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[New information on the pathophysiology of atherosclerosis].
Lijec Vjesn. 2001 Jan-Feb; 123(1-2):26-31.LV

Abstract

The past decade has witnessed enormous progress in our understanding of the nature of this process. The development of an atherosclerotic plaque is a complex process which begins with endothelial dysfunction, the trigger for which are factors such as hypercholesterolemia, smoking, hypertension, hyperhomocysteinemia and impaired glucose metabolism. This dysfunction includes increased endothelial permeability to lipoproteins and other plasma constituents, which is mediated by NO, PDGF, prostacyclin, angiotensin II and endothelin; up-regulation of endothelial adhesion molecules including VCAM-1, ICAM-1, and selectins and migration of leukocytes and monocytes-macrophages in the subendothelial space mediated by oxidized LDL, MCP-1, PDGF and MCSF. The next step includes smooth-muscle cells migration (stimulated by PDGF and TGF-beta), T-cell activation (mediated by TNF-alpha and IL-2), formation of foam-cells from macrophages (mediated by oxidized LDL, MCSF, TNF-alpha and IL-1) and platelet adherence and aggregation (stimulated by thromboxane A2, tissue factor etc). The smooth muscle cells form a fibrous cap which confers mechanical stability of the plaque and separates the lipid rich thrombogenic core from the lumen and circulating blood. Whether a plaque will remain intact and therefore stable or rupture and lead to thrombosis causing an acute coronary syndrome (MI, unstable angina pectoris) depends upon a number of factors, the most important of which is its composition. Plaque size plays only a minor role in determining risk of an acute coronary syndrome. Rupture of the fibrous cap occurs due to thinning of the cap caused by an influx and activation of macrophages which release metalloproteinases and other proteolytic enzymes (stimulated by inflammatory cells, particularly T-lymphocytes). These enzymes cause degradation of the fibrous tissue of the cap which can result in thrombous formation and occlusion of the artery. Stable plaques have a thick fibrous cap, a small lipid core, and few inflammatory cells. In contrast, vulnerable plaques have a high lipid content, numerous inflammatory cells, and a thin fibrous cap with reduced collagen and vascular smooth muscle cells in it. Although vulnerable plaques are believed to account for only a small number of all coronary atheromas, they are responsible for most acute coronary events.

Authors+Show Affiliations

Klinika za unutrasnje bolesti Medicinskog fakulteta i KBC-a Zagreb, Rebro, Kispatićeva 12, 10000 Zagreb.No affiliation info available

Pub Type(s)

English Abstract
Journal Article
Review

Language

hrv

PubMed ID

11379194

Citation

Reiner, Z, and E Tedeschi-Reiner. "[New Information On the Pathophysiology of Atherosclerosis]." Lijecnicki Vjesnik, vol. 123, no. 1-2, 2001, pp. 26-31.
Reiner Z, Tedeschi-Reiner E. [New information on the pathophysiology of atherosclerosis]. Lijec Vjesn. 2001;123(1-2):26-31.
Reiner, Z., & Tedeschi-Reiner, E. (2001). [New information on the pathophysiology of atherosclerosis]. Lijecnicki Vjesnik, 123(1-2), 26-31.
Reiner Z, Tedeschi-Reiner E. [New Information On the Pathophysiology of Atherosclerosis]. Lijec Vjesn. 2001 Jan-Feb;123(1-2):26-31. PubMed PMID: 11379194.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [New information on the pathophysiology of atherosclerosis]. AU - Reiner,Z, AU - Tedeschi-Reiner,E, PY - 2001/5/31/pubmed PY - 2001/7/6/medline PY - 2001/5/31/entrez SP - 26 EP - 31 JF - Lijecnicki vjesnik JO - Lijec Vjesn VL - 123 IS - 1-2 N2 - The past decade has witnessed enormous progress in our understanding of the nature of this process. The development of an atherosclerotic plaque is a complex process which begins with endothelial dysfunction, the trigger for which are factors such as hypercholesterolemia, smoking, hypertension, hyperhomocysteinemia and impaired glucose metabolism. This dysfunction includes increased endothelial permeability to lipoproteins and other plasma constituents, which is mediated by NO, PDGF, prostacyclin, angiotensin II and endothelin; up-regulation of endothelial adhesion molecules including VCAM-1, ICAM-1, and selectins and migration of leukocytes and monocytes-macrophages in the subendothelial space mediated by oxidized LDL, MCP-1, PDGF and MCSF. The next step includes smooth-muscle cells migration (stimulated by PDGF and TGF-beta), T-cell activation (mediated by TNF-alpha and IL-2), formation of foam-cells from macrophages (mediated by oxidized LDL, MCSF, TNF-alpha and IL-1) and platelet adherence and aggregation (stimulated by thromboxane A2, tissue factor etc). The smooth muscle cells form a fibrous cap which confers mechanical stability of the plaque and separates the lipid rich thrombogenic core from the lumen and circulating blood. Whether a plaque will remain intact and therefore stable or rupture and lead to thrombosis causing an acute coronary syndrome (MI, unstable angina pectoris) depends upon a number of factors, the most important of which is its composition. Plaque size plays only a minor role in determining risk of an acute coronary syndrome. Rupture of the fibrous cap occurs due to thinning of the cap caused by an influx and activation of macrophages which release metalloproteinases and other proteolytic enzymes (stimulated by inflammatory cells, particularly T-lymphocytes). These enzymes cause degradation of the fibrous tissue of the cap which can result in thrombous formation and occlusion of the artery. Stable plaques have a thick fibrous cap, a small lipid core, and few inflammatory cells. In contrast, vulnerable plaques have a high lipid content, numerous inflammatory cells, and a thin fibrous cap with reduced collagen and vascular smooth muscle cells in it. Although vulnerable plaques are believed to account for only a small number of all coronary atheromas, they are responsible for most acute coronary events. SN - 0024-3477 UR - https://www.unboundmedicine.com/medline/citation/11379194/[New_information_on_the_pathophysiology_of_atherosclerosis]_ DB - PRIME DP - Unbound Medicine ER -