Haemochromatosis gene mutations and risk of coronary heart disease: a west of Scotland coronary prevention study (WOSCOPS) substudy
Objectives: To measure the frequency of genotypes of the HFE (haemochromatosis) gene in patients recruited to the west of Scotland coronary prevention study (WOSCOPS), and relate them to the subsequent occurrence of coronary clinical events. Design: Nested case–control study, drawing samples of DNA...
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| Veröffentlicht in: | Heart (British Cardiac Society) 2004-03, Vol.90 (3), p.304-306 |
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| creator | Gunn, I R Maxwell, F K Gaffney, D McMahon, A D Packard, C J |
| description | Objectives: To measure the frequency of genotypes of the HFE (haemochromatosis) gene in patients recruited to the west of Scotland coronary prevention study (WOSCOPS), and relate them to the subsequent occurrence of coronary clinical events. Design: Nested case–control study, drawing samples of DNA from the biological bank of a cohort study. Patients: Men aged 45–64 years in 1989, with moderate hypercholesterolaemia and no evidence of coronary heart disease at baseline. Interventions: Follow up for a mean period of 4.9 years. Typing for C282Y and H63D mutations of the HFE gene in 482 subjects with a subsequent coronary event and 1104 without an event. Results: The C282Y mutation was present in 81 of 482 cases (16.8%) and 182 of 1104 controls (16.5%). Comparing the prevalence of gene mutations in the cases and controls, there were no significant differences. The hazard ratio for C282Y heterozygotes was 1.03 (95% confidence interval (CI) 0.77 to 1.36) and for C282Y/H63D compound heterozygotes 1.04 (95% CI 0.50 to 2.14). Prespecified subgroup analyses of the pravastatin, placebo, smoking, and non-smoking groups showed no significant differences between cases and controls. Repeating the analyses after adjusting for possible confounding factors produced no change in the results. Conclusions: In a population of moderately hypercholesterolaemic middle aged Scottish men who did not have any evidence of coronary heart disease at baseline, the presence of a C282Y mutation in the HFE gene did not predict the occurrence of coronary events over a mean follow up of 4.9 years. |
| doi_str_mv | 10.1136/hrt.2003.015149 |
| format | Article |
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Design: Nested case–control study, drawing samples of DNA from the biological bank of a cohort study. Patients: Men aged 45–64 years in 1989, with moderate hypercholesterolaemia and no evidence of coronary heart disease at baseline. Interventions: Follow up for a mean period of 4.9 years. Typing for C282Y and H63D mutations of the HFE gene in 482 subjects with a subsequent coronary event and 1104 without an event. Results: The C282Y mutation was present in 81 of 482 cases (16.8%) and 182 of 1104 controls (16.5%). Comparing the prevalence of gene mutations in the cases and controls, there were no significant differences. The hazard ratio for C282Y heterozygotes was 1.03 (95% confidence interval (CI) 0.77 to 1.36) and for C282Y/H63D compound heterozygotes 1.04 (95% CI 0.50 to 2.14). Prespecified subgroup analyses of the pravastatin, placebo, smoking, and non-smoking groups showed no significant differences between cases and controls. Repeating the analyses after adjusting for possible confounding factors produced no change in the results. Conclusions: In a population of moderately hypercholesterolaemic middle aged Scottish men who did not have any evidence of coronary heart disease at baseline, the presence of a C282Y mutation in the HFE gene did not predict the occurrence of coronary events over a mean follow up of 4.9 years.