Interaction Between Endothelial Nitric Oxide Synthase Gene Polymorphisms (−786T>C, 894G>T and Intron 4 a/b) and Cardiovascular Risk Factors in Acute Coronary Syndromes
Background and Aims Endothelial rupture of coronary plaque can represent the pathomorphological substratum of acute coronary syndrome (ACS). Polymorphisms in the NOS3 gene (eNOS) –786T>C, 894G>T and intron 4 a/b VNTR can be associated with a higher susceptibility for ACS. The present study is...
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creator | da Costa Escobar Piccoli, Jacqueline Manfredini, Vanusa Hamester, Fernanda Irma Bandinelli, Josiane Bettim Turkienicz, Ilan Maltz Chies, José Artur Bogo Peres, Alessandra Bodanese, Luiz Carlos Bogo, Maurício Reis |
description | Background and Aims Endothelial rupture of coronary plaque can represent the pathomorphological substratum of acute coronary syndrome (ACS). Polymorphisms in the NOS3 gene (eNOS) –786T>C, 894G>T and intron 4 a/b VNTR can be associated with a higher susceptibility for ACS. The present study is focused on the investigation of the interaction of these polymorphisms and cardiovascular risk factors in 135 patients with ACS and 115 control subjects. Methods Case–control study where the allele and genotype frequencies of the polymorphisms –786T> C, 894G> T and intron 4 VNTR of the gene encoding eNOS were determined by PCR-RFLP associated with cardiovascular risk factors. Results An association of the 894TT genotype and 894GT+GG (OR 1.4; 95% CI 1.0–1.8) in ACS has been observed. Subjects without dyslipidemia and intron 4 a/b genotype present a lower chance for ACS development, whereas subjects without diabetes and 894TT genotype show a higher risk for ACS (OR 1.7; 95% CI 1.2–2.3). In patients without dyslipidemia, the 894GG genotype presented a tendency to behave as a protector factor against ACS. Also, the 894GG genotype has been a protective factor for ACS in females (OR 0.5; CI 95% 0.2–0.9). Conclusions Our results suggest that eNOS polymorphisms may be an additional risk factor in development of ACS. |
doi_str_mv | 10.1016/j.arcmed.2012.03.011 |
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Polymorphisms in the NOS3 gene (eNOS) –786T>C, 894G>T and intron 4 a/b VNTR can be associated with a higher susceptibility for ACS. The present study is focused on the investigation of the interaction of these polymorphisms and cardiovascular risk factors in 135 patients with ACS and 115 control subjects. Methods Case–control study where the allele and genotype frequencies of the polymorphisms –786T> C, 894G> T and intron 4 VNTR of the gene encoding eNOS were determined by PCR-RFLP associated with cardiovascular risk factors. Results An association of the 894TT genotype and 894GT+GG (OR 1.4; 95% CI 1.0–1.8) in ACS has been observed. Subjects without dyslipidemia and intron 4 a/b genotype present a lower chance for ACS development, whereas subjects without diabetes and 894TT genotype show a higher risk for ACS (OR 1.7; 95% CI 1.2–2.3). In patients without dyslipidemia, the 894GG genotype presented a tendency to behave as a protector factor against ACS. Also, the 894GG genotype has been a protective factor for ACS in females (OR 0.5; CI 95% 0.2–0.9). Conclusions Our results suggest that eNOS polymorphisms may be an additional risk factor in development of ACS.