Chlamydia pneumoniae-atherosclerosis link: a sound concept in search for clinical relevance.

The potential role of Chlamydia pneumoniae (Cpn) in atherosclerosis has attracted considerable attention. On the basis of early encouraging results, it was anticipated that infection with Cpn might prove a novel treatable risk factor for atherosclerosis, with a relevance comparable to that of Helicobacter pylori in peptic ulcer disease. The effect of antibiotic treatment on clinical outcome became widely accepted as benchmark for the Cpn–atherosclerosis link. Several studies investigated macrolide antibiotics for secondary prevention in vascular disease.1–4 Due to limited sample sizes, however, most of these trials need to be interpreted cautiously. At the 51st Annual Scientific Sessions of American College of Cardiology, 2002, two adequately sized antibiotic trials, WIZARD (Weekly Intervention with Zithromax for Atherosclerosis and its Related Disorders) and AZACS (AZithromycin in Acute Coronary Syndromes), were reported. The negative results of these trials deadened the enthusiasm for the role of Cpn in atherosclerosis. WIZARD included 7747 patients with previous myocardial infarction (MI) and elevated Cpn titers who were randomly assigned to placebo or azithromycin for 11 weeks. During 2-year followup, the composite of all-cause mortality, recurrent MI, revascularization, and hospitalization for angina was not significantly affected by antibiotic treatment. Likewise, AZACS did not show a significant effect of short-term treatment with azithromycin on 6-month rate of all-cause mortality, nonfatal MI, or recurrent ischemia requiring revascularization in 1400 patients with unstable angina.