Atherosklerose--Suche nach einer neuen Entität [Atherosclerosis--search for a new entity].

Details

Serval ID
serval:BIB_310C4313DEB6
Type
Article: article from journal or magazin.
Collection
Publications
Title
Atherosklerose--Suche nach einer neuen Entität [Atherosclerosis--search for a new entity].
Journal
Verhandlungen Der Deutschen Gesellschaft Für Pathologie
Author(s)
Lehr H.A., Kirkpatrick C.J.
ISSN
0070-4113 (Print)
ISSN-L
0070-4113
Publication state
Published
Issued date
2001
Volume
85
Pages
132-141
Language
german
Notes
Publication types: English Abstract ; Journal ArticlePublication Status: ppublish
Abstract
Atherogenesis is a disease of middle-sized and large caliber blood vessels that can be divided into three major phases. The initial lesions of early atherosclerosis are characterized by the adhesion and subendothelial emigration of blood-borne monocytes, which differentiate into macrophages and provide the morphological basis for the formation of foam cells and fatty streak lesions. These lesions are found in most children and teenagers in industrialized nations. The next key event in atherogenesis is the proliferation of smooth muscle cells within the intima and media, resulting in the gradual compromise of the vessel lumen. Myofibroblastic cells also contribute to lesion growth through the production of excessive amounts of extracellular matrix. Such lesions are clinically silent unless progression to the next phase continues: the lesions degenerate, forming a mostly necrotic "lipid core" consisting of extracellular lipid, cholesterol crystals, inflammatory cells and necrotic debris. A fibrous cap is formed which prevents the interaction of blood cells, particularly of platelets with the highly proaggregatory material found in the lipid core. However, continuous inflammatory activity and/or heightened mechanical stress (i.e. in hypertension) tends to weaken the fibrous caps. Eventually, plaque rupture ensues, platelets aggregate, and the lesions become clinically manifest in such dramatic events as myocardial infarction, stroke, or mesenteric ischemia. Research into lesion formation and progression is limited by the fact that lesions develop in silence over many decades and that animal models only incompletely model the situation in humans. Most currently debated concepts accept the "response to injury" hypothesis formulated by the late Russell Ross and the multifactorial nature of atherogenesis. The discussion today circles around the relative contributions of low density lipoproteins (oxidized or enzymatically modified LDL?), the immune response (adaptive or innate?), infectious agents (CMV, chlamydia pneumoniae?), and/or hereditary factors, to name only a few of the most widely debated concepts. Irrespective of the outcome of this pathomechanistic discussion, the knowledge of established risk factors (hypercholesterolemia, hypertension, diabetes, smoking, etc.) and protective interventions (lifestyle changes, physical exercise, "healthy" diets, effective dietary and pharmacological control of hyperglycemia, blood pressure or hyperlipidemia) has helped to define atherosclerosis as a "new entity" that has little to do with the archaic concept of a "degenerative" vessel disease.
Keywords
Arteriosclerosis/classification, Arteriosclerosis/pathology, Extracellular Matrix/pathology, Humans, Muscle, Smooth, Vascular/pathology, Tunica Intima/pathology, Tunica Media/pathology
Pubmed
Create date
27/11/2011 19:32
Last modification date
20/08/2019 13:16
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