The M235T polymorphism in the AGT gene and CHD risk: evidence of a Hardy-Weinberg equilibrium violation and publication bias in a meta-analysis
The M235T polymorphism in the AGT gene has been related to an increased risk of hypertension. This finding may also suggest an increased risk of coronary heart disease (CHD). A case-cohort study was conducted in 1,732 unrelated middle-age women (210 CHD cases and 1,522 controls) from a prospective c...
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| Veröffentlicht in: | PloS one 2008-06, Vol.3 (6), p.e2533-e2533 |
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| description | The M235T polymorphism in the AGT gene has been related to an increased risk of hypertension. This finding may also suggest an increased risk of coronary heart disease (CHD).
A case-cohort study was conducted in 1,732 unrelated middle-age women (210 CHD cases and 1,522 controls) from a prospective cohort of 15,236 initially healthy Dutch women. We applied a Cox proportional hazards model to study the association of the polymorphism with acute myocardial infarction (AMI) (n = 71) and CHD. In the case-cohort study, no increased risk for CHD was found under the additive genetic model (hazard ratio [HR] = 1.20; 95% confidence interval [CI], 0.86 to 1.68; P = 0.28). This result was not changed by adjustment (HR = 1.17; 95% CI, 0.83 to 1.64; P = 0.38) nor by using dominant, recessive and pairwise genetic models. Analyses for AMI risk under the additive genetic model also did not show any statistically significant association (crude HR = 1.14; 95% CI, 0.93 to 1.39; P = 0.20). To evaluate the association, a comprehensive systematic review and meta-analysis were undertaken of all studies published up to February 2007 (searched through PubMed/MEDLINE, Web of Science and EMBASE). The meta-analysis (38 studies with 13284 cases and 18722 controls) showed a per-allele odds ratio (OR) of 1.08 (95% CI, 1.01 to 1.15; P = 0.02). Moderate to large levels of heterogeneity were identified between studies. Hardy-Weinberg equilibrium (HWE) violation and the mean age of cases were statistically significant sources of the observed variation. In a stratum of non-HWE violation studies, there was no effect. An asymmetric funnel plot, the Egger's test (P = 0.066), and the Begg-Mazumdar test (P = 0.074) were all suggestive of the presence of publication bias.
The pooled OR of the present meta-analysis, including our own data, presented evidence that there is an increase in the risk of CHD conferred by the M235T variant of the AGT gene. However, the relevance of this weakly positive overall association remains uncertain because it may be due to various residual biases, including HWE-violation and publication biases. |
| doi_str_mv | 10.1371/journal.pone.0002533 |
| format | Article |
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A case-cohort study was conducted in 1,732 unrelated middle-age women (210 CHD cases and 1,522 controls) from a prospective cohort of 15,236 initially healthy Dutch women. We applied a Cox proportional hazards model to study the association of the polymorphism with acute myocardial infarction (AMI) (n = 71) and CHD. In the case-cohort study, no increased risk for CHD was found under the additive genetic model (hazard ratio [HR] = 1.20; 95% confidence interval [CI], 0.86 to 1.68; P = 0.28). This result was not changed by adjustment (HR = 1.17; 95% CI, 0.83 to 1.64; P = 0.38) nor by using dominant, recessive and pairwise genetic models. Analyses for AMI risk under the additive genetic model also did not show any statistically significant association (crude HR = 1.14; 95% CI, 0.93 to 1.39; P = 0.20). To evaluate the association, a comprehensive systematic review and meta-analysis were undertaken of all studies published up to February 2007 (searched through PubMed/MEDLINE, Web of Science and EMBASE). The meta-analysis (38 studies with 13284 cases and 18722 controls) showed a per-allele odds ratio (OR) of 1.08 (95% CI, 1.01 to 1.15; P = 0.02). Moderate to large levels of heterogeneity were identified between studies. Hardy-Weinberg equilibrium (HWE) violation and the mean age of cases were statistically significant sources of the observed variation. In a stratum of non-HWE violation studies, there was no effect. An asymmetric funnel plot, the Egger's test (P = 0.066), and the Begg-Mazumdar test (P = 0.074) were all suggestive of the presence of publication bias.
