Pathogenesis of atherosclerosis: a possible relation to infection

Authors
Citation
G. Noll, Pathogenesis of atherosclerosis: a possible relation to infection, ATHEROSCLER, 140, 1998, pp. S3-S9
Citations number
31
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
ATHEROSCLEROSIS
ISSN journal
00219150 → ACNP
Volume
140
Year of publication
1998
Supplement
1
Pages
S3 - S9
Database
ISI
SICI code
0021-9150(199810)140:<S3:POAAPR>2.0.ZU;2-I
Abstract
Atherosclerosis is the main underlying cause of coronary heart disease, whi ch in turn is the most common cause of death in the industrialized world. A n acute event in coronary heart disease is typically precipitated by thromb osis occurring at the site of atherosclerotic plaque disruption. Atheroscle rotic plaques consist of a fibrous cap overlying a lipid-rich core. Many ce ll types are involved in their formation, including platelets, endothelial cells, activated monocytes, macrophages derived from monocytes and smooth m uscle cells. The currently accepted hypothesis is that atherosclerosis deve lops as a response to injury and that it is primarily a chronic inflammator y condition. The endothelium plays an important role in regulating vascular blood flow and it is now apparent that endothelial dysfunction is an impor tant contributor to the pathogenesis of atherosclerosis. There is growing e vidence that infection may be a risk factor for atherosclerosis and myocard ial infarction. Numerous studies have reported associations between human c oronary heart disease (CHD) and bacterial and viral infections. At present, interest is focused on the potential aetiological role of C. pneumoniae wh ich has been repeatedly identified, using various diagnostic techniques, in atherosclerotic lesions. There is also increasing seroepidemiological evid ence of the association between C. pneumoniae and CHD. The role of this org anism in atherosclerosis may be analogous to that of chronic C. trachomatis infection in trachoma. (C) 1998 Elsevier Science Ireland Ltd. All rights r eserved.