The Anti-Oxidative Capacity of High-Density Lipoprotein Is Reduced in Acute Coronary Syndrome But Not in Stable Coronary Artery Disease

Objectives This study examined an anti-inflammatory property of high-density lipoprotein (HDL) in subjects with acute coronary syndrome (ACS) and stable coronary artery disease (CAD) compared with control subjects. Background HDL has anti-inflammatory properties in vitro, but its relationship to cor...

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Veröffentlicht in:Journal of the American College of Cardiology 2011-11, Vol.58 (20), p.2068-2075
Hauptverfasser: Patel, Parin J., MD, Khera, Amit V., MD, Jafri, Kashif, BA, Wilensky, Robert L., MD, Rader, Daniel J., MD
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container_issue 20
container_start_page 2068
container_title Journal of the American College of Cardiology
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creator Patel, Parin J., MD
Khera, Amit V., MD
Jafri, Kashif, BA
Wilensky, Robert L., MD
Rader, Daniel J., MD
description Objectives This study examined an anti-inflammatory property of high-density lipoprotein (HDL) in subjects with acute coronary syndrome (ACS) and stable coronary artery disease (CAD) compared with control subjects. Background HDL has anti-inflammatory properties in vitro, but its relationship to coronary disease in humans is unclear. The high-density lipoprotein inflammatory index (HII) measures the ability of HDL to mitigate oxidation of low-density lipoprotein; this function may be impaired in ACS and/or CAD. Methods We measured HII in 193 patients undergoing angiography for symptoms of CAD. Control subjects (n = 99) had no angiographic CAD, chronic CAD subjects (n = 51) had ≥70% vessel stenosis, and ACS subjects (n = 43) had ≥20% vessel stenosis and ischemia or infarction. We also examined HII in a cohort of healthy subjects randomly assigned to a statin or placebo. Results Subjects who had ACS had higher HII (less antioxidative capacity) compared with controls (1.57 vs. 1.17, p = 0.005) or those with chronic CAD (1.57 vs. 1.11, p = 0.006). HII was not different in subjects with stable CAD compared with controls. Furthermore, those subjects with higher HII were more likely to have ACS than no CAD (quartile 4 vs. 1, odds ratio [OR]: 1.74, p = 0.008). In a multivariate logistic regression model, HII was associated with ACS after adjusting for traditional cardiac risk factors (OR: 3.8, p = 0.003). There was a small improvement in HII after statin therapy compared with placebo (−14%, p = 0.03). Conclusions HDL has less anti-inflammatory capacity as assessed by HII in the setting of ACS compared with controls or subjects with chronic CAD.
doi_str_mv 10.1016/j.jacc.2011.08.030
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Background HDL has anti-inflammatory properties in vitro, but its relationship to coronary disease in humans is unclear. The high-density lipoprotein inflammatory index (HII) measures the ability of HDL to mitigate oxidation of low-density lipoprotein; this function may be impaired in ACS and/or CAD. Methods We measured HII in 193 patients undergoing angiography for symptoms of CAD. Control subjects (n = 99) had no angiographic CAD, chronic CAD subjects (n = 51) had ≥70% vessel stenosis, and ACS subjects (n = 43) had ≥20% vessel stenosis and ischemia or infarction. We also examined HII in a cohort of healthy subjects randomly assigned to a statin or placebo. Results Subjects who had ACS had higher HII (less antioxidative capacity) compared with controls (1.57 vs. 1.17, p = 0.005) or those with chronic CAD (1.57 vs. 1.11, p = 0.006). HII was not different in subjects with stable CAD compared with controls. Furthermore, those subjects with higher HII were more likely to have ACS than no CAD (quartile 4 vs. 1, odds ratio [OR]: 1.74, p = 0.008). In a multivariate logistic regression model, HII was associated with ACS after adjusting for traditional cardiac risk factors (OR: 3.8, p = 0.003). There was a small improvement in HII after statin therapy compared with placebo (−14%, p = 0.03). Conclusions HDL has less anti-inflammatory capacity as assessed by HII in the setting of ACS compared with controls or subjects with chronic CAD.