White Cell Telomere Length and Risk of Premature Myocardial Infarction
OBJECTIVE—Biological age may be distinct from chronological age and contribute to the pathogenesis of age-related diseases. Mean telomeres lengths provide an assessment of biological age with shorter telomeres, indicating increased biological age. We investigated whether subjects with premature myoc...
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| Veröffentlicht in: | Arteriosclerosis, thrombosis, and vascular biology thrombosis, and vascular biology, 2003-05, Vol.23 (5), p.842-846 |
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| container_title | Arteriosclerosis, thrombosis, and vascular biology |
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| creator | Brouilette, Scott Singh, Ravi K Thompson, John R Goodall, Alison H Samani, Nilesh J |
| description | OBJECTIVE—Biological age may be distinct from chronological age and contribute to the pathogenesis of age-related diseases. Mean telomeres lengths provide an assessment of biological age with shorter telomeres, indicating increased biological age. We investigated whether subjects with premature myocardial infarction (MI) had shorter leukocyte telomeres.
METHODS AND RESULTS—Mean terminal restriction fragment (TRF) length, a measure of average telomere size, was compared in leukocyte DNA of 203 cases with a premature MI ( |
| doi_str_mv | 10.1161/01.ATV.0000067426.96344.32 |
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METHODS AND RESULTS—Mean terminal restriction fragment (TRF) length, a measure of average telomere size, was compared in leukocyte DNA of 203 cases with a premature MI (<50 years) and 180 controls. Age- and sex-adjusted mean TRF length of cases was significantly shorter than that of controls (difference 299.7±69.3 base pairs, P <0.0001) and on average equivalent to controls 11.3 years older. The difference in mean TRF length between cases and controls was not accounted for by other coronary risk factors. Compared with subjects in the highest quartile for telomere length, the risk of myocardial infarction was increased between 2.8- and 3.2-fold (P <0.0001) in subjects with shorter than average telomeres.
CONCLUSIONS—The findings support the concept that biological age may play a role in the etiology of coronary heart disease and have potentially important implications for our understanding of its genetic etiology, pathogenesis, and variable age of onset.</description><identifier>ISSN: 1079-5642</identifier><identifier>EISSN: 1524-4636</identifier><identifier>DOI: 10.1161/01.ATV.0000067426.96344.32</identifier><identifier>PMID: 12649083</identifier><identifier>CODEN: ATVBFA</identifier><language>eng</language><publisher>Philadelphia, PA: American Heart Association, Inc</publisher><subject>Adult ; Age of Onset ; Aging - genetics ; Biological and medical sciences ; Cardiology. Vascular system ; Coronary Disease - epidemiology ; Coronary Disease - genetics ; Coronary heart disease ; England - epidemiology ; Female ; Heart ; Humans ; Leukocytes - ultrastructure ; Male ; Medical sciences ; Middle Aged ; Myocardial Infarction - epidemiology ; Myocardial Infarction - genetics ; Retrospective Studies ; Risk ; Risk Factors ; Telomere - ultrastructure</subject><ispartof>Arteriosclerosis, thrombosis, and vascular biology, 2003-05, Vol.23 (5), p.842-846</ispartof><rights>2003 American Heart Association, Inc.</rights><rights>2003 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. May 1 2003</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c6252-1fcdb76ca396ef2c2ce0645b02913063b01a421e702ef2ca3aac83d91bd973be3</citedby><cites>FETCH-LOGICAL-c6252-1fcdb76ca396ef2c2ce0645b02913063b01a421e702ef2ca3aac83d91bd973be3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14790057$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12649083$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Brouilette, Scott</creatorcontrib><creatorcontrib>Singh, Ravi K</creatorcontrib><creatorcontrib>Thompson, John R</creatorcontrib><creatorcontrib>Goodall, Alison H</creatorcontrib><creatorcontrib>Samani, Nilesh J</creatorcontrib><title>White Cell Telomere Length and Risk of Premature Myocardial Infarction</title><title>Arteriosclerosis, thrombosis, and vascular biology</title><addtitle>Arterioscler Thromb Vasc Biol</addtitle><description>OBJECTIVE—Biological age may be distinct from chronological age and contribute to the pathogenesis of age-related diseases. Mean telomeres lengths provide an assessment of biological age with shorter telomeres, indicating increased biological age. We investigated whether subjects with premature myocardial infarction (MI) had shorter leukocyte telomeres.
METHODS AND RESULTS—Mean terminal restriction fragment (TRF) length, a measure of average telomere size, was compared in leukocyte DNA of 203 cases with a premature MI (<50 years) and 180 controls. Age- and sex-adjusted mean TRF length of cases was significantly shorter than that of controls (difference 299.7±69.3 base pairs, P <0.0001) and on average equivalent to controls 11.3 years older. The difference in mean TRF length between cases and controls was not accounted for by other coronary risk factors. Compared with subjects in the highest quartile for telomere length, the risk of myocardial infarction was increased between 2.8- and 3.2-fold (P <0.0001) in subjects with shorter than average telomeres.
