Genetically Reduced Soluble Epoxide Hydrolase Activity and Risk of Stroke and Other Cardiovascular Disease
The development of stroke has been linked to lowered levels of epoxyeicosatrienoic acids in the cerebral microvasculature. These substances are metabolized by the enzyme-soluble epoxide hydrolase encoded by the EPHX2 gene. We tested whether genetically reduced soluble epoxide hydrolase activity is a...
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| Veröffentlicht in: | Stroke (1970) 2010, Vol.41 (1), p.27-33 |
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| creator | LEE, Julie DAHL, Morten GRANDE, Peer TYBJAERG-HANSEN, Anne NORDESTGAARD, Børge G |
| description | The development of stroke has been linked to lowered levels of epoxyeicosatrienoic acids in the cerebral microvasculature. These substances are metabolized by the enzyme-soluble epoxide hydrolase encoded by the EPHX2 gene. We tested whether genetically reduced soluble epoxide hydrolase activity is associated with risk of ischemic stroke, myocardial infarction, and ischemic heart disease.
We genotyped participants from the Copenhagen City Heart Study (n=10 352), the Copenhagen General Population Study (n=26 042), the Copenhagen Carotid Stroke Study (n=398 cases+796 control subjects), and the Copenhagen Ischemic Heart Disease Study (n=4901 cases+9798 control subjects) for the R103C, R287Q, and Arg(402-403ins) variants in the EPHX2 gene and recorded hospital admissions due to ischemic stroke, myocardial infarction, and ischemic heart disease.
The hazard/odds ratio for ischemic stroke did not differ from 1.0 for any of the EPHX2 genotypes or genotype combinations in the Copenhagen City Heart Study (P for trend=0.15 to 0.76), in the Copenhagen General Population Study (P for trend=0.75 to 0.95), and the Copenhagen Carotid Stroke Study (P for trend=0.08 to 1.00). Similar results were obtained for myocardial infarction and ischemic heart disease in the 3 studies.
Our results show with significant power that genetically reduced soluble epoxide hydrolase activity is not a major risk factor for ischemic stroke, myocardial infarction, or ischemic heart disease in the Danish population. This suggests that the relationship between the EPHX2 gene and risk of ischemic stroke and other cardiovascular disease does not exist or its effect size is likely to be quite small. |
| doi_str_mv | 10.1161/STROKEAHA.109.567768 |
| format | Article |
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We genotyped participants from the Copenhagen City Heart Study (n=10 352), the Copenhagen General Population Study (n=26 042), the Copenhagen Carotid Stroke Study (n=398 cases+796 control subjects), and the Copenhagen Ischemic Heart Disease Study (n=4901 cases+9798 control subjects) for the R103C, R287Q, and Arg(402-403ins) variants in the EPHX2 gene and recorded hospital admissions due to ischemic stroke, myocardial infarction, and ischemic heart disease.
The hazard/odds ratio for ischemic stroke did not differ from 1.0 for any of the EPHX2 genotypes or genotype combinations in the Copenhagen City Heart Study (P for trend=0.15 to 0.76), in the Copenhagen General Population Study (P for trend=0.75 to 0.95), and the Copenhagen Carotid Stroke Study (P for trend=0.08 to 1.00). Similar results were obtained for myocardial infarction and ischemic heart disease in the 3 studies.
Our results show with significant power that genetically reduced soluble epoxide hydrolase activity is not a major risk factor for ischemic stroke, myocardial infarction, or ischemic heart disease in the Danish population. This suggests that the relationship between the EPHX2 gene and risk of ischemic stroke and other cardiovascular disease does not exist or its effect size is likely to be quite small.</description><identifier>ISSN: 0039-2499</identifier><identifier>EISSN: 1524-4628</identifier><identifier>DOI: 10.1161/STROKEAHA.109.567768</identifier><identifier>PMID: 19940276</identifier><identifier>CODEN: SJCCA7</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Biological and medical sciences ; Brain Ischemia - enzymology ; Brain Ischemia - genetics ; Case-Control Studies ; Cohort Studies ; Cross-Sectional Studies ; Enzyme Activation - genetics ; Epoxide Hydrolases - antagonists & inhibitors ; Epoxide Hydrolases - genetics ; Epoxide Hydrolases - metabolism ; Female ; Genetic Predisposition to Disease ; Genetic Variation - genetics ; Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy ; Humans ; Male ; Medical sciences ; Myocardial Ischemia - enzymology ; Myocardial Ischemia - genetics ; Nervous system (semeiology, syndromes) ; Neurology ; Prospective Studies ; Risk Factors ; Vascular diseases and vascular malformations of the nervous system</subject><ispartof>Stroke (1970), 2010, Vol.41 (1), p.27-33</ispartof><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c416t-47d6c2744e60e65c148752f0e66ff47e5b4fccd7697285b882f6a8ed385a10ff3</citedby><cites>FETCH-LOGICAL-c416t-47d6c2744e60e65c148752f0e66ff47e5b4fccd7697285b882f6a8ed385a10ff3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3687,4024,27923,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=22336990$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19940276$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>LEE, Julie</creatorcontrib><creatorcontrib>DAHL, Morten</creatorcontrib><creatorcontrib>GRANDE, Peer</creatorcontrib><creatorcontrib>TYBJAERG-HANSEN, Anne</creatorcontrib><creatorcontrib>NORDESTGAARD, Børge G</creatorcontrib><title>Genetically Reduced Soluble Epoxide Hydrolase Activity and Risk of Stroke and Other Cardiovascular Disease</title><title>Stroke (1970)</title><addtitle>Stroke</addtitle><description>The development of stroke has been linked to lowered levels of epoxyeicosatrienoic acids in the cerebral microvasculature. These substances are metabolized by the enzyme-soluble epoxide hydrolase encoded by the EPHX2 gene. We tested whether genetically reduced soluble epoxide hydrolase activity is associated with risk of ischemic stroke, myocardial infarction, and ischemic heart disease.