</description><identifier>ISSN: 1355-6037</identifier><identifier>EISSN: 1468-201X</identifier><identifier>DOI: 10.1136/hrt.2003.015149</identifier><identifier>PMID: 14966054</identifier><language>eng</language><publisher>London: BMJ Publishing Group Ltd and British Cardiovascular Society</publisher><subject>ARIC ; atherosclerosis risk in communities ; Biological and medical sciences ; Cardiology. Vascular system ; Cardiovascular disease ; Cardiovascular Medicine ; Case-Control Studies ; Coronary Disease - epidemiology ; Coronary Disease - genetics ; Coronary Disease - prevention & control ; Coronary heart disease ; Follow-Up Studies ; Gene Frequency ; genetics ; haemochromatosis ; Health risk assessment ; Heart ; Heart attacks ; Hemochromatosis Protein ; Heterozygote ; Histocompatibility Antigens Class I - genetics ; Humans ; Hypercholesterolemia - complications ; Hypercholesterolemia - epidemiology ; iron ; KIHD ; Kuopio ischaemic risk factor study ; Low density lipoprotein ; Male ; Medical sciences ; Membrane Proteins - genetics ; Metabolic diseases ; Metals (hemochromatosis...) ; Middle Aged ; Mutation ; Mutation - genetics ; Other metabolic disorders ; Risk Factors ; Scotland - epidemiology ; Studies ; west of Scotland coronary prevention study ; WOSCOPS</subject><ispartof>Heart (British Cardiac Society), 2004-03, Vol.90 (3), p.304-306</ispartof><rights>Copyright 2004 by Heart</rights><rights>2004 INIST-CNRS</rights><rights>COPYRIGHT 2004 BMJ Publishing Group Ltd.</rights><rights>Copyright: 2004 Copyright 2004 by Heart</rights><rights>Copyright © Copyright 2004 by Heart 2004</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b597t-d3eea10f50f9a950ebb87f148eabcae6331d22da12a258bf9d71d54f5915cf5a3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1768115/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1768115/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15573251$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14966054$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gunn, I R</creatorcontrib><creatorcontrib>Maxwell, F K</creatorcontrib><creatorcontrib>Gaffney, D</creatorcontrib><creatorcontrib>McMahon, A D</creatorcontrib><creatorcontrib>Packard, C J</creatorcontrib><title>Haemochromatosis gene mutations and risk of coronary heart disease: a west of Scotland coronary prevention study (WOSCOPS) substudy</title><title>Heart (British Cardiac Society)</title><addtitle>Heart</addtitle><description>Objectives: To measure the frequency of genotypes of the HFE (haemochromatosis) gene in patients recruited to the west of Scotland coronary prevention study (WOSCOPS), and relate them to the subsequent occurrence of coronary clinical events. Design: Nested case–control study, drawing samples of DNA from the biological bank of a cohort study. Patients: Men aged 45–64 years in 1989, with moderate hypercholesterolaemia and no evidence of coronary heart disease at baseline. Interventions: Follow up for a mean period of 4.9 years. Typing for C282Y and H63D mutations of the HFE gene in 482 subjects with a subsequent coronary event and 1104 without an event. Results: The C282Y mutation was present in 81 of 482 cases (16.8%) and 182 of 1104 controls (16.5%). Comparing the prevalence of gene mutations in the cases and controls, there were no significant differences. The hazard ratio for C282Y heterozygotes was 1.03 (95% confidence interval (CI) 0.77 to 1.36) and for C282Y/H63D compound heterozygotes 1.04 (95% CI 0.50 to 2.14). Prespecified subgroup analyses of the pravastatin, placebo, smoking, and non-smoking groups showed no significant differences between cases and controls. Repeating the analyses after adjusting for possible confounding factors produced no change in the results. Conclusions: In a population of moderately hypercholesterolaemic middle aged Scottish men who did not have any evidence of coronary heart disease at baseline, the presence of a C282Y mutation in the HFE gene did not predict the occurrence of coronary events over a mean follow up of 4.9 years.