Linked Life Data

11296789

Source:http://linkedlifedata.com/resource/pubmed/id/11296789

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2001-4-11
pubmed:abstractText
Landmark pathological studies have deepened our understanding of the mechanisms behind acute coronary syndromes over the last decade. Thrombosis plays a key role and is a unifying feature in the pathogenesis. Platelet-rich thrombus superimposed over the disrupted atherosclerotic plaque or eroded plaque endothelium, with or without fibrin-thrombus extension, is evident in postmortem necropsy, angiographic and angioscopic studies. However features which contribute to the risk of acute events lie in the atherosclerotic plaque itself. Plaque content and not plaque size is the important factor. A vulnerable plaque may be invisible on clinical stress testing and even coronary angiography; but it is prone to rupture if it has only a thin cap and a proportionally larger lipid core. There is a cellular preponderance of activated macrophages and T-lymphocytes; and high activity of matrix metalloproteinases in vulnerable plaques. Smooth muscle cell proliferation and collagen synthesis are downregulated. These features may serve as possible targets for detecting plaques at risk or for reversing the risk of vulnerable plaques.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0037-5675
pubmed:author
pubmed:issnType
Print
pubmed:volume
41
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
606-10
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
Concepts in acute coronary syndromes.
pubmed:affiliation
Division of Cardiology, Department of Medicine and Therapeutics, Leicester University, Glenfield Hospital, Clinical Sciences Wing, Leicester LE3 9QP, UK. rf226@medschl.cam.ac.uk
pubmed:publicationType
Journal Article, Review