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Lack of association between Chlamydia Pneumoniae serology and endothelial dysfunction of coronary arteries
Markus Ferrari1, Gerald S Werner, Barbara M Richartz
1Clinic of Internal Medicine I, Friedrich-Schiller-University, D - 07740 Jena, Germany. markus.ferrari@med.uni-jena.de
Insights
A previous Chlamydia Pneumoniae (CP) infection did not correlate with endothelial dysfunction in patients exhibiting coronary artery disease symptoms but lacking visible blockages. Further research is needed to understand CP
Area of Science:
- Cardiology
- Infectious Diseases
- Vascular Biology
Background:
- Coronary artery disease (CAD) hypothesis links Chlamydia Pneumoniae (CP) infection.
- Investigated endothelial dysfunction (ED) as an atherosclerosis precursor in CP-infected patients without angiographic CAD.
Purpose of the Study:
- To determine if endothelial dysfunction (ED) is detectable in patients with prior Chlamydia Pneumoniae (CP) infection but no visible coronary artery disease (CAD).
Main Methods:
- 16 patients with prior CP infection (elevated aCP-IgG) and 6 controls (negative aCP-IgG) were studied.
- Endothelial function assessed via acetylcholine (ACh) response in the left anterior descending coronary artery (LAD).
- Coronary flow velocity reserve (CFVR) measured using adenosine.
Main Results:
- 30% of CP-positive patients showed evidence of ED post-ACh.
- 67% of control patients exhibited ED.
- No association found between aCP-IgG levels and coronary blood flow changes after ACh.
- All patients had normal CFVR, regardless of CP status.
Conclusions:
- In patients with ischemic symptoms but no angiographic CAD or other risk factors, prior CP infection is not linked to endothelial dysfunction.
- Findings suggest CP infection may not be a primary driver of ED in this specific patient group.
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 microg/min and 36 microg/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 microg adenosine i. c.
Results:
10 patients had an elevated aCP-IgG (> 1:8). 6 patients with negative titers (aCP-IgG
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.
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