The pooled OR of the present meta-analysis, including our own data, presented evidence that there is an increase in the risk of CHD conferred by the M235T variant of the AGT gene. However, the relevance of this weakly positive overall association remains uncertain because it may be due to various residual biases, including HWE-violation and publication biases.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0002533</identifier><identifier>PMID: 18575631</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>AGT gene ; Angiotensinogen - genetics ; Bias ; Biomarkers ; Blood pressure ; Cancer ; Cardiovascular disease ; Cardiovascular diseases ; Cardiovascular Disorders/Coronary Artery Disease ; Cardiovascular Disorders/Myocardial Infarction ; Case-Control Studies ; Codes ; Cohort Studies ; Confidence intervals ; Coronary artery disease ; Coronary Disease - genetics ; Deoxyribonucleic acid ; DNA ; Epidemiology ; Equilibrium ; Female ; Gene polymorphism ; Genes ; Genetic aspects ; Genetic polymorphisms ; Genetic Predisposition to Disease ; Genetic testing ; Genetics and Genomics/Complex Traits ; Genetics and Genomics/Genetics of Disease ; Genomes ; Hazards ; Health risk assessment ; Health risks ; Health services ; Heart attack ; Heart attacks ; Heart diseases ; Hospitals ; Humans ; Hypertension ; Internal medicine ; Laboratories ; Medical ethics ; Medical research ; Meta-analysis ; Middle Aged ; Myocardial infarction ; Plasma ; Polymorphism ; Polymorphism, Genetic ; Population ; Proportional Hazards Models ; Risk ; Risk Factors ; Statistical analysis ; Statistical models ; Statistical significance ; Womens health</subject><ispartof>PloS one, 2008-06, Vol.3 (6), p.e2533-e2533</ispartof><rights>COPYRIGHT 2008 Public Library of Science</rights><rights>2008 Zafarmand et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Zafarmand et al. 2008</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c693t-7c85ca6b818f92600a90479bc6fc6d9c1e4df0c8cf508f0db9b80c1922d77f6b3</citedby><cites>FETCH-LOGICAL-c693t-7c85ca6b818f92600a90479bc6fc6d9c1e4df0c8cf508f0db9b80c1922d77f6b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2432037/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2432037/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79342,79343</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18575631$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zafarmand, Mohammad Hadi</creatorcontrib><creatorcontrib>van der Schouw, Yvonne T</creatorcontrib><creatorcontrib>Grobbee, Diederick E</creatorcontrib><creatorcontrib>de Leeuw, Peter W</creatorcontrib><creatorcontrib>Bots, Michiel L</creatorcontrib><title>The M235T polymorphism in the AGT gene and CHD risk: evidence of a Hardy-Weinberg equilibrium violation and publication bias in a meta-analysis</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>The M235T polymorphism in the AGT gene has been related to an increased risk of hypertension. This finding may also suggest an increased risk of coronary heart disease (CHD).
A case-cohort study was conducted in 1,732 unrelated middle-age women (210 CHD cases and 1,522 controls) from a prospective cohort of 15,236 initially healthy Dutch women. We applied a Cox proportional hazards model to study the association of the polymorphism with acute myocardial infarction (AMI) (n = 71) and CHD. In the case-cohort study, no increased risk for CHD was found under the additive genetic model (hazard ratio [HR] = 1.20; 95% confidence interval [CI], 0.86 to 1.68; P = 0.28). This result was not changed by adjustment (HR = 1.17; 95% CI, 0.83 to 1.64; P = 0.38) nor by using dominant, recessive and pairwise genetic models. Analyses for AMI risk under the additive genetic model also did not show any statistically significant association (crude HR = 1.14; 95% CI, 0.93 to 1.39; P = 0.20). To evaluate the association, a comprehensive systematic review and meta-analysis were undertaken of all studies published up to February 2007 (searched through PubMed/MEDLINE, Web of Science and EMBASE). The meta-analysis (38 studies with 13284 cases and 18722 controls) showed a per-allele odds ratio (OR) of 1.08 (95% CI, 1.01 to 1.15; P = 0.02). Moderate to large levels of heterogeneity were identified between studies. Hardy-Weinberg equilibrium (HWE) violation and the mean age of cases were statistically significant sources of the observed variation. In a stratum of non-HWE violation studies, there was no effect. An asymmetric funnel plot, the Egger's test (P = 0.066), and the Begg-Mazumdar test (P = 0.074) were all suggestive of the presence of publication bias.
The pooled OR of the present meta-analysis, including our own data, presented evidence that there is an increase in the risk of CHD conferred by the M235T variant of the AGT gene. However, the relevance of this weakly positive overall association remains uncertain because it may be due to various residual biases, including HWE-violation and publication biases.</description><subject>AGT gene</subject><subject>Angiotensinogen - genetics</subject><subject>Bias</subject><subject>Biomarkers</subject><subject>Blood pressure</subject><subject>Cancer</subject><subject>Cardiovascular disease</subject><subject>Cardiovascular diseases</subject><subject>Cardiovascular Disorders/Coronary Artery Disease</subject><subject>Cardiovascular Disorders/Myocardial Infarction</subject><subject>Case-Control Studies</subject><subject>Codes</subject><subject>Cohort Studies</subject><subject>Confidence intervals</subject><subject>Coronary artery disease</subject><subject>Coronary Disease - genetics</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>Epidemiology</subject><subject>Equilibrium</subject><subject>Female</subject><subject>Gene polymorphism</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Genetic polymorphisms</subject><subject>Genetic Predisposition to Disease</subject><subject>Genetic testing</subject><subject>Genetics and Genomics/Complex Traits</subject><subject>Genetics and