</description><identifier>ISSN: 0188-4409</identifier><identifier>EISSN: 1873-5487</identifier><identifier>DOI: 10.1016/j.arcmed.2012.03.011</identifier><identifier>PMID: 22475779</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Acute coronary syndrome ; Acute Coronary Syndrome - enzymology ; Acute Coronary Syndrome - genetics ; Adult ; Aged ; Aged, 80 and over ; Animals ; Cardiovascular risk factors ; Case-Control Studies ; Diabetes mellitus ; Diabetes Mellitus - enzymology ; Diabetes Mellitus - genetics ; Dyslipidemias - enzymology ; Dyslipidemias - genetics ; Endothelial nitric oxide polymorphisms ; eNOS ; Female ; Genetic Predisposition to Disease ; Genotypes ; Humans ; Internal Medicine ; Introns ; Male ; Medical research ; Middle Aged ; Nitric oxide ; Nitric Oxide Synthase Type III - genetics ; Polymorphism, Single Nucleotide ; Risk factors</subject><ispartof>Archives of medical research, 2012-04, Vol.43 (3), p.205-211</ispartof><rights>IMSS</rights><rights>2012 IMSS</rights><rights>Copyright © 2012 IMSS. Published by Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c516t-22b21cfcb4895a7a57c6e65d60eeeba15bd61770fd25281707f49fa8739262e63</citedby><cites>FETCH-LOGICAL-c516t-22b21cfcb4895a7a57c6e65d60eeeba15bd61770fd25281707f49fa8739262e63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0188440912000811$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22475779$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>da Costa Escobar Piccoli, Jacqueline</creatorcontrib><creatorcontrib>Manfredini, Vanusa</creatorcontrib><creatorcontrib>Hamester, Fernanda Irma</creatorcontrib><creatorcontrib>Bandinelli, Josiane Bettim</creatorcontrib><creatorcontrib>Turkienicz, Ilan Maltz</creatorcontrib><creatorcontrib>Chies, José Artur Bogo</creatorcontrib><creatorcontrib>Peres, Alessandra</creatorcontrib><creatorcontrib>Bodanese, Luiz Carlos</creatorcontrib><creatorcontrib>Bogo, Maurício Reis</creatorcontrib><title>Interaction Between Endothelial Nitric Oxide Synthase Gene Polymorphisms (−786T>C, 894G>T and Intron 4 a/b) and Cardiovascular Risk Factors in Acute Coronary Syndromes</title><title>Archives of medical research</title><addtitle>Arch Med Res</addtitle><description>Background and Aims Endothelial rupture of coronary plaque can represent the pathomorphological substratum of acute coronary syndrome (ACS). Polymorphisms in the NOS3 gene (eNOS) –786T>C, 894G>T and intron 4 a/b VNTR can be associated with a higher susceptibility for ACS. The present study is focused on the investigation of the interaction of these polymorphisms and cardiovascular risk factors in 135 patients with ACS and 115 control subjects. Methods Case–control study where the allele and genotype frequencies of the polymorphisms –786T> C, 894G> T and intron 4 VNTR of the gene encoding eNOS were determined by PCR-RFLP associated with cardiovascular risk factors. Results An association of the 894TT genotype and 894GT+GG (OR 1.4; 95% CI 1.0–1.8) in ACS has been observed. Subjects without dyslipidemia and intron 4 a/b genotype present a lower chance for ACS development, whereas subjects without diabetes and 894TT genotype show a higher risk for ACS (OR 1.7; 95% CI 1.2–2.3). In patients without dyslipidemia, the 894GG genotype presented a tendency to behave as a protector factor against ACS. Also, the 894GG genotype has been a protective factor for ACS in females (OR 0.5; CI 95% 0.2–0.9). Conclusions Our results suggest that eNOS polymorphisms may be an additional risk factor in development of ACS.