Am Fam Physician. 2002;65(9):1935-1936
Evidence is accumulating that atherosclerosis is related to inflammatory disease. Infectious microorganisms such as herpes viruses and Chlamydia pneumoniae are among the factors that may promote inflammation and subsequent atherogenesis. C. pneumoniae has been isolated in coronary artery and thoracic aorta atherosclerotic lesions. Studies have demonstrated conflicting evidence regarding an increased prevalence of C. pneumoniae antibodies in patients with acute myocardial infarction (MI). Studies demonstrating that treatment with an antibiotic effective against C. pneumoniae may decrease the likelihood of a cardiac event are raising interest in this field. Pilote and associates used a retrospective case-review study to determine the ability of these types of antibiotics to improve a patient's prognosis following acute MI.
The researchers assessed the vital status of patients using in-hospital records, the Quebec drug claims database, and other administrative and vital statistics databases of men older than 64 years who were admitted with a first acute MI. These data were used to confirm the diagnosis, identify antibiotic use, and provide a two-year health status follow-up. Antibiotic users were divided into three groups: group 1 received antibiotics to which C. pneumoniae is sensitive (i.e., tetracyclines, macrolides, and quinolones); group 2 received sulfa-derived antibiotics to which C. pneumoniae organisms are not sensitive; and group 3 received other antibiotics to which C. pneumoniae organisms are not sensitive or no antibiotics at all. These groups were further broken down into two different times of exposure to antibiotics. Group 1, patients who survived at least three months following MI received antibiotics for those three months, and group 2, patients who received antibiotics for six months before the MI. Patients who received antibiotics during both periods were excluded.
Among patients exposed to antibiotics within three months following MI, the one-year mortality rate was similar across all three groups; however, the two-year mortality rate favored patients who had received antichlamydial therapy. Exposure during the six months before MI had no effect on one- or two-year mortality. Although the relationship between C. pneumoniae is unclear, possible effects of infection may relate to progression of atherosclerosis or plaque stability.
The authors conclude that although exposure to antichlamydial antibiotics during the six months before MI does not affect survival, exposure within three months after MI may improve survival. This potential benefit is intriguing, but more studies must be performed before the widespread use of antichlamydial antibiotics to prevent or improve survival following MI can be recommended.
editor's note: Interest in the effect of inflammation and infection on atherosclerotic disease has been stimulated by the findings of higher levels of Chlamydia pneumoniae antibody titers, C-reactive protein, and fibrinogen in patients with coronary artery disease. The role of these markers is unclear. Muhlestein and associates used a placebo-controlled study to evaluate the effect of C. pneumoniae treatment on the development of acute coronary and stroke events among patients with previous coronary artery disease and evidence of exposure to C. pneumoniae, based on positive IgG titers. The intervention group received azithromycin (500 mg per day for three days and then 500 mg per week for three months). Clinical end points representing worsening of coronary artery disease and stroke occurred with similar frequency during the two-year follow-up of patients in the treated and placebo groups, but there was a tendency for fewer end points to occur between six and 24 months in the treated group. The authors concluded that longer and larger studies are needed, since antibiotic therapy with azithromycin was not associated with an early reduction of cardiac events but may have a more delayed benefit.—r.s.