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Systemic inflammation, Chlamydia pneumoniae DNA in circulating leukocytes and coronary atherosclerosis
Vicky Hoymans1, Johan Bosmans, Dominique Ursi
1Department of Cardiology, University Hospital Antwerp, Edegem, Belgium.
Insights
Chlamydia pneumoniae DNA was not detected in white blood cells of patients with ischemic heart disease. This suggests no link between circulating C. pneumoniae, inflammation, and coronary atherosclerosis extent.
Area of Science:
- Cardiovascular Medicine
- Infectious Diseases
- Molecular Biology
Background:
- Emerging evidence suggests Chlamydia pneumoniae (C. pneumoniae) may drive atherosclerosis through vascular wall inflammation.
- Understanding the role of C. pneumoniae in cardiovascular disease is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate the prevalence of C. pneumoniae DNA in leukocytes of patients with ischemic heart disease.
- To correlate C. pneumoniae detection with coronary atherosclerosis severity and systemic inflammation markers.
Main Methods:
- Polymerase chain reaction (PCR) was used to detect C. pneumoniae DNA in circulating white blood cells of 203 patients.
- Coronary angiography assessed the extent of coronary atherosclerosis.
- Serum levels of C-reactive protein (CRP) and fibrinogen were measured as inflammation markers.
Main Results:
- C. pneumoniae DNA was not detected in the leukocytes of any patient.
- Serum CRP levels were significantly elevated in patients with significant coronary artery disease compared to those with normal arteries.
- Higher CRP levels correlated with the extent of coronary atherosclerosis, and a positive correlation was observed between CRP and fibrinogen.
Conclusions:
- Despite a clear association between systemic inflammation markers (CRP) and the severity of coronary atherosclerosis, circulating C. pneumoniae was not detected.
- These findings indicate no apparent relationship between circulating C. pneumoniae, systemic inflammation, and the extent of coronary atherosclerosis.
Objective:
Earlier studies have suggested that C. pneumoniae may be involved in the progression of atherosclerosis by contributing to the pathogenesis of inflammation in the vessel wall. The aim of the present study was to determine the prevalence of C. pneumoniae DNA in circulating white blood cells of patients with ischaemic heart disease and to correlate these findings with the extent of coronary atherosclerosis and serum markers of inflammation.
Methods And Results:
In 203 consecutive patients undergoing diagnostic coronary angiography for different coronary syndromes, presence of C. pneumoniae DNA in circulating leukocytes could not be demonstrated by the polymerase chain reaction. Serum concentrations of CRP were significantly higher in patients with significant coronary artery disease compared to those with normal coronary arteries. In addition, patients with a three-vessel disease had significantly higher serum CRP compared to patients with diffuse, non-critical coronary atherosclerosis. A positive correlation was found between serum fibrinogen and serum CRP.
Conclusion:
In spite of a significant relation between serum CRP and the extent of atherosclerotic coronary artery disease, we were unable to detect C. pneumoniae DNA in circulating white blood cells. This observation suggests that there is no relation between circulating C. pneumoniae, systemic inflammation and extent of coronary atherosclerosis.