</description><subject>Acute coronary syndrome</subject><subject>Acute Coronary Syndrome - enzymology</subject><subject>Acute Coronary Syndrome - genetics</subject><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Animals</subject><subject>Cardiovascular risk factors</subject><subject>Case-Control Studies</subject><subject>Diabetes mellitus</subject><subject>Diabetes Mellitus - enzymology</subject><subject>Diabetes Mellitus - genetics</subject><subject>Dyslipidemias - enzymology</subject><subject>Dyslipidemias - genetics</subject><subject>Endothelial nitric oxide polymorphisms</subject><subject>eNOS</subject><subject>Female</subject><subject>Genetic Predisposition to Disease</subject><subject>Genotypes</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Introns</subject><subject>Male</subject><subject>Medical research</subject><subject>Middle Aged</subject><subject>Nitric oxide</subject><subject>Nitric Oxide Synthase Type III - genetics</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Risk factors</subject><issn>0188-4409</issn><issn>1873-5487</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNUsFu1DAUjBCILoU_QMjHIpGt7Th2clmprNqlUkURXc6WY79ovU3srZ0U9g848xf8Fl-Cw7YXLnCyZM_Me56ZLHtN8Jxgwk-3cxV0D2ZOMaFzXMwxIU-yGalEkZesEk-zGSZVlTOG66PsRYxbjHHFuHieHVHKRClEPct-XroBgtKD9Q69h-ErgEPnzvhhA51VHfpoh2A1uv5mDaCbvRs2KgJagQP0yXf73ofdxsY-opNf33-Iiq8Xy3eoqtlqsUbKGZT0Q5JmSJ02b__cLFUw1t-rqMdOBfTZxlt0kTbwISLr0JkeB0BLn1gq7KeRJvge4svsWau6CK8ezuPsy8X5evkhv7peXS7PrnJdEj7klDaU6FY3rKpLJVQpNAdeGo4BoFGkbAwnQuDW0JJWRGDRsrpVybWacgq8OM5ODrq74O9GiIPsbdTQdcqBH6MkuC5YyRnG_wGlGJe4wjRB2QGqg48xQCt3wfbpgwkkpzzlVh7ylFOeEhcy5Zlobx4mjM309kh6DDABFgcAJEvuLQQZtQWnwdgAepDG239N-FtAd9ZZrbpb2EPc-jG4ZLckMiaOvJk6NVWK0KlOSeA3zZrH8g</recordid><startdate>20120401</startdate><enddate>20120401</enddate><creator>da Costa Escobar Piccoli, Jacqueline</creator><creator>Manfredini, Vanusa</creator><creator>Hamester, Fernanda Irma</creator><creator>Bandinelli, Josiane Bettim</creator><creator>Turkienicz, Ilan Maltz</creator><creator>Chies, José Artur Bogo</creator><creator>Peres, Alessandra</creator><creator>Bodanese, Luiz Carlos</creator><creator>Bogo, Maurício Reis</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>7T2</scope><scope>7U1</scope><scope>7U2</scope><scope>C1K</scope></search><sort><creationdate>20120401</creationdate><title>Interaction Between Endothelial Nitric Oxide Synthase Gene Polymorphisms (−786T>C, 894G>T and Intron 4 a/b) and Cardiovascular Risk Factors in Acute Coronary Syndromes</title><author>da Costa Escobar Piccoli, Jacqueline ; Manfredini, Vanusa ; Hamester, Fernanda Irma ; Bandinelli, Josiane Bettim ; Turkienicz, Ilan Maltz ; Chies, José Artur Bogo ; Peres, Alessandra ; Bodanese, Luiz Carlos ; Bogo, Maurício Reis</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c516t-22b21cfcb4895a7a57c6e65d60eeeba15bd61770fd25281707f49fa8739262e63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Acute coronary syndrome</topic><topic>Acute Coronary Syndrome - enzymology</topic><topic>Acute Coronary Syndrome - genetics</topic><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Animals</topic><topic>Cardiovascular risk factors</topic><topic>Case-Control Studies</topic><topic>Diabetes mellitus</topic><topic>Diabetes Mellitus - enzymology</topic><topic>Diabetes Mellitus - genetics</topic><topic>Dyslipidemias - enzymology</topic><topic>Dyslipidemias - genetics</topic><topic>Endothelial nitric oxide polymorphisms</topic><topic>eNOS</topic><topic>Female</topic><topic>Genetic Predisposition to Disease</topic><topic>Genotypes</topic><topic>Humans</topic><topic>Internal Medicine</topic><topic>Introns</topic><topic>Male</topic><topic>Medical research</topic><topic>Middle Aged</topic><topic>Nitric oxide</topic><topic>Nitric Oxide Synthase Type III - genetics</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Risk factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>da Costa Escobar Piccoli, Jacqueline</creatorcontrib><creatorcontrib>Manfredini, Vanusa</creatorcontrib><creatorcontrib>Hamester, Fernanda Irma</creatorcontrib><creatorcontrib>Bandinelli, Josiane Bettim</creatorcontrib><creatorcontrib>Turkienicz, Ilan