</description><subject>ARIC</subject><subject>atherosclerosis risk in communities</subject><subject>Biological and medical sciences</subject><subject>Cardiology. Vascular system</subject><subject>Cardiovascular disease</subject><subject>Cardiovascular Medicine</subject><subject>Case-Control Studies</subject><subject>Coronary Disease - epidemiology</subject><subject>Coronary Disease - genetics</subject><subject>Coronary Disease - prevention & control</subject><subject>Coronary heart disease</subject><subject>Follow-Up Studies</subject><subject>Gene Frequency</subject><subject>genetics</subject><subject>haemochromatosis</subject><subject>Health risk assessment</subject><subject>Heart</subject><subject>Heart attacks</subject><subject>Hemochromatosis Protein</subject><subject>Heterozygote</subject><subject>Histocompatibility Antigens Class I - genetics</subject><subject>Humans</subject><subject>Hypercholesterolemia - complications</subject><subject>Hypercholesterolemia - epidemiology</subject><subject>iron</subject><subject>KIHD</subject><subject>Kuopio ischaemic risk factor study</subject><subject>Low density lipoprotein</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Membrane Proteins - genetics</subject><subject>Metabolic diseases</subject><subject>Metals (hemochromatosis...)</subject><subject>Middle Aged</subject><subject>Mutation</subject><subject>Mutation - genetics</subject><subject>Other metabolic disorders</subject><subject>Risk Factors</subject><subject>Scotland - epidemiology</subject><subject>Studies</subject><subject>west of Scotland coronary prevention study</subject><subject>WOSCOPS</subject><issn>1355-6037</issn><issn>1468-201X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqFkttrFDEUxgdRbK0--yYBUVSYba5z8UEoi1qxdIX1UnwJmczJbrYzkzWZqfbZf9yMu-yqFCQPCcnvfOd84UuShwRPCGHZ8dL3E4oxm2AiCC9vJYeEZ0VKMbm4Hc9MiDTDLD9I7oWwwhjzssjuJgcRzTIs-GHy81RB6_TSu1b1LtiAFtABaode9dZ1AamuRt6GS-QM0s67TvlrtATle1TbACrAS6TQdwj9SMy165uxZIeuPVxBN2qh0A_1NXr2ZTafzj7Mn6MwVL-v7id3jGoCPNjuR8mnN68_Tk_Ts9nbd9OTs7QSZd6nNQNQBBuBTalKgaGqitwQXoCqtIKMMVJTWitCFRVFZco6J7XgRpREaCMUO0pebXTXQ9VCreNYXjVy7W0bJ5VOWfn3S2eXcuGuJMmzghARBZ5uBbz7NkTLsrVBQxMdgxuCLDDJeImLCD7-B1y5wXfRXNQqcMZ5SXGk0g21UA1I2xkXu-rx_2Nz14Gx8fqEEE5FTvnIT27g46qhtfrGguNNgfYuBA9m55VgOeZHxvzIMT9yk59Y8ejPL9rz28BE4MkWUEGrxnjVaRv2nBA5o4LsvdnQw4_du_KXMstZLuT556n8evGeU0bn8jzyLzZ81a7-O-UvPMvskg</recordid><startdate>20040301</startdate><enddate>20040301</enddate><creator>Gunn, I R</creator><creator>Maxwell, F K</creator><creator>Gaffney, D</creator><creator>McMahon, A D</creator><creator>Packard, C J</creator><general>BMJ Publishing Group Ltd and British Cardiovascular Society</general><general>BMJ</general><general>BMJ Publishing Group Ltd</general><general>BMJ Publishing Group LTD</general><general>Copyright 2004 by Heart</general><scope>BSCLL</scope><scope>IQODW</scope><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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>BTHHO</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20040301</creationdate><title>Haemochromatosis gene mutations and risk of coronary heart disease: a west of Scotland coronary prevention study (WOSCOPS) substudy</title><author>Gunn, I R ; Maxwell, F K ; Gaffney, D ; McMahon, A D ; Packard, C J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b597t-d3eea10f50f9a950ebb87f148eabcae6331d22da12a258bf9d71d54f5915cf5a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>ARIC</topic><topic>atherosclerosis risk in communities</topic><topic>Biological and medical sciences</topic><topic>Cardiology. Vascular system</topic><topic>Cardiovascular disease</topic><topic>Cardiovascular Medicine</topic><topic>Case-Control Studies</topic><topic>Coronary Disease - epidemiology</topic><topic>Coronary Disease - genetics</topic><topic>Coronary Disease - prevention & control</topic><topic>Coronary heart disease</topic><topic>Follow-Up Studies</topic><topic>Gene Frequency</topic><topic>genetics</topic><topic>haemochromatosis</topic><topic>Health risk assessment</topic><topic>Heart</topic><topic>Heart attacks</topic><topic>Hemochromatosis Protein</topic><topic>Heterozygote</topic><topic>Histocompatibility Antigens Class I - genetics</topic><topic>Humans</topic><topic>Hypercholesterolemia - complications</topic><topic>Hypercholesterolemia - epidemiology</topic><topic>iron</topic><topic>KIHD</topic><topic>Kuopio ischaemic risk factor study</topic><topic>Low density lipoprotein</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Membrane Proteins - genetics</topic><topic>Metabolic diseases</topic><topic>Metals (hemochromatosis...)