Lack of association between Chlamydia Pneumoniae serology and endothelial dysfunction of coronary arteries

Markus Ferrari¹ , Gerald S Werner¹ , Barbara M Richartz¹ , Albrecht Oehme² , Eberhard Straube² and Hans R Figulla¹

¹Clinic of Internal Medicine I, Friedrich-Schiller-University, D – 07740 Jena, Germany

²Institute of Microbiology, Friedrich-Schiller-University, D – 07740 Jena, Germany

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Cardiovascular Ultrasound 2005, 3:12doi:10.1186/1476-7120-3-12


Published:	27 April 2005

Abstract

Background

Recent publications brought up the hypothesis that an infection with Chlamydia Pneumoniae (CP) might be a major cause of coronary artery disease (CAD). Therefore, we investigated whether endothelial dysfunction (ED) as a precursor of atherosclerosis might be detectable in patients with previous infection with CP but without angiographic evidence of CAD.

Methods

We included 16 patients (6 male / 10 female) of 52 consecutive patients with normal coronary angiography who had typical angina pectoris and pathologic findings in the stress test. Exclusion criteria were: active smoker, elevated cholesterol, hypertension, age > 65 years, diabetes mellitus, treatment with ACE-inhibitors, or known CAD. Blood sample analysis for serum titer against CP (aCP-IgG) was performed after coronary angiography. We looked for endothelial dysfunction analyzing the diameter of the left anterior descending coronary artery (LAD) before and after acetylcholine (ACh) i. c. Quantitative analysis of luminal diameter (LD) was performed in at least two planes during baseline conditions and after ACh for 2 minutes in dosages of 7.2 μg/min and 36 μg/min with an infusion speed of 2 ml/min. Using Doppler guide wire, the coronary flow velocity was measured continuously in the LAD. The coronary flow velocity reserve (CFVR) was measured after 20 μg adenosine i. c.

Results

10 patients had an elevated aCP-IgG (> 1:8). 6 patients with negative titers (aCP-IgG ≤ 1:8) served as control (CTRL). Both groups were comparable in age, gender, angina class, results of non-invasive stress-test and the baseline values of LD and flow. In the CP positive group 3 patients (30%) did not show an increase of LD after ACh as evidence of ED. In the CTRL group 4 patients (67 %) had ED. There was no association between aCP-IgG and changes of coronary blood flow after ACh. All patients showed normal CFVR (3.0 ± 0.27) irrespective of their aCP-IgG values.

Conclusion

In patients with typical symptoms of coronary ischemia but without angiographically visible CAD and absence of other factors affecting the endothelial function, a previous infection with CP is not associated with endothelial dysfunction.