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[Chlamydia pneumoniae in coronary plaques: Increased detection with acute coronary syndrome]
G Bauriedel1, U Welsch, J A Likungu
1Medizinische Klinik und Poliklinik II, Universität Bonn.
Insights
Chlamydia pneumoniae was found in 63% of coronary plaques, with a significantly higher prevalence in unstable angina and acute myocardial infarction cases. These findings suggest Chlamydia pneumoniae plays a role in human coronary plaque rupture.
Area of Science:
- Cardiovascular pathology
- Infectious disease research
- Microbiology
Context:
- Growing evidence links Chlamydia pneumoniae infection to atherosclerosis.
- The precise clinical significance and pathogenic mechanisms remain incompletely understood.
- This study investigates the presence and location of C. pneumoniae in coronary atheroma.
Purpose:
- To evaluate the presence and location of Chlamydia pneumoniae in coronary atheroma.
- To determine the prevalence of C. pneumoniae in relation to unstable versus stable angina.
- To explore potential associations with intimal features in coronary lesions.
Summary:
- Chlamydia pneumoniae was detected in 63% of coronary plaques from symptomatic patients.
- Immunoreaction for C. pneumoniae was significantly more frequent in lesions associated with unstable angina (84%) compared to stable angina (30%).
- Ultrastructural analysis revealed elementary bodies within foam cells and macrophages in areas of plaque rupture.
Impact:
- These in situ findings provide evidence for a pathogenic role of Chlamydia pneumoniae in human coronary plaque rupture.
- The study highlights C. pneumoniae's predilection for areas with signs of healing activity or propensity for rupture.
- Results contribute to understanding the infectious etiology of acute coronary syndromes.
Background And Objective:
There is seroepidemiologic and experimental evidence for a link between Chlamydia (C.) pneumoniae and arteriosclerosis. However, the clinical importance and the pathogenic pathways implicated remain unclear. In the present study, we sought to evaluate the presence and the location of C. pneumoniae in coronary atheroma, as well as a potential prevalence with unstable versus stable angina.
Patients And Methods:
Retrospectively, coronary plaque material of primary lesions from 51 consecutive patients (44 men, 7 women, mean age 59.6 +/- 9.4 years) was examined for the presence of C. pneumoniae by use of immuno-histochemistry and transmission electron microscopy. The findings associated with clinically acute coronary syndrome according to Braunwald's classification (n = 31) were compared to those with stable angina (n = 20) and regarded for potential relations to characteristic intimal features.
Results:
Immunoreaction for C. pneumoniae was found in 32 of 51 (63%) coronary plaques. Signals (% prevalence of specific intimal features) were present with necrotic areas (40%), sparse cellularity (40%), neo-vascularization (29%), thrombi (20%), ruptured plaque areas (19%), and fields rich in foam cells and calcifications (13%). Intimal hyperplasia and inflammatory infiltrates showed no signals. As the central finding in this report, C. pneumoniae immunoreaction was more frequently (P < 0.001) found in 26 of 31 (84%) lesions associated with unstable angina or acute myocardial infarction, compared to 6 of 20 (30%) lesions with stable angina (P < 0.001). Intact vessels devoid of arteriosclerotic disease, such as mammarial arteries and saphenous veins, were without C. pneumoniae signals (negative controls). Ultrastructurally, chlamydial elementary bodies were found in foam cells and phagocytosing macrophages, also in fragmented extracellular matrix adjacent to apoptotic and necrotic intimal cells.
Conclusions:
Chlamydiae pneumoniae were detected in 32 of 51 (63%) coronary primary lesions of symptomatic patients. Most importantly, there was a highly significant prevalence of lesions associated with acute coronary syndrome. Predilection sites of C. pneumoniae were areas that revealed small healing activity and (or) propensity to plaque rupture. The present in situ findings indicate a pathogenic role of Chlamydiae pneumoniae in human (coronary) plaque rupture.