</topic><topic>Middle Aged</topic><topic>Mutation</topic><topic>Mutation - genetics</topic><topic>Other metabolic disorders</topic><topic>Risk Factors</topic><topic>Scotland - epidemiology</topic><topic>Studies</topic><topic>west of Scotland coronary prevention study</topic><topic>WOSCOPS</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gunn, I R</creatorcontrib><creatorcontrib>Maxwell, F K</creatorcontrib><creatorcontrib>Gaffney, D</creatorcontrib><creatorcontrib>McMahon, A D</creatorcontrib><creatorcontrib>Packard, C J</creatorcontrib><collection>Istex</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>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>BMJ Journals</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Heart (British Cardiac Society)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gunn, I R</au><au>Maxwell, F K</au><au>Gaffney, D</au><au>McMahon, A D</au><au>Packard, C J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Haemochromatosis gene mutations and risk of coronary heart disease: a west of Scotland coronary prevention study (WOSCOPS) substudy</atitle><jtitle>Heart (British Cardiac Society)</jtitle><addtitle>Heart</addtitle><date>2004-03-01</date><risdate>2004</risdate><volume>90</volume><issue>3</issue><spage>304</spage><epage>306</epage><pages>304-306</pages><issn>1355-6037</issn><eissn>1468-201X</eissn><abstract>Objectives: To measure the frequency of genotypes of the HFE (haemochromatosis) gene in patients recruited to the west of Scotland coronary prevention study (WOSCOPS), and relate them to the subsequent occurrence of coronary clinical events. Design: Nested case–control study, drawing samples of DNA from the biological bank of a cohort study. Patients: Men aged 45–64 years in 1989, with moderate hypercholesterolaemia and no evidence of coronary heart disease at baseline. Interventions: Follow up for a mean period of 4.9 years. Typing for C282Y and H63D mutations of the HFE gene in 482 subjects with a subsequent coronary event and 1104 without an event. Results: The C282Y mutation was present in 81 of 482 cases (16.8%) and 182 of 1104 controls (16.5%). Comparing the prevalence of gene mutations in the cases and controls, there were no significant differences. The hazard ratio for C282Y heterozygotes was 1.03 (95% confidence interval (CI) 0.77 to 1.36) and for C282Y/H63D compound heterozygotes 1.04 (95% CI 0.50 to 2.14). Prespecified subgroup analyses of the pravastatin, placebo, smoking, and non-smoking groups showed no significant differences between cases and controls. Repeating the analyses after adjusting for possible confounding factors produced no change in the results. Conclusions: In a population of moderately hypercholesterolaemic middle aged Scottish men who did not have any evidence of coronary heart disease at baseline, the presence of a C282Y mutation in the HFE gene did not predict the occurrence of coronary events over a mean follow up of 4.9 years.</abstract><cop>London</cop><pub>BMJ Publishing Group Ltd and British Cardiovascular Society</pub><pmid>14966054</pmid><doi>10.1136/hrt.2003.015149</doi><tpages>3</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | ARIC atherosclerosis risk in communities Biological and medical sciences Cardiology. Vascular system Cardiovascular disease Cardiovascular Medicine Case-Control Studies Coronary Disease - epidemiology Coronary Disease - genetics Coronary Disease - prevention & control Coronary heart disease Follow-Up Studies Gene Frequency genetics haemochromatosis Health risk assessment Heart Heart attacks Hemochromatosis Protein Heterozygote Histocompatibility Antigens Class I - genetics Humans Hypercholesterolemia - complications Hypercholesterolemia - epidemiology iron KIHD Kuopio ischaemic risk factor study Low density lipoprotein Male Medical sciences Membrane Proteins - genetics Metabolic diseases Metals (hemochromatosis...) Middle Aged Mutation Mutation - genetics Other metabolic disorders Risk Factors Scotland - epidemiology Studies west of Scotland coronary prevention study WOSCOPS |
| title | Haemochromatosis gene mutations and risk of coronary heart disease: a west of Scotland coronary prevention study (WOSCOPS) substudy |
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