Document Detail

Is there life after plaque rupture?
MedLine Citation:
PMID:  17956238     Owner:  NLM     Status:  MEDLINE    
Little is known of the relationship between plaque rupture and adaptive geometric remodelling, especially in the context of unstable atherosclerosis. We have assessed remodelling in the proximal brachiocephalic arteries of fat-fed apoE (apolipoprotein E)-knockout mice. The rate of vessel expansive remodelling is similar in vessels with plaques and without plaques, suggesting that the presence of plaque is not necessary for remodelling to occur. In vessels with plaques, the degree of expansive remodelling was strongly associated with the stability of the plaque. Vessels with stable plaques (i.e. with neither buried fibrous caps nor acute plaque ruptures) showed no expansion, whereas those with evidence of plaque rupture expanded at a significant rate. Vessels with stable plaques suffered significant loss of lumen over time, but those with unstable plaques maintained lumen area over time. Pravastatin treatment of male apoE-knockout mice caused a 5-fold increase in fibrous cap thickness and, although it did not influence overall rates of vessel remodelling, it significantly increased both the amount of vessel expansion and the period of time between plaque ruptures, suggesting that it increases the ability of the plaque to resist the rupturing force caused by vessel expansion. These results suggest that vessel expansion in brachiocephalic arteries of fat-fed apoE-knockout mouse does not require the presence of plaque. When a plaque is present, the outward remodelling force is exerted across its cap: vessels with smaller outward remodelling forces cannot overcome the strength of the cap, and the plaque remains stable. When the remodelling force is greater than the strength of the cap, the plaque ruptures. Thus plaque rupture can be viewed as a consequence of vessel remodelling. Interventions that strengthen the plaque, such as pravastatin therapy, do not alter remodelling parameters but instead allow for more outward remodelling before a rupture is caused.
C L Jackson
Related Documents :
1601918 - Parietal inflammatory infiltrate in peripheral aneurysms of atherosclerotic origin.
15047378 - Tissue velocity imaging of coronary artery by rotating-type intravascular ultrasound.
1579968 - Amount of smoking independently predicts carotid artery atherosclerosis severity.
11442968 - Doppler microembolic signals for diagnosis of ulcerated carotid artery plaques.
2012418 - Tricuspid valve repair for tricuspid valve endocarditis: tricuspid valve "recycling".
21789748 - The prevalence and distribution of coronary artery calcium in asymptomatic korean popul...
Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Biochemical Society transactions     Volume:  35     ISSN:  0300-5127     ISO Abbreviation:  Biochem. Soc. Trans.     Publication Date:  2007 Nov 
Date Detail:
Created Date:  2007-10-24     Completed Date:  2008-02-05     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7506897     Medline TA:  Biochem Soc Trans     Country:  England    
Other Details:
Languages:  eng     Pagination:  887-9     Citation Subset:  IM    
Bristol Heart Institute, University of Bristol, Level 7, Bristol Royal Infirmary, Bristol BS2 8HW, U.K.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Apolipoproteins E / genetics,  physiology
Atherosclerosis / pathology*
Mice, Knockout
Reg. No./Substance:
0/Apolipoproteins E

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Peroxisomal disorders affecting phytanic acid alpha-oxidation: a review.
Next Document:  Ion channel switching and activation in smooth-muscle cells of occlusive vascular diseases.