The role of inflammation and infection in coronary artery disease

New insights into atherosclerosis, the most common disease affecting coronary arteries, may change therapeutic strategies from largely symptomatic to causal. Atherosclerotic plaques contain a lipid-related, immune-mediated inflammation, with release of secretory products capable of changing plaque m...

Full description

Saved in:
Bibliographic Details
Published in:Annual review of medicine Vol. 52; p. 289
Main Authors: Becker, A E, de Boer, O J, van Der Wal, A C
Format: Journal Article
Language:English
Published: United States Annual Reviews, Inc 01.01.2001
Subjects:
Chlamydia Infections - complications
Chlamydophila pneumoniae
Chronic Disease
Coronary Artery Disease - immunology
Coronary Artery Disease - microbiology
Coronary Artery Disease - pathology
Humans
Infection - complications
Inflammation
ISSN:0066-4219, 1545-326X
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:New insights into atherosclerosis, the most common disease affecting coronary arteries, may change therapeutic strategies from largely symptomatic to causal. Atherosclerotic plaques contain a lipid-related, immune-mediated inflammation, with release of secretory products capable of changing plaque morphology. Plaques prone to complications contain large numbers of inflammatory cells; stable plaques contain little inflammation. Similarly, atherectomy specimens from patients with coronary syndromes revealed more inflammatory cells in unstable than in stable patients. These observations, and the fact that acute coronary syndromes are associated with increased blood levels of inflammatory markers, have renewed interest in the possible relationship between infection and atherogenesis. Of all potential candidate antigens, Chlamydia pneumoniae presently is considered the most likely because a substantial number of patients with unstable syndromes contain C. pneumoniae-reactive T cells, both in blood and within the atherosclerotic plaque, suggesting enhancement of intraplaque inflammation.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 14
ObjectType-Review-3
content type line 23
ISSN:0066-4219
1545-326X
DOI:10.1146/annurev.med.52.1.289