Risk Factors, biochemical markers, and genetic polymorphisms in early coronary artery disease
To assess the risk factors, lipid and apolipoprotein profile, hemostasis variables, and polymorphisms of the apolipoprotein AI-CIII gene in early coronary artery disease (CAD). Case-control study with 112 patients in each group controlled by sex and age. After clinical evaluation and nutritional ins...
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Veröffentlicht in: | Arquivos brasileiros de cardiologia 2003-04, Vol.80 (4), p.379-395 |
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creator | Izar, Maria Cristina Fonseca, Francisco Antonio Helfenstein Ihara, Sílvia Saiuli Miki Kasinski, Nelson Sang, Won Han Lopes, Ieda Edite Lanzarini Pinto, Leonor do Espírito Santo de Almeida Relvas, Waldir Gabriel Miranda Lourenço, Daisy Tufik, Sérgio de Paola, Angelo Amato Vincenzo Carvalho, Antonio Carlos Camargo |
description | To assess the risk factors, lipid and apolipoprotein profile, hemostasis variables, and polymorphisms of the apolipoprotein AI-CIII gene in early coronary artery disease (CAD).
Case-control study with 112 patients in each group controlled by sex and age. After clinical evaluation and nutritional instruction, blood samples were collected for biochemical assays and genetic study.
Familial history of early CAD (64 vs 39%), arterial hypertension (69 vs 36%), diabetes mellitus (25 vs 3%), and previous smoking (71 vs 46%) were more prevalent in the case group (p |
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Case-control study with 112 patients in each group controlled by sex and age. After clinical evaluation and nutritional instruction, blood samples were collected for biochemical assays and genetic study.
Familial history of early CAD (64 vs 39%), arterial hypertension (69 vs 36%), diabetes mellitus (25 vs 3%), and previous smoking (71 vs 46%) were more prevalent in the case group (p<0.001). Hypertension and diabetes were independent risk factors. Early CAD was characterized by higher serum levels of total cholesterol (235 +/-6 vs 209 +/- 4 mg/dL), of LDL-c (154 +/- 5 vs 135 +/- 4 mg/dL), triglycerides (205 +/- 12 vs 143 +/- 9 mg/dL), and apolipoprotein B (129 +/- 3 vs 105 +/- 3 mg/dL), and lower serum levels of HDL-c (40 +/- 1 vs 46 +/- 1 mg/dL) and apolipoprotein AI (134 +/- 2 vs 146 +/- 2mg/dL) [p<0.01], in addition to an elevation in fibrinogen and D-dimer (p<0.02). The simultaneous presence of the rare alleles of the APO AI-CIII genes in early CAD are associated with hypertriglyceridemia (p=0.03).
Of the classical risk factors, hypertension and diabetes mellitus were independently associated with early CAD. In addition to an unfavorable lipid profile, an increase in the thrombotic risk was identified in this population. An additive effect of the APO AI-CIII genes was observed in triglyceride levels.</description><identifier>ISSN: 0066-782X</identifier><identifier>PMID: 12754559</identifier><language>eng ; por</language><publisher>Brazil</publisher><subject>Adult ; Apolipoprotein A-I - genetics ; Apolipoprotein C-III ; Apolipoproteins C - genetics ; Biomarkers - blood ; Case-Control Studies ; Coronary Artery Disease - blood ; Coronary Artery Disease - etiology ; Coronary Artery Disease - genetics ; Female ; Hemostasis ; Humans ; Lipids - blood ; Male ; Middle Aged ; Polymorphism, Genetic ; Risk Factors</subject><ispartof>Arquivos brasileiros de cardiologia, 2003-04, Vol.80 (4), p.379-395</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12754559$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Izar, Maria Cristina</creatorcontrib><creatorcontrib>Fonseca, Francisco Antonio Helfenstein</creatorcontrib><creatorcontrib>Ihara, Sílvia Saiuli Miki</creatorcontrib><creatorcontrib>Kasinski, Nelson</creatorcontrib><creatorcontrib>Sang, Won Han</creatorcontrib><creatorcontrib>Lopes, Ieda Edite Lanzarini</creatorcontrib><creatorcontrib>Pinto, Leonor do Espírito Santo de Almeida</creatorcontrib><creatorcontrib>Relvas, Waldir Gabriel Miranda</creatorcontrib><creatorcontrib>Lourenço, Daisy</creatorcontrib><creatorcontrib>Tufik, Sérgio</creatorcontrib><creatorcontrib>de Paola, Angelo Amato Vincenzo</creatorcontrib><creatorcontrib>Carvalho, Antonio Carlos Camargo</creatorcontrib><title>Risk Factors, biochemical markers, and genetic polymorphisms in early coronary artery disease</title><title>Arquivos brasileiros de cardiologia</title><addtitle>Arq Bras Cardiol</addtitle><description>To assess the risk factors, lipid and apolipoprotein profile, hemostasis variables, and polymorphisms of the apolipoprotein AI-CIII gene in early coronary artery disease (CAD).
