Document Detail


The effect of lipid and inflammatory profiles on the morphological changes of lipid-rich plaques in patients with non-ST-segment elevated acute coronary syndrome: follow-up study by optical coherence tomography and intravascular ultrasound.
MedLine Citation:
PMID:  20650439     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVES: The aim of this study was to determine the relationship between the morphological changes of nonculprit lipid-rich plaques and several clinical profiles in patients with non-ST-segment elevated acute coronary syndrome (NSTEACS).
BACKGROUND: Identification of coronary lesion with morphological characteristics of rupture-prone plaques is still difficult.
METHODS: Eighty-two consecutive patients with NSTEACS who underwent percutaneous coronary intervention were enrolled. The changes in total atheroma volume (TAV) of residual nonculprit lipid-rich plaques and the changes in the corresponding fibrous cap thickness (FCT) were assessed by intravascular ultrasound and optical coherence tomography, respectively, at baseline and after 9 months.
RESULTS: The percentage changes in TAV (mm(3)) of lipid-rich plaques and in the corresponding FCT (microm) over the 9-month follow-up period were 3.1 +/- 11% and 15 +/- 17%, respectively. There was no significant correlation between the changes in TAV and those in FCT. The change in TAV showed a significant correlation with reduction of the low-density lipoprotein/high-density lipoprotein (LDL/HDL) ratio (r = 0.42, p < 0.01). In contrast, the change in FCT showed no correlation with LDL/HDL ratio but had a significant positive correlation with changes in high-sensitivity C-reactive protein (r = 0.44, p < 0.01). Furthermore, in multivariate logistic analysis, statin use was an independent predictor of changes in well-stabilized plaques that showed both TAV reduction and FCT increase.
CONCLUSIONS: The changes in TAV and FCT of coronary plaques over a 9-month observation period were related to 2 different independent factors (i.e., reduction of LDL-cholesterol and high-sensitivity C-reactive protein, respectively). Furthermore, lipid-lowering therapy with statin has the potential to stabilize these parameters by both plaque reduction and FCT.
Authors:
Shigeho Takarada; Toshio Imanishi; Kohei Ishibashi; Takashi Tanimoto; Kenichi Komukai; Yasushi Ino; Hironori Kitabata; Takashi Kubo; Atsushi Tanaka; Keizo Kimura; Masato Mizukoshi; Takashi Akasaka
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Publication Detail:
Type:  Comparative Study; Journal Article    
Journal Detail:
Title:  JACC. Cardiovascular interventions     Volume:  3     ISSN:  1876-7605     ISO Abbreviation:  JACC Cardiovasc Interv     Publication Date:  2010 Jul 
Date Detail:
Created Date:  2010-07-23     Completed Date:  2010-11-08     Revised Date:  2014-09-05    
Medline Journal Info:
Nlm Unique ID:  101467004     Medline TA:  JACC Cardiovasc Interv     Country:  United States    
Other Details:
Languages:  eng     Pagination:  766-72     Citation Subset:  IM    
Copyright Information:
Copyright 2010 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.
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MeSH Terms
Descriptor/Qualifier:
Acute Coronary Syndrome / blood,  diagnosis,  etiology,  therapy*
Aged
Aged, 80 and over
Angioplasty, Balloon, Coronary*
Biological Markers / blood
C-Reactive Protein / metabolism*
Cholesterol, HDL / blood
Cholesterol, LDL / blood*
Coronary Angiography
Coronary Artery Disease / blood,  complications,  diagnosis,  therapy*
Coronary Vessels* / pathology,  ultrasonography
Cross-Sectional Studies
Female
Fibrosis
Humans
Hydroxymethylglutaryl-CoA Reductase Inhibitors
Inflammation Mediators / blood*
Japan
Logistic Models
Male
Middle Aged
Odds Ratio
Risk Assessment
Risk Factors
Time Factors
Tomography, Optical Coherence*
Treatment Outcome
Ultrasonography, Interventional*
Chemical
Reg. No./Substance:
0/Biological Markers; 0/Cholesterol, HDL; 0/Cholesterol, LDL; 0/Hydroxymethylglutaryl-CoA Reductase Inhibitors; 0/Inflammation Mediators; 9007-41-4/C-Reactive Protein

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


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