We genotyped participants from the Copenhagen City Heart Study (n=10 352), the Copenhagen General Population Study (n=26 042), the Copenhagen Carotid Stroke Study (n=398 cases+796 control subjects), and the Copenhagen Ischemic Heart Disease Study (n=4901 cases+9798 control subjects) for the R103C, R287Q, and Arg(402-403ins) variants in the EPHX2 gene and recorded hospital admissions due to ischemic stroke, myocardial infarction, and ischemic heart disease.
The hazard/odds ratio for ischemic stroke did not differ from 1.0 for any of the EPHX2 genotypes or genotype combinations in the Copenhagen City Heart Study (P for trend=0.15 to 0.76), in the Copenhagen General Population Study (P for trend=0.75 to 0.95), and the Copenhagen Carotid Stroke Study (P for trend=0.08 to 1.00). Similar results were obtained for myocardial infarction and ischemic heart disease in the 3 studies.
Our results show with significant power that genetically reduced soluble epoxide hydrolase activity is not a major risk factor for ischemic stroke, myocardial infarction, or ischemic heart disease in the Danish population. This suggests that the relationship between the EPHX2 gene and risk of ischemic stroke and other cardiovascular disease does not exist or its effect size is likely to be quite small.</description><subject>Biological and medical sciences</subject><subject>Brain Ischemia - enzymology</subject><subject>Brain Ischemia - genetics</subject><subject>Case-Control Studies</subject><subject>Cohort Studies</subject><subject>Cross-Sectional Studies</subject><subject>Enzyme Activation - genetics</subject><subject>Epoxide Hydrolases - antagonists & inhibitors</subject><subject>Epoxide Hydrolases - genetics</subject><subject>Epoxide Hydrolases - metabolism</subject><subject>Female</subject><subject>Genetic Predisposition to Disease</subject><subject>Genetic Variation - genetics</subject><subject>Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Myocardial Ischemia - enzymology</subject><subject>Myocardial Ischemia - genetics</subject><subject>Nervous system (semeiology, syndromes)</subject><subject>Neurology</subject><subject>Prospective Studies</subject><subject>Risk Factors</subject><subject>Vascular diseases and vascular malformations of the nervous system</subject><issn>0039-2499</issn><issn>1524-4628</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkE1PGzEQhi3UCtKUf1AhXypOG2yv1x_HKARSgRQpgfPKsceqwYmDvYvIv--2iehpRqPnndE8CP2gZEKpoDfrp9XyYT5dTCeU6EkjpBTqDI1ow3jFBVNf0IiQWleMa32BvpXyQghhtWrO0QXVmhMmxQi93MMOumBNjAe8AtdbcHidYr-JgOf79BEc4MXB5RRNATy1XXgP3QGbncOrUF5x8njd5fQK_0bL7jdkPDPZhfRuiu2jyfg2FBjC39FXb2KBy1Mdo-e7-dNsUT0u73_Npo-V5VR0FZdOWCY5B0FANJZyJRvmh154zyU0G-6tdVJoyVSzUYp5YRS44TNDiff1GF0f9-5zeuuhdO02FAsxmh2kvrSy5owKNcgZI34kbU6lZPDtPoetyYeWkvav5PZT8jDR7VHyELs6Heg3W3D_QyerA_DzBAwKTPTZ7GwonxxjdS20JvUflxmGXg</recordid><startdate>2010</startdate><enddate>2010</enddate><creator>LEE, Julie</creator><creator>DAHL, Morten</creator><creator>GRANDE, Peer</creator><creator>TYBJAERG-HANSEN, Anne</creator><creator>NORDESTGAARD, Børge G</creator><general>Lippincott Williams & Wilkins</general><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>7X8</scope></search><sort><creationdate>2010</creationdate><title>Genetically Reduced Soluble Epoxide Hydrolase Activity and Risk of Stroke and Other Cardiovascular Disease</title><author>LEE, Julie ; DAHL, Morten ; GRANDE, Peer ; TYBJAERG-HANSEN, Anne ; NORDESTGAARD, Børge G</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c416t-47d6c2744e60e65c148752f0e66ff47e5b4fccd7697285b882f6a8ed385a10ff3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Biological and medical sciences</topic><topic>Brain Ischemia - enzymology</topic><topic>Brain Ischemia - genetics</topic><topic>Case-Control Studies</topic><topic>Cohort Studies</topic><topic>Cross-Sectional Studies</topic><topic>Enzyme Activation - genetics</topic><topic>Epoxide Hydrolases - antagonists & inhibitors</topic><topic>Epoxide Hydrolases - genetics</topic><topic>Epoxide Hydrolases - metabolism</topic><topic>Female</topic><topic>Genetic Predisposition to Disease</topic><topic>Genetic Variation - genetics</topic><topic>Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Myocardial