Linked Life Data

11977579

Source:http://linkedlifedata.com/resource/pubmed/id/11977579

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2002-4-29
pubmed:abstractText
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 morphologic 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 multi-factorial 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 pharmacologic 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. The new concept takes us into the responsibility--puts us in charge of our own and our patients' cardiovascular risk--whether we like it or not. The smoking obese doctor no longer fits into the modern medical landscape.
pubmed:language
ger
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0723-5003
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
97
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
229-35
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
[Atherosclerosis--progression by nonspecific activation of the immune system].
pubmed:affiliation
Institut für Pathologie der Johannes Gutenberg-Universität Mainz. lehr@pathologie.klinik.uni-mainz.de
pubmed:publicationType
Journal Article, English Abstract, Review