CONCLUSIONS—The findings support the concept that biological age may play a role in the etiology of coronary heart disease and have potentially important implications for our understanding of its genetic etiology, pathogenesis, and variable age of onset.</description><subject>Adult</subject><subject>Age of Onset</subject><subject>Aging - genetics</subject><subject>Biological and medical sciences</subject><subject>Cardiology. Vascular system</subject><subject>Coronary Disease - epidemiology</subject><subject>Coronary Disease - genetics</subject><subject>Coronary heart disease</subject><subject>England - epidemiology</subject><subject>Female</subject><subject>Heart</subject><subject>Humans</subject><subject>Leukocytes - ultrastructure</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Myocardial Infarction - epidemiology</subject><subject>Myocardial Infarction - genetics</subject><subject>Retrospective Studies</subject><subject>Risk</subject><subject>Risk Factors</subject><subject>Telomere - ultrastructure</subject><issn>1079-5642</issn><issn>1524-4636</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkG-L1DAQh4Mo3nn6FaQc6LvWyeRPW98di6cHK4qs-jKk6dTtXdreJS3HfXtTd2HBQEjCPJPf8DB2yaHgXPMPwIur3a8C1qVLibqotZCyEPiMnXOFMpda6OfpDmWdKy3xjL2K8TbhEhFesjOOWtZQiXN2_Xvfz5RtyPtsR34aKFC2pfHPvM_s2GY_-niXTV32PdBg5yUVvz5Nzoa2tz67GTsb3NxP42v2orM-0pvjecF-Xn_abb7k22-fbzZX29xpVJjzzrVNqZ0VtaYOHToCLVUDWHMBWjTArUROJeBatsJaV4m25k1bl6IhccHeH_69D9PDQnE2Qx9dGt6ONC3RlAIrhRoTePkfeDstYUyzGUwWKlVxnqCPB8iFKcZAnbkP_WDDk-FgVtUGuEmqzUm1-afaiDXh7TFhaQZqT61Htwl4dwRsdNZ3wY6ujydOljWAKhMnD9zj5GcK8c4vjxTMnqyf92u0FBpUjgACVHrmaSOKv7EUlSg</recordid><startdate>200305</startdate><enddate>200305</enddate><creator>Brouilette, Scott</creator><creator>Singh, Ravi K</creator><creator>Thompson, John R</creator><creator>Goodall, Alison H</creator><creator>Samani, Nilesh J</creator><general>American Heart Association, Inc</general><general>Lippincott</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>K9.</scope><scope>7X8</scope></search><sort><creationdate>200305</creationdate><title>White Cell Telomere Length and Risk of Premature Myocardial Infarction</title><author>Brouilette, Scott ; Singh, Ravi K ; Thompson, John R ; Goodall, Alison H ; Samani, Nilesh J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c6252-1fcdb76ca396ef2c2ce0645b02913063b01a421e702ef2ca3aac83d91bd973be3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Adult</topic><topic>Age of Onset</topic><topic>Aging - genetics</topic><topic>Biological and medical sciences</topic><topic>Cardiology. Vascular system</topic><topic>Coronary Disease - epidemiology</topic><topic>Coronary Disease - genetics</topic><topic>Coronary heart disease</topic><topic>England - epidemiology</topic><topic>Female</topic><topic>Heart</topic><topic>Humans</topic><topic>Leukocytes - ultrastructure</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Myocardial Infarction - epidemiology</topic><topic>Myocardial Infarction - genetics</topic><topic>Retrospective Studies</topic><topic>Risk</topic><topic>Risk Factors</topic><topic>Telomere - ultrastructure</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Brouilette, Scott</creatorcontrib><creatorcontrib>Singh, Ravi K</creatorcontrib><creatorcontrib>Thompson, John R</creatorcontrib><creatorcontrib>Goodall, Alison H</creatorcontrib><creatorcontrib>Samani, Nilesh J</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>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Arteriosclerosis, thrombosis, and vascular biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Brouilette, Scott</au><au>Singh, Ravi K</au><au>Thompson, John R</au><au>Goodall, Alison H</au><au>Samani, Nilesh J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>White Cell Telomere Length and Risk of Premature Myocardial Infarction</atitle><jtitle>Arteriosclerosis, thrombosis, and vascular biology</jtitle><addtitle>Arterioscler Thromb Vasc Biol</addtitle><date>2003-05</date><risdate>2003</risdate><volume>23</volume><issue>5</issue><spage>842</spage><epage>846</epage><pages>842-846</pages><issn>1079-5642</issn><eissn>1524-4636</eissn><coden>ATVBFA</coden><abstract>OBJECTIVE—Biological age may be distinct from chronological age and contribute to the pathogenesis of age-related diseases. Mean telomeres lengths provide an assessment of biological age with shorter telomeres, indicating increased biological age. We investigated whether subjects with premature myocardial infarction (MI) had shorter leukocyte telomeres.
METHODS AND RESULTS—Mean terminal restriction fragment (TRF) length, a measure of average telomere size, was compared in leukocyte DNA of 203 cases with a premature MI (<50 years) and 180 controls. Age- and sex-adjusted mean TRF length of cases was significantly shorter than that of controls (difference 299.7±69.3 base pairs, P <0.0001) and on average equivalent to controls 11.3 years older. The difference in mean TRF length between cases and controls was not accounted for by other coronary risk factors. Compared with subjects in the highest quartile for telomere length, the risk of myocardial infarction was increased between 2.8- and 3.2-fold (P <0.0001) in subjects with shorter than average telomeres.
CONCLUSIONS—The findings support the concept that biological age may play a role in the etiology of coronary heart disease and have potentially important implications for our understanding of its genetic etiology, pathogenesis, and variable age of onset.</abstract><cop>Philadelphia, PA</cop><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>12649083</pmid><doi>10.1161/01.ATV.0000067426.96344.32</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Age of Onset Aging - genetics Biological and medical sciences Cardiology. Vascular system Coronary Disease - epidemiology Coronary Disease - genetics Coronary heart disease England - epidemiology Female Heart Humans Leukocytes - ultrastructure Male Medical sciences Middle Aged Myocardial Infarction - epidemiology Myocardial Infarction - genetics Retrospective Studies Risk Risk Factors Telomere - ultrastructure |
| title | White Cell Telomere Length and Risk of Premature Myocardial Infarction |
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