Genomics/Genetics of Disease</subject><subject>Genomes</subject><subject>Hazards</subject><subject>Health risk assessment</subject><subject>Health risks</subject><subject>Health services</subject><subject>Heart attack</subject><subject>Heart attacks</subject><subject>Heart diseases</subject><subject>Hospitals</subject><subject>Humans</subject><subject>Hypertension</subject><subject>Internal medicine</subject><subject>Laboratories</subject><subject>Medical ethics</subject><subject>Medical research</subject><subject>Meta-analysis</subject><subject>Middle Aged</subject><subject>Myocardial infarction</subject><subject>Plasma</subject><subject>Polymorphism</subject><subject>Polymorphism, Genetic</subject><subject>Population</subject><subject>Proportional Hazards Models</subject><subject>Risk</subject><subject>Risk Factors</subject><subject>Statistical analysis</subject><subject>Statistical models</subject><subject>Statistical significance</subject><subject>Womens 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M235T polymorphism in the AGT gene and CHD risk: evidence of a Hardy-Weinberg equilibrium violation and publication bias in a meta-analysis</title><author>Zafarmand, Mohammad Hadi ; van der Schouw, Yvonne T ; Grobbee, Diederick E ; de Leeuw, Peter W ; Bots, Michiel L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c693t-7c85ca6b818f92600a90479bc6fc6d9c1e4df0c8cf508f0db9b80c1922d77f6b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>AGT gene</topic><topic>Angiotensinogen - genetics</topic><topic>Bias</topic><topic>Biomarkers</topic><topic>Blood pressure</topic><topic>Cancer</topic><topic>Cardiovascular disease</topic><topic>Cardiovascular diseases</topic><topic>Cardiovascular Disorders/Coronary Artery Disease</topic><topic>Cardiovascular Disorders/Myocardial Infarction</topic><topic>Case-Control Studies</topic><topic>Codes</topic><topic>Cohort 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Hardy-Weinberg equilibrium violation and publication bias in a meta-analysis</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2008-06-25</date><risdate>2008</risdate><volume>3</volume><issue>6</issue><spage>e2533</spage><epage>e2533</epage><pages>e2533-e2533</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>The M235T polymorphism in the AGT gene has been related to an increased risk of hypertension. This finding may also suggest an increased risk of coronary heart disease (CHD).
A case-cohort study was conducted in 1,732 unrelated middle-age women (210 CHD cases and 1,522 controls) from a prospective cohort of 15,236 initially healthy Dutch women. We applied a Cox proportional hazards model to study the association of the polymorphism with acute myocardial infarction (AMI) (n = 71) and CHD. In the case-cohort study, no increased risk for CHD was found under the additive genetic model (hazard ratio [HR] = 1.20; 95% confidence interval [CI], 0.86 to 1.68; P = 0.28). This result was not changed by adjustment (HR = 1.17; 95% CI, 0.83 to 1.64; P = 0.38) nor by using dominant, recessive and pairwise genetic models. Analyses for AMI risk under the additive genetic model also did not show any statistically significant association (crude HR = 1.14; 95% CI, 0.93 to 1.39; P = 0.20). To evaluate the association, a comprehensive systematic review and meta-analysis were undertaken of all studies published up to February 2007 (searched through PubMed/MEDLINE, Web of Science and EMBASE). The meta-analysis (38 studies with 13284 cases and 18722 controls) showed a per-allele odds ratio (OR) of 1.08 (95% CI, 1.01 to 1.15; P = 0.02). Moderate to large levels of heterogeneity were identified between studies. Hardy-Weinberg equilibrium (HWE) violation and the mean age of cases were statistically significant sources of the observed variation. In a stratum of non-HWE violation studies, there was no effect. An asymmetric funnel plot, the Egger's test (P = 0.066), and the Begg-Mazumdar test (P = 0.074) were all suggestive of the presence of publication bias.
The pooled OR of the present meta-analysis, including our own data, presented evidence that there is an increase in the risk of CHD conferred by the M235T variant of the AGT gene. However, the relevance of this weakly positive overall association remains uncertain because it may be due to various residual biases, including HWE-violation and publication biases.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>18575631</pmid><doi>10.1371/journal.pone.0002533</doi><tpages>e2533</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2008-06, Vol.3 (6), p.e2533-e2533 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1312290703 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Free Full-Text Journals in Chemistry; Public Library of Science (PLoS) |
| subjects | AGT gene Angiotensinogen - genetics Bias Biomarkers Blood pressure Cancer Cardiovascular disease Cardiovascular diseases Cardiovascular Disorders/Coronary Artery Disease Cardiovascular Disorders/Myocardial Infarction Case-Control Studies Codes Cohort Studies Confidence intervals Coronary artery disease Coronary Disease - genetics Deoxyribonucleic acid DNA Epidemiology Equilibrium Female Gene polymorphism Genes Genetic aspects Genetic polymorphisms Genetic Predisposition to Disease Genetic testing Genetics and Genomics/Complex Traits Genetics and Genomics/Genetics of Disease Genomes Hazards Health risk assessment Health risks Health services Heart attack Heart attacks Heart diseases Hospitals Humans Hypertension Internal medicine Laboratories Medical ethics Medical research Meta-analysis Middle Aged Myocardial infarction Plasma Polymorphism Polymorphism, Genetic Population Proportional Hazards Models Risk Risk Factors Statistical analysis Statistical models Statistical significance Womens health |
| title | The M235T polymorphism in the AGT gene and CHD risk: evidence of a Hardy-Weinberg equilibrium violation and publication bias in a meta-analysis |
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