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Projects / Programmes source: ARIS

The role of bacteria chlamydia pneumoniae in the pathogenesis of diffuse coronary disease

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Research activity

Code Science Field Subfield
3.06.00  Medical sciences  Cardiovascular system   

Code Science Field
B530  Biomedical sciences  Cardiovascular system 
Keywords
coronary heart disease, Chlamydia pneumoniae, atherosclerosis, pathogenesis, risk factors
Evaluation (rules)
source: COBISS
Evaluation of bibliographic research performance indicators according to ARIS methodology
Citations Citations for bibliographic records in COBIB.SI that are linked to records in citation databases
source: WoS source: Scopus source: COBISS
Researchers (6)
no. Code Name and surname Research area Role Period No. of publications
1.  05381  PhD Darja Keše  Microbiology and immunology  Researcher  2002 - 2004  268 
2.  12888  PhD Mateja Legan  Metabolic and hormonal disorders  Head  2002 - 2004  84 
3.  11252  PhD Danijel Petrovič  Cardiovascular system  Researcher  2002 - 2004  318 
4.  01862  PhD Olga Vraspir-Porenta  Cardiovascular system  Researcher  2002 - 2004  108 
5.  03287  PhD Marjeta Zorc  Cardiovascular system  Researcher  2002 - 2004  181 
6.  07797  PhD Rudolfina Zorc-Pleskovič  Cardiovascular system  Researcher  2002 - 2004  138 
Organisations (1)
no. Code Research organisation City Registration number No. of publications
1.  0381  University of Ljubljana, Faculty of Medicine  Ljubljana  1627066  49,102 
Abstract
The inflammatory process causes diffuse and distal coronary disease. There are the evidences in literature datas on possible link between persistent bacterial infection with Chlamydia pneumoniae (CP) and atherosclerotic process. Besides experimental animals (mouses, rabbits) where CP was found and showed the acceleration of atherosclerosis, the seroepidemiological studies confirm higher incidency of chronical infection with CP in patients with acute myocardial infarction and unstable angina pectoris than in control group.The bactery was found in the vascular tissue of patients who died of coronary heart disease. The mechanism of artery wall damage by CP has not been explained yet. It is possible that CP is an incidental "passenger" in atheromatotic plaque. Maybe it accounts to local inflammation in the atheromatotic artery wall. Maybe it increases koagulability of blood leading to fatal incidents in atherosclerosis. It may influence the metabolism of holesterol and the formation of foam cells. In the prospective clinical study we want to find out whether our population of patients with diffuse and distal coronary heart disease differ in incidency of CP infection according to healthy population. The higher prevalency of chlamydial infection (as well as chronic CP infection) is expected in patients with coronary heart disease than in healthy controls. The single and cummulative role of CP will be evaluated, including other risk factors for atherosclerosis (hyperlipidaemia, arterial hypertension, diabetes, obesity, smoking). The histological and immunohistological analyses of endarterectomised sequesters of coronary artery patiets after the operation will contribute to eventually clearify the reason for the artery wall damage. The diagnostic screening of our patients and the subsequent antibiotic therapy of serological determined infection of CP will hopefully lead to better treatment of coronary heart disease.
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