Case-control study with 112 patients in each group controlled by sex and age. After clinical evaluation and nutritional instruction, blood samples were collected for biochemical assays and genetic study.
Familial history of early CAD (64 vs 39%), arterial hypertension (69 vs 36%), diabetes mellitus (25 vs 3%), and previous smoking (71 vs 46%) were more prevalent in the case group (p<0.001). Hypertension and diabetes were independent risk factors. Early CAD was characterized by higher serum levels of total cholesterol (235 +/-6 vs 209 +/- 4 mg/dL), of LDL-c (154 +/- 5 vs 135 +/- 4 mg/dL), triglycerides (205 +/- 12 vs 143 +/- 9 mg/dL), and apolipoprotein B (129 +/- 3 vs 105 +/- 3 mg/dL), and lower serum levels of HDL-c (40 +/- 1 vs 46 +/- 1 mg/dL) and apolipoprotein AI (134 +/- 2 vs 146 +/- 2mg/dL) [p<0.01], in addition to an elevation in fibrinogen and D-dimer (p<0.02). The simultaneous presence of the rare alleles of the APO AI-CIII genes in early CAD are associated with hypertriglyceridemia (p=0.03).
Of the classical risk factors, hypertension and diabetes mellitus were independently associated with early CAD. In addition to an unfavorable lipid profile, an increase in the thrombotic risk was identified in this population. An additive effect of the APO AI-CIII genes was observed in triglyceride levels.</description><subject>Adult</subject><subject>Apolipoprotein A-I - genetics</subject><subject>Apolipoprotein C-III</subject><subject>Apolipoproteins C - genetics</subject><subject>Biomarkers - blood</subject><subject>Case-Control Studies</subject><subject>Coronary Artery Disease - blood</subject><subject>Coronary Artery Disease - etiology</subject><subject>Coronary Artery Disease - genetics</subject><subject>Female</subject><subject>Hemostasis</subject><subject>Humans</subject><subject>Lipids - blood</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Polymorphism, Genetic</subject><subject>Risk Factors</subject><issn>0066-782X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo1kEFLwzAYhnNQ3Jz-BcnJk4U0yde0RxlOBwNBdvAiJU2-urimqUl76L934jw98PLwwvtekCVjRZGpkr8vyHVKX4xxrgRckUXOFUiAakk-3lw60o02Y4jpgTYumAN6Z3RHvY5H_A11b-kn9jg6Q4fQzT7E4eCST9T1FHXsZmpCDL2OM9VxxBOsS6gT3pDLVncJb89ckf3mab9-yXavz9v14y4bQFaZbEsujQQrEJTAAsoSWwENMGglU8pKVVWytDoXXDPT8MIYaFqFphLKVo1Ykfu_2iGG7wnTWHuXDHad7jFMqVZCMJkzOIl3Z3FqPNp6iO60cq7__xA_DVZcTg</recordid><startdate>200304</startdate><enddate>200304</enddate><creator>Izar, Maria Cristina</creator><creator>Fonseca, Francisco Antonio Helfenstein</creator><creator>Ihara, Sílvia Saiuli Miki</creator><creator>Kasinski, Nelson</creator><creator>Sang, Won Han</creator><creator>Lopes, Ieda Edite Lanzarini</creator><creator>Pinto, Leonor do Espírito Santo de Almeida</creator><creator>Relvas, Waldir Gabriel Miranda</creator><creator>Lourenço, Daisy</creator><creator>Tufik, Sérgio</creator><creator>de Paola, Angelo Amato Vincenzo</creator><creator>Carvalho, Antonio Carlos Camargo</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>200304</creationdate><title>Risk Factors, biochemical markers, and genetic polymorphisms in early coronary artery disease</title><author>Izar, Maria Cristina ; Fonseca, Francisco Antonio Helfenstein ; Ihara, Sílvia Saiuli Miki ; Kasinski, Nelson ; Sang, Won Han ; Lopes, Ieda Edite Lanzarini ; Pinto, Leonor do Espírito Santo de Almeida ; Relvas, Waldir Gabriel Miranda ; Lourenço, Daisy ; Tufik, Sérgio ; de Paola, Angelo Amato Vincenzo ; Carvalho, Antonio Carlos Camargo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p549-4f824c45d3e573e6588ef35b505f4077d479948da132a0cb26cc5bf7ec937d9b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng ; por</language><creationdate>2003</creationdate><topic>Adult</topic><topic>Apolipoprotein A-I - genetics</topic><topic>Apolipoprotein C-III</topic><topic>Apolipoproteins C - genetics</topic><topic>Biomarkers - blood</topic><topic>Case-Control Studies</topic><topic>Coronary Artery Disease - blood</topic><topic>Coronary Artery Disease - etiology</topic><topic>Coronary Artery