</description><identifier>ISSN: 0735-1097</identifier><identifier>EISSN: 1558-3597</identifier><identifier>DOI: 10.1016/j.jacc.2011.08.030</identifier><identifier>PMID: 22051328</identifier><identifier>CODEN: JACCDI</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Acute Coronary Syndrome - metabolism ; acute coronary syndrome(s) ; Acute coronary syndromes ; Aged ; Atherosclerosis ; Biological and medical sciences ; Cardiology ; Cardiology. Vascular system ; Cardiovascular ; Cardiovascular disease ; Case-Control Studies ; Cholesterol ; Chronic illnesses ; Colleges &amp; universities ; Confidence intervals ; coronary artery disease ; Coronary Artery Disease - metabolism ; Coronary heart disease ; Coronary vessels ; Female ; HDL function ; HDL inflammatory index ; Heart ; Heart attacks ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology ; Internal Medicine ; Intubation ; Lipoproteins ; Lipoproteins, HDL - drug effects ; Lipoproteins, HDL - metabolism ; Male ; Medical sciences ; Middle Aged ; Myocarditis. Cardiomyopathies ; oxidized LDL ; Risk Factors ; Triglycerides</subject><ispartof>Journal of the American College of Cardiology, 2011-11, Vol.58 (20), p.2068-2075</ispartof><rights>American College of Cardiology Foundation</rights><rights>2011 American College of Cardiology Foundation</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2011 American College of Cardiology Foundation. 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Background HDL has anti-inflammatory properties in vitro, but its relationship to coronary disease in humans is unclear. The high-density lipoprotein inflammatory index (HII) measures the ability of HDL to mitigate oxidation of low-density lipoprotein; this function may be impaired in ACS and/or CAD. Methods We measured HII in 193 patients undergoing angiography for symptoms of CAD. Control subjects (n = 99) had no angiographic CAD, chronic CAD subjects (n = 51) had ≥70% vessel stenosis, and ACS subjects (n = 43) had ≥20% vessel stenosis and ischemia or infarction. We also examined HII in a cohort of healthy subjects randomly assigned to a statin or placebo. Results Subjects who had ACS had higher HII (less antioxidative capacity) compared with controls (1.57 vs. 1.17, p = 0.005) or those with chronic CAD (1.57 vs. 1.11, p = 0.006). HII was not different in subjects with stable CAD compared with controls. Furthermore, those subjects with higher HII were more likely to have ACS than no CAD (quartile 4 vs. 1, odds ratio [OR]: 1.74, p = 0.008). In a multivariate logistic regression model, HII was associated with ACS after adjusting for traditional cardiac risk factors (OR: 3.8, p = 0.003). There was a small improvement in HII after statin therapy compared with placebo (−14%, p = 0.03). Conclusions HDL has less anti-inflammatory capacity as assessed by HII in the setting of ACS compared with controls or subjects with chronic CAD.</description><subject>Acute Coronary Syndrome - metabolism</subject><subject>acute coronary syndrome(s)</subject><subject>Acute coronary syndromes</subject><subject>Aged</subject><subject>Atherosclerosis</subject><subject>Biological and medical sciences</subject><subject>Cardiology</subject><subject>Cardiology. Vascular system</subject><subject>Cardiovascular</subject><subject>Cardiovascular disease</subject><subject>Case-Control Studies</subject><subject>Cholesterol</subject><subject>Chronic illnesses</subject><subject>Colleges &amp; universities</subject><subject>Confidence intervals</subject><subject>coronary artery disease</subject><subject>Coronary Artery Disease - metabolism</subject><subject>Coronary heart disease</subject><subject>Coronary vessels</subject><subject>Female</subject><subject>HDL function</subject><subject>HDL inflammatory index</subject><subject>Heart</subject><subject>Heart attacks</subject><subject>Humans</subject><subject>Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology</subject><subject>Internal Medicine</subject><subject>Intubation</subject><subject>Lipoproteins</subject><subject>Lipoproteins, HDL - drug effects</subject><subject>Lipoproteins, HDL - metabolism</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Myocarditis. 