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The ACADEMIC Study in Perspective (Azithromycin in Coronary Artery Disease: Elimination of Myocardial Infection with Chlamydia)
Author(s) -
Jeffrey L. Anderson,
Joseph B. Muhlestein
Publication year - 2000
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/315635
Subject(s) - azithromycin , chlamydia , medicine , coronary artery disease , placebo , chlamydophila pneumoniae , antibody titer , c reactive protein , immunology , gastroenterology , inflammation , titer , antibody , chlamydiaceae , antibiotics , pathology , biology , alternative medicine , microbiology and biotechnology
Chlamydia pneumoniae, a common cause of respiratory infection, is vasotropic and frequently found in human atheromas. Whether it plays a causal role in coronary artery disease (CAD) is uncertain. The effects of 3 months of azithromycin treatment or placebo were tested in 302 patients with chronic CAD seropositive to C. pneumoniae at 3-6 months. Azithromycin reduced a global rank sum score of 4 inflammatory markers (C-reactive protein [CRP], interleukin [IL]-1, IL-6, tumor necrosis factor-alpha; P=.011) and a global rank sum change score (+/-SD) (from 535+/-201 to 587+/-190; P=.027) at 6 (but not 3) months. Change scores for CRP and IL-6 and median IL-1 levels were lower. C. pneumoniae IgG and IgA antibody titers were unchanged. Clinical cardiovascular events at 6 months did not differ between groups (azithromycin, 9; placebo, 7). Infections were reduced and drug was well tolerated. Thus, azithromycin caused modest but significant reductions in markers of inflammation, but differences in clinical events were not evident at 6 months. However, power was limited and conclusions should await results of the 2-year evaluation and larger studies.

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