic heart disease. It is not known whether this is caused by eradicating C. pneumoniae organisms, or by the macrolide's non-specific anti-inflammatory effect. Since both C. pneumoniae and inflammation are found in the AAA wall, it may be considered that macrolide would also improve the outcome of AAA and other diseases related to vascular surgery. In order to confirm this, randomised trials with macrolide therapy are needed, as well as diagnostic methods that can differentiate between individuals who are or are not infected with C. pneumoniae. The latter are needed in order to clarify the impact of the presence of C. pneumoniae and to avoid indiscriminate use of antimicrobials.