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Relation of Chlamydia Pneumoniae Infection to Documented Coronary Artery Disease in Shiraz, Southern Iran

Cardiovascular Research Center and Prof. Alborzi Clinical Microbiology Research Center, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran, Zibaeem2{at}sums.ac.ir

A. Amanat, MD

Cardiovascular Research Center and Prof. Alborzi Clinical Microbiology Research Center, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran

A. Alborzi, MD

Cardiovascular Research Center and Prof. Alborzi Clinical Microbiology Research Center, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran

A. Obudi

Cardiovascular Research Center and Prof. Alborzi Clinical Microbiology Research Center, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran

The possibility that infectious agents may trigger a cascade of reactions leading to inflammation, atherogenesis, and vascular thrombotic events has recently been raised. Chlamydia pneumoniae is one of those that have received the most investigative attention with respect to coronary artery disease (CAD). This study was undertaken for the first time in Shiraz, Iran to determine this relationship. A case-control study was conducted in 167 subjects (81 women and 86 men) who underwent coronary angiography at cardiac catheterization laboratories of Shiraz University of Medical Sciences Hospitals. Immunoglobulin G (IgG), and IgA antibodies to C. pneumoniae antigen were estimated in baseline serum samples from 109 patients (mean age 57 years) experiencing a coronary event and from their matched controls (n=58, mean age 50 years) by ELISA method. The prevalence of IgG and IgA antibodies to C. pneumoniae did not show any case-control differences (82.6% vs 74.1% and 22% vs 15.5%, respectively). These results suggest that although C. pneumoniae was highly prevalent among these patients, it did not appear to be associated with angiographically documented CAD and cannot be regarded as a positive predictor for the development of acute coronary syndrome.

Angiology, Vol. 56, No. 1, 43-48 (2005)
DOI: 10.1177/000331970505600106


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