The prevalence of chronicChlamydia pneumoniaeinfection as detected by polymerase chain reaction in pharyngeal samples from patients with ischaemic heart disease
Open Access
- 1 September 1998
- journal article
- clinical trial
- Published by Oxford University Press (OUP) in European Heart Journal
- Vol. 19 (9) , 1321-1327
- https://doi.org/10.1053/euhj.1998.1010
Abstract
Aims Cross-sectional serological studies have suggested an association between ischaemic heart disease and infections fromChlamydia pneumoniaeandHelicobacter pylori. We therefore sought to find out if patients with ischaemic heart disease had an increased prevalence ofC. pneumoniaein the pharynx. As the course of theC. pneumoniaeinfection remains unclear, both acute and follow-up samples were taken and compared with antibody levels. Methods and Results We studied 282 patients with ischaemic heart disease. One hundred and two subjects without history or symptoms of ischaemic heart disease served as controls. Pharyngeal specimens for polymerase chain reaction detection ofC. pneumoniae, and blood samples forC. pneumoniaeandH. pyloriantibody detection, were collected. In patients with positive polymerase chain reaction orC. pneumoniaeIgA titres ≥32, indicating current infection, convalescent samples were taken at least 6 weeks later. An immunofluorescent antigen detection test was used to confirm the presence ofC. pneumoniaeelementary bodies in specimens found to be polymerase chain reaction positive. The prevalence of positive polymerase chain reaction tests was 36% among patients and 22% among controls (PC. pneumoniaeIgG titres ≥512 were found in 39% of patients and 26% of the controls (P16. There was no link between positiveH. pyloriserology and positiveC. pneumoniaepolymerase chain reaction tests. Conclusions The high prevalence and persistence of positive pharyngealC. pneumoniaepolymerase chain reaction and elevated antibody titres in patients with ischaemic heart disease indicate a chronic infection. The pharyngeal presence ofC. pneumoniaemight contribute to a low grade inflammatory activation or be a source for further spread of the bacteria to atherosclerotic vessels.Keywords
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