Presence of <i>Chlamydia pneumoniae</i> DNA in the Artery Wall – Biomarker of Coronary Artery Disease

Kirbiš, J.; Keše, D.; Petrovič, Daniel

doi:10.14712/fb2005051050145

Fol. Biol. 2005, 51, 145-147

https://doi.org/10.14712/fb2005051050145

Presence of Chlamydia pneumoniae DNA in the Artery Wall – Biomarker of Coronary Artery Disease

J. Kirbiš¹, D. Keše², Daniel Petrovič³

¹Department of Cardiovascular Surgery, University Medical Centre Ljubljana, Slovenia
²Institute of Microbiology and Immunology, Medical Faculty, University of Ljubljana, Slovenia
³Institute of Histology and Embryology, Medical Faculty, University of Ljubljana, Slovenia

Received May 2005
Accepted July 2005

Many authors have shown an association between Chlamydia pneumoniae (CPn) infection and coronary artery disease (CAD). However, whether CPn infection demonstrated by CPn DNA presence in the artery wall plays an important role in pathogenesis of CAD and acute coronary events (i.e. unstable angina) remains to be elucidated. One hundred and fifteen consecutive patients with CAD (51 with unstable angina and 64 with stable angina) were compared with 52 control subjects with aortic valve disease without angiographic evidence of CAD. The presence of CPn DNA in the aortic wall was assessed with nested polymerase chain reaction (PCR), and the IgM, IgG and IgA antiCPn titres were assessed with microimmunofluorescence test. CPn DNA presence in the artery (i.e. aortic) wall was associated with 3.7-fold increased risk of CAD (95% CI 1.2-11.3, P < 0.01); however, no statistically significant difference in CPn DNA presence was demonstrated between unstable and stable angina (17.6% vs. 25%). In the CPn DNA positive group more often than in the CPn DNA negative group, serological signs of chronic infection (55.2% vs. 27%, P = 0.004) were demonstrated, whereas no statistically significant differences were demonstrated in prevalence of either acute infection (9.3% vs. 0%) or reinfection (0% vs. 0%). In conclusion, CPn DNA presence in the artery (i.e. aortic) wall was associated with CAD, therefore may be used as a biomarker for CAD. Moreover, no statistically significant differences in CPn DNA presence in the artery wall and in serology were present between unstable and stable angina; therefore, CPn infection does not seem implicated in triggering an acute coronary event.