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Vascular system</topic><topic>Cardiovascular</topic><topic>Cardiovascular disease</topic><topic>Case-Control Studies</topic><topic>Cholesterol</topic><topic>Chronic illnesses</topic><topic>Colleges &amp; universities</topic><topic>Confidence intervals</topic><topic>coronary artery disease</topic><topic>Coronary Artery Disease - metabolism</topic><topic>Coronary heart disease</topic><topic>Coronary vessels</topic><topic>Female</topic><topic>HDL function</topic><topic>HDL inflammatory index</topic><topic>Heart</topic><topic>Heart attacks</topic><topic>Humans</topic><topic>Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology</topic><topic>Internal Medicine</topic><topic>Intubation</topic><topic>Lipoproteins</topic><topic>Lipoproteins, HDL - drug effects</topic><topic>Lipoproteins, HDL - metabolism</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Myocarditis. Cardiomyopathies</topic><topic>oxidized LDL</topic><topic>Risk Factors</topic><topic>Triglycerides</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Patel, Parin J., MD</creatorcontrib><creatorcontrib>Khera, Amit V., MD</creatorcontrib><creatorcontrib>Jafri, Kashif, BA</creatorcontrib><creatorcontrib>Wilensky, Robert L., MD</creatorcontrib><creatorcontrib>Rader, Daniel J., MD</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>Nursing &amp; Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of the American College of Cardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Patel, Parin J., MD</au><au>Khera, Amit V., MD</au><au>Jafri, Kashif, BA</au><au>Wilensky, Robert L., MD</au><au>Rader, Daniel J., MD</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Anti-Oxidative Capacity of High-Density Lipoprotein Is Reduced in Acute Coronary Syndrome But Not in Stable Coronary Artery Disease</atitle><jtitle>Journal of the American College of Cardiology</jtitle><addtitle>J Am Coll Cardiol</addtitle><date>2011-11-08</date><risdate>2011</risdate><volume>58</volume><issue>20</issue><spage>2068</spage><epage>2075</epage><pages>2068-2075</pages><issn>0735-1097</issn><eissn>1558-3597</eissn><coden>JACCDI</coden><abstract>Objectives This study examined an anti-inflammatory property of high-density lipoprotein (HDL) in subjects with acute coronary syndrome (ACS) and stable coronary artery disease (CAD) compared with control subjects. Background HDL has anti-inflammatory properties in vitro, but its relationship to coronary disease in humans is unclear. The high-density lipoprotein inflammatory index (HII) measures the ability of HDL to mitigate oxidation of low-density lipoprotein; this function may be impaired in ACS and/or CAD. Methods We measured HII in 193 patients undergoing angiography for symptoms of CAD. Control subjects (n = 99) had no angiographic CAD, chronic CAD subjects (n = 51) had ≥70% vessel stenosis, and ACS subjects (n = 43) had ≥20% vessel stenosis and ischemia or infarction. We also examined HII in a cohort of healthy subjects randomly assigned to a statin or placebo. Results Subjects who had ACS had higher HII (less antioxidative capacity) compared with controls (1.57 vs. 1.17, p = 0.005) or those with chronic CAD (1.57 vs. 1.11, p = 0.006). HII was not different in subjects with stable CAD compared with controls. Furthermore, those subjects with higher HII were more likely to have ACS than no CAD (quartile 4 vs. 1, odds ratio [OR]: 1.74, p = 0.008). In a multivariate logistic regression model, HII was associated with ACS after adjusting for traditional cardiac risk factors (OR: 3.8, p = 0.003). There was a small improvement in HII after statin therapy compared with placebo (−14%, p = 0.03). Conclusions HDL has less anti-inflammatory capacity as assessed by HII in the setting of ACS compared with controls or subjects with chronic CAD.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>22051328</pmid><doi>10.1016/j.jacc.2011.08.030</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record>
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subjects Acute Coronary Syndrome - metabolism
acute coronary syndrome(s)
Acute coronary syndromes
Aged
Atherosclerosis
Biological and medical sciences
Cardiology
Cardiology. Vascular system
Cardiovascular
Cardiovascular disease
Case-Control Studies
Cholesterol
Chronic illnesses
Colleges & universities
Confidence intervals
coronary artery disease
Coronary Artery Disease - metabolism
Coronary heart disease
Coronary vessels
Female
HDL function
HDL inflammatory index
Heart
Heart attacks
Humans
Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology
Internal Medicine
Intubation
Lipoproteins
Lipoproteins, HDL - drug effects
Lipoproteins, HDL - metabolism
Male
Medical sciences
Middle Aged
Myocarditis. Cardiomyopathies
oxidized LDL
Risk Factors
Triglycerides
title The Anti-Oxidative Capacity of High-Density Lipoprotein Is Reduced in Acute Coronary Syndrome But Not in Stable Coronary Artery Disease
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