| Arterial remodeling in [corrected] subclinical carotid artery disease. | |
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MedLine Citation:
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PMID: 20083072 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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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:
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Type: Journal Article; Research Support, N.I.H., Extramural |
Journal Detail:
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Title: JACC. Cardiovascular imaging Volume: 2 ISSN: 1876-7591 ISO Abbreviation: JACC Cardiovasc Imaging Publication Date: 2009 Dec |
Date Detail:
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Created Date: 2010-01-19 Completed Date: 2010-03-29 Revised Date: 2011-09-26 |
Medline Journal Info:
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Nlm Unique ID: 101467978 Medline TA: JACC Cardiovasc Imaging Country: United States |
Other Details:
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Languages: eng Pagination: 1381-9 Citation Subset: IM |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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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:
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P01 HL072262-01/HL/NHLBI NIH HHS; P01 HL072262-010002/HL/NHLBI NIH HHS; P01-HL072262/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Hydroxymethylglutaryl-CoA Reductase Inhibitors |
| Comments/Corrections | |
Comment In:
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JACC Cardiovasc Imaging. 2009 Dec;2(12):1390-2
[PMID:
20083073
]
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Erratum In:
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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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