Ischemia - enzymology</topic><topic>Myocardial Ischemia - genetics</topic><topic>Nervous system (semeiology, syndromes)</topic><topic>Neurology</topic><topic>Prospective Studies</topic><topic>Risk Factors</topic><topic>Vascular diseases and vascular malformations of the nervous system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>LEE, Julie</creatorcontrib><creatorcontrib>DAHL, Morten</creatorcontrib><creatorcontrib>GRANDE, Peer</creatorcontrib><creatorcontrib>TYBJAERG-HANSEN, Anne</creatorcontrib><creatorcontrib>NORDESTGAARD, Børge G</creatorcontrib><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>MEDLINE - Academic</collection><jtitle>Stroke (1970)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>LEE, Julie</au><au>DAHL, Morten</au><au>GRANDE, Peer</au><au>TYBJAERG-HANSEN, Anne</au><au>NORDESTGAARD, Børge G</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Genetically Reduced Soluble Epoxide Hydrolase Activity and Risk of Stroke and Other Cardiovascular Disease</atitle><jtitle>Stroke (1970)</jtitle><addtitle>Stroke</addtitle><date>2010</date><risdate>2010</risdate><volume>41</volume><issue>1</issue><spage>27</spage><epage>33</epage><pages>27-33</pages><issn>0039-2499</issn><eissn>1524-4628</eissn><coden>SJCCA7</coden><abstract>The development of stroke has been linked to lowered levels of epoxyeicosatrienoic acids in the cerebral microvasculature. These substances are metabolized by the enzyme-soluble epoxide hydrolase encoded by the EPHX2 gene. We tested whether genetically reduced soluble epoxide hydrolase activity is associated with risk of ischemic stroke, myocardial infarction, and ischemic heart disease.
We genotyped participants from the Copenhagen City Heart Study (n=10 352), the Copenhagen General Population Study (n=26 042), the Copenhagen Carotid Stroke Study (n=398 cases+796 control subjects), and the Copenhagen Ischemic Heart Disease Study (n=4901 cases+9798 control subjects) for the R103C, R287Q, and Arg(402-403ins) variants in the EPHX2 gene and recorded hospital admissions due to ischemic stroke, myocardial infarction, and ischemic heart disease.
The hazard/odds ratio for ischemic stroke did not differ from 1.0 for any of the EPHX2 genotypes or genotype combinations in the Copenhagen City Heart Study (P for trend=0.15 to 0.76), in the Copenhagen General Population Study (P for trend=0.75 to 0.95), and the Copenhagen Carotid Stroke Study (P for trend=0.08 to 1.00). Similar results were obtained for myocardial infarction and ischemic heart disease in the 3 studies.
Our results show with significant power that genetically reduced soluble epoxide hydrolase activity is not a major risk factor for ischemic stroke, myocardial infarction, or ischemic heart disease in the Danish population. This suggests that the relationship between the EPHX2 gene and risk of ischemic stroke and other cardiovascular disease does not exist or its effect size is likely to be quite small.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>19940276</pmid><doi>10.1161/STROKEAHA.109.567768</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Stroke (1970), 2010, Vol.41 (1), p.27-33 |
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| source | MEDLINE; American Heart Association Journals; Journals@Ovid Complete; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Biological and medical sciences Brain Ischemia - enzymology Brain Ischemia - genetics Case-Control Studies Cohort Studies Cross-Sectional Studies Enzyme Activation - genetics Epoxide Hydrolases - antagonists & inhibitors Epoxide Hydrolases - genetics Epoxide Hydrolases - metabolism Female Genetic Predisposition to Disease Genetic Variation - genetics Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy Humans Male Medical sciences Myocardial Ischemia - enzymology Myocardial Ischemia - genetics Nervous system (semeiology, syndromes) Neurology Prospective Studies Risk Factors Vascular diseases and vascular malformations of the nervous system |
| title | Genetically Reduced Soluble Epoxide Hydrolase Activity and Risk of Stroke and Other Cardiovascular Disease |
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