Linked Life Data

12615292

Source:http://linkedlifedata.com/resource/pubmed/id/12615292

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4A
pubmed:dateCreated
2003-3-4
pubmed:abstractText
The traditional view of cardiovascular disease held that the degree of stenosis defined high-risk lesions and that removal of cholesterol shrank these lesions and thereby enlarged the lumen. Advances in understanding of the pathophysiology of the acute coronary syndromes refute this view. We now appreciate that vascular biology determines plaque stability and that statins stabilize plaque by favorably altering this biology. They do so chiefly (but probably not exclusively) by cholesterol lowering. In addition to reducing the cholesterol content of plaque, lipid lowering inhibits inflammation, and decreases collagenolytic activity and thrombotic potential. The role of lipid-independent effects remains unclear because many studies used statin concentrations too high to have any clinical relevance. However, data suggest that statin-induced alterations in the function of small G proteins may contribute to the anti-inflammatory and antithrombotic actions of statins in clinical practice.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0002-9149
pubmed:author
pubmed:issnType
Print
pubmed:day
20
pubmed:volume
91
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4B-8B
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Mechanisms of plaque stabilization with statins.
pubmed:affiliation
Leducq Center for Cardiovascular Research, Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA. plibby@rics.harvard.edu
pubmed:publicationType
Journal Article, Review