Disease - genetics</topic><topic>Female</topic><topic>Hemostasis</topic><topic>Humans</topic><topic>Lipids - blood</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Polymorphism, Genetic</topic><topic>Risk Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Izar, Maria Cristina</creatorcontrib><creatorcontrib>Fonseca, Francisco Antonio Helfenstein</creatorcontrib><creatorcontrib>Ihara, Sílvia Saiuli Miki</creatorcontrib><creatorcontrib>Kasinski, Nelson</creatorcontrib><creatorcontrib>Sang, Won Han</creatorcontrib><creatorcontrib>Lopes, Ieda Edite Lanzarini</creatorcontrib><creatorcontrib>Pinto, Leonor do Espírito Santo de Almeida</creatorcontrib><creatorcontrib>Relvas, Waldir Gabriel Miranda</creatorcontrib><creatorcontrib>Lourenço, Daisy</creatorcontrib><creatorcontrib>Tufik, Sérgio</creatorcontrib><creatorcontrib>de Paola, Angelo Amato Vincenzo</creatorcontrib><creatorcontrib>Carvalho, Antonio Carlos Camargo</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Arquivos brasileiros de cardiologia</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Izar, Maria Cristina</au><au>Fonseca, Francisco Antonio Helfenstein</au><au>Ihara, Sílvia Saiuli Miki</au><au>Kasinski, Nelson</au><au>Sang, Won Han</au><au>Lopes, Ieda Edite Lanzarini</au><au>Pinto, Leonor do Espírito Santo de Almeida</au><au>Relvas, Waldir Gabriel Miranda</au><au>Lourenço, Daisy</au><au>Tufik, Sérgio</au><au>de Paola, Angelo Amato Vincenzo</au><au>Carvalho, Antonio Carlos Camargo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Risk Factors, biochemical markers, and genetic polymorphisms in early coronary artery disease</atitle><jtitle>Arquivos brasileiros de cardiologia</jtitle><addtitle>Arq Bras Cardiol</addtitle><date>2003-04</date><risdate>2003</risdate><volume>80</volume><issue>4</issue><spage>379</spage><epage>395</epage><pages>379-395</pages><issn>0066-782X</issn><abstract>To assess the risk factors, lipid and apolipoprotein profile, hemostasis variables, and polymorphisms of the apolipoprotein AI-CIII gene in early coronary artery disease (CAD).
Case-control study with 112 patients in each group controlled by sex and age. After clinical evaluation and nutritional instruction, blood samples were collected for biochemical assays and genetic study.
Familial history of early CAD (64 vs 39%), arterial hypertension (69 vs 36%), diabetes mellitus (25 vs 3%), and previous smoking (71 vs 46%) were more prevalent in the case group (p<0.001). Hypertension and diabetes were independent risk factors. Early CAD was characterized by higher serum levels of total cholesterol (235 +/-6 vs 209 +/- 4 mg/dL), of LDL-c (154 +/- 5 vs 135 +/- 4 mg/dL), triglycerides (205 +/- 12 vs 143 +/- 9 mg/dL), and apolipoprotein B (129 +/- 3 vs 105 +/- 3 mg/dL), and lower serum levels of HDL-c (40 +/- 1 vs 46 +/- 1 mg/dL) and apolipoprotein AI (134 +/- 2 vs 146 +/- 2mg/dL) [p<0.01], in addition to an elevation in fibrinogen and D-dimer (p<0.02). The simultaneous presence of the rare alleles of the APO AI-CIII genes in early CAD are associated with hypertriglyceridemia (p=0.03).
Of the classical risk factors, hypertension and diabetes mellitus were independently associated with early CAD. In addition to an unfavorable lipid profile, an increase in the thrombotic risk was identified in this population. An additive effect of the APO AI-CIII genes was observed in triglyceride levels.</abstract><cop>Brazil</cop><pmid>12754559</pmid><tpages>17</tpages></addata></record> |
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subjects | Adult Apolipoprotein A-I - genetics Apolipoprotein C-III Apolipoproteins C - genetics Biomarkers - blood Case-Control Studies Coronary Artery Disease - blood Coronary Artery Disease - etiology Coronary Artery Disease - genetics Female Hemostasis Humans Lipids - blood Male Middle Aged Polymorphism, Genetic Risk Factors |
title | Risk Factors, biochemical markers, and genetic polymorphisms in early coronary artery disease |
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