title: Randomized secondary prevention trial of azithromycin in patients with coronary artery disease and serological evidence for Chlamydia pneumoniae infection: The Azithromycin in Coronary Artery Disease: Elimination of Myocardial Infection with Chlamydia (ACADEMIC) study.
abstract: BACKGROUND
  Chlamydia pneumoniae commonly causes respiratory infection, is vasotropic, causes atherosclerosis in animal models, and has been found in human atheromas. Whether it plays a causal role in clinical coronary artery disease (CAD) and is amenable to antibiotic therapy is uncertain.
  
  
  RESULTS
  CAD patients (n=302) who had a seropositive reaction to C pneumoniae (IgG titers >/=1:16) were randomized to receive placebo or azithromycin, 500 mg/d for 3 days, then 500 mg/wk for 3 months. Circulating markers of inflammation (C-reactive protein [CRP], interleukin [IL]-1, IL-6, and tumor necrosis factor [TNF]-alpha), C pneumoniae antibody titers, and cardiovascular events were assessed at 3 and 6 months. Treatment groups were balanced, with age averaging 64 (SD=10) years; 89% of the patients were male. Azithromycin reduced a global rank sum score of the 4 inflammatory markers at 6 (but not 3) months (P=0. 011) as well as the mean global rank sum change score: 531 (SD=201) for active drug and 587 (SD=190) for placebo (P=0.027). Specifically, change-score ranks were significantly lower for CRP (P=0.011) and IL-6 (P=0.043). Antibody titers were unchanged, and number of clinical cardiovascular events at 6 months did not differ by therapy (9 for active drug, 7 for placebo). Azithromycin decreased infections requiring antibiotics (1 versus 12 at 3 months, P=0.002) but caused more mild, primarily gastrointestinal, adverse effects (36 versus 17, P=0.003).
  
  
  CONCLUSIONS
  In CAD patients positive for C pneumoniae antibodies, global tests of 4 markers of inflammation improved at 6 months with azithromycin. However, unlike another smaller study, no differences in antibody titers and clinical events were observed. Longer-term and larger studies of antichlamydial therapy are indicated.
authors: Department of Medicine, Division of Cardiology, University of Utah, LDS Hospital, Salt Lake City, Utah 84143, USA.
authors: J L
authors: JL
authors: Anderson
authors: J B
authors: JB
authors: Muhlestein
authors: J
authors: J
authors: Carlquist
authors: A
authors: A
authors: Allen
authors: S
authors: S
authors: Trehan
authors: C
authors: C
authors: Nielson
authors: S
authors: S
authors: Hall
authors: J
authors: J
authors: Brady
authors: M
authors: M
authors: Egger
authors: B
authors: B
authors: Horne
authors: T
authors: T
authors: Lim
mesh_terms: D000900:Anti-Bacterial Agents / Q000008:administration & dosage / Q000009:adverse effects / Q000627:therapeutic use*; D000907:Antibodies, Bacterial / Q000097:blood; D017963:Azithromycin / Q000008:administration & dosage / Q000009:adverse effects / Q000627:therapeutic use*; D002097:C-Reactive Protein / Q000032:analysis; D002690:Chlamydia Infections / Q000188:drug therapy*; D016993:Chlamydophila pneumoniae / Q000276:immunology; D003327:Coronary Disease / Q000188:drug therapy* / Q000517:prevention & control; D004311:Double-Blind Method; D004361:Drug Tolerance; D005260:Female; D006801:Humans; D007375:Interleukin-1 / Q000032:analysis; D015850:Interleukin-6 / Q000032:analysis; D007958:Leukocyte Count; D008297:Male; D008875:Middle Aged; D010342:Patient Acceptance of Health Care; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: D000900:Anti-Bacterial Agents; D000907:Antibodies, Bacterial; D007375:Interleukin-1; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D017963:Azithromycin; D002097:C-Reactive Protein