Maltz</creatorcontrib><creatorcontrib>Chies, José Artur Bogo</creatorcontrib><creatorcontrib>Peres, Alessandra</creatorcontrib><creatorcontrib>Bodanese, Luiz Carlos</creatorcontrib><creatorcontrib>Bogo, Maurício Reis</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Health and Safety Science Abstracts (Full archive)</collection><collection>Risk Abstracts</collection><collection>Safety Science and Risk</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>Archives of medical research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>da Costa Escobar Piccoli, Jacqueline</au><au>Manfredini, Vanusa</au><au>Hamester, Fernanda Irma</au><au>Bandinelli, Josiane Bettim</au><au>Turkienicz, Ilan Maltz</au><au>Chies, José Artur Bogo</au><au>Peres, Alessandra</au><au>Bodanese, Luiz Carlos</au><au>Bogo, Maurício Reis</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Interaction Between Endothelial Nitric Oxide Synthase Gene Polymorphisms (−786T>C, 894G>T and Intron 4 a/b) and Cardiovascular Risk Factors in Acute Coronary Syndromes</atitle><jtitle>Archives of medical research</jtitle><addtitle>Arch Med Res</addtitle><date>2012-04-01</date><risdate>2012</risdate><volume>43</volume><issue>3</issue><spage>205</spage><epage>211</epage><pages>205-211</pages><issn>0188-4409</issn><eissn>1873-5487</eissn><abstract>Background and Aims Endothelial rupture of coronary plaque can represent the pathomorphological substratum of acute coronary syndrome (ACS). Polymorphisms in the NOS3 gene (eNOS) –786T>C, 894G>T and intron 4 a/b VNTR can be associated with a higher susceptibility for ACS. The present study is focused on the investigation of the interaction of these polymorphisms and cardiovascular risk factors in 135 patients with ACS and 115 control subjects. Methods Case–control study where the allele and genotype frequencies of the polymorphisms –786T> C, 894G> T and intron 4 VNTR of the gene encoding eNOS were determined by PCR-RFLP associated with cardiovascular risk factors. Results An association of the 894TT genotype and 894GT+GG (OR 1.4; 95% CI 1.0–1.8) in ACS has been observed. Subjects without dyslipidemia and intron 4 a/b genotype present a lower chance for ACS development, whereas subjects without diabetes and 894TT genotype show a higher risk for ACS (OR 1.7; 95% CI 1.2–2.3). In patients without dyslipidemia, the 894GG genotype presented a tendency to behave as a protector factor against ACS. Also, the 894GG genotype has been a protective factor for ACS in females (OR 0.5; CI 95% 0.2–0.9). Conclusions Our results suggest that eNOS polymorphisms may be an additional risk factor in development of ACS.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>22475779</pmid><doi>10.1016/j.arcmed.2012.03.011</doi><tpages>7</tpages></addata></record> |
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subjects | Acute coronary syndrome Acute Coronary Syndrome - enzymology Acute Coronary Syndrome - genetics Adult Aged Aged, 80 and over Animals Cardiovascular risk factors Case-Control Studies Diabetes mellitus Diabetes Mellitus - enzymology Diabetes Mellitus - genetics Dyslipidemias - enzymology Dyslipidemias - genetics Endothelial nitric oxide polymorphisms eNOS Female Genetic Predisposition to Disease Genotypes Humans Internal Medicine Introns Male Medical research Middle Aged Nitric oxide Nitric Oxide Synthase Type III - genetics Polymorphism, Single Nucleotide Risk factors |
title | Interaction Between Endothelial Nitric Oxide Synthase Gene Polymorphisms (−786T>C, 894G>T and Intron 4 a/b) and Cardiovascular Risk Factors in Acute Coronary Syndromes |
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