Document Detail


Arterial remodeling in [corrected] subclinical carotid artery disease.
MedLine Citation:
PMID:  20083072     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVES: We sought to identify clinical and/or plaque characteristics that affect atherosclerotic disease progression and arterial remodeling in the carotid artery with subclinical stenosis.
BACKGROUND: Increasing severity of stenosis has been associated with a higher risk of stroke. Factors that drive subclinical lesions to become stenotic plaques remain ambiguous. Carotid magnetic resonance imaging (MRI) has been validated with histology to accurately quantify in vivo arterial morphology and plaque composition.
METHODS: A total of 67 asymptomatic participants with 16% to 49% carotid stenosis as demonstrated by duplex ultrasonography were imaged at 1.5-T with a carotid MRI protocol at baseline and at 18-month follow-up. Clinical and/or intra-arterial metrics with a significant association with change in plaque burden during multivariate analysis were evaluated for effects on lumen, wall, and total vessel volume.
RESULTS: From multiple regression analysis, intraplaque hemorrhage (IPH) (p < 0.001) and statin therapy (p = 0.015) were identified as key determinants of change in plaque burden. The group with IPH compared with the group without IPH demonstrated luminal narrowing, with a mean +/- SD decrease in lumen volume (-24.9 +/- 21.1 mm(3)/year vs. -0.5 +/- 26.9 mm(3)/year; p = 0.005), a larger increase in wall volume (44.1 +/- 36.1 mm(3)/year vs. 0.8 +/- 34.5 mm(3)/year; p < 0.001), and no difference in total vessel volume (19.3 +/- 27.4 mm(3)/year vs. 0.4 +/- 42.4 mm(3)/year; p = 0.15). The nonstatin group compared with the statin group demonstrated outward remodeling, with an increase in wall volume (22.4 +/- 35.6 mm(3)/year(3)/year vs. 0.9 +/- 38.0 mm(3)/year; p = 0.026) and total vessel volume (19.2 +/- 36.9 mm(3)/year vs. -4.9 +/- 40.4 mm(3)/year; p = 0.019) and no difference in lumen volume (-5.8 +/- 26.6 mm(3)/year vs. -3.2 +/- 29.5 mm(3)/year; p = 0.72).
CONCLUSIONS: IPH may represent an indication of accelerated plaque growth and impending luminal compromise in the subclinical carotid artery. Statin therapy may stabilize lesions by slowing or halting lesion progression. This phase of plaque stenosis (16% to 49%) may be a critical stage for intrinsic and extrinsic factors to affect the atherosclerotic disease process.
Authors:
Hunter R Underhill; Chun Yuan; Vasily L Yarnykh; Baocheng Chu; Minako Oikawa; Nayak L Polissar; Stephen M Schwartz; Gail P Jarvik; Thomas S Hatsukami
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  JACC. Cardiovascular imaging     Volume:  2     ISSN:  1876-7591     ISO Abbreviation:  JACC Cardiovasc Imaging     Publication Date:  2009 Dec 
Date Detail:
Created Date:  2010-01-19     Completed Date:  2010-03-29     Revised Date:  2013-05-31    
Medline Journal Info:
Nlm Unique ID:  101467978     Medline TA:  JACC Cardiovasc Imaging     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1381-9     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Aged
Aged, 80 and over
Blood Pressure
Carotid Arteries / pathology*,  ultrasonography
Carotid Stenosis / complications,  drug therapy,  pathology*,  physiopathology
Disease Progression
Female
Hemorrhage / etiology*,  pathology,  physiopathology,  prevention & control
Humans
Hydroxymethylglutaryl-CoA Reductase Inhibitors / therapeutic use
Magnetic Resonance Angiography
Male
Middle Aged
Predictive Value of Tests
Prospective Studies
Risk Factors
Severity of Illness Index
Time Factors
Ultrasonography, Doppler, Duplex
Grant Support
ID/Acronym/Agency:
P01 HL072262-01/HL/NHLBI NIH HHS; P01 HL072262-010002/HL/NHLBI NIH HHS; P01-HL072262/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Hydroxymethylglutaryl-CoA Reductase Inhibitors
Comments/Corrections
Comment In:
JACC Cardiovasc Imaging. 2009 Dec;2(12):1390-2   [PMID:  20083073 ]
Erratum In:
JACC Cardiovasc Imaging. 2010 Feb;3(2):226

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


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