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Reduced carriership of 4G allele of plasminogen activator inhibitor-1 4G/5G polymorphism in very young survivors of myocardial infarction
There are limited and controversial data regarding the impact of 4G/5G polymorphism of the plasminogen activator inhibitor-1 (PAI-1) gene in the pathogenesis of premature myocardial infarction (MI). We explored whether 4G/5G polymorphism of the PAI-1 gene is associated with the development of MI ≤ 3...
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Published in: | Journal of thrombosis and thrombolysis 2010-05, Vol.29 (4), p.497-502 |
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creator | Rallidis, Loukianos S. Gialeraki, Argyri Merkouri, Efrosyni Liakos, George Dagres, Nikolaos Sionis, Dimitrios Travlou, Anthi Lekakis, John Kremastinos, Dimitrios T. |
description | There are limited and controversial data regarding the impact of 4G/5G polymorphism of the plasminogen activator inhibitor-1 (PAI-1) gene in the pathogenesis of premature myocardial infarction (MI). We explored whether 4G/5G polymorphism of the PAI-1 gene is associated with the development of MI ≤ 35 years of age. We recruited 201 consecutive patients who had survived their first acute MI ≤ 35 years of age (mean age = 32.2 ± 3.4 years). The control group consisted of 140 healthy individuals matched with cases for age and sex, without a family history of premature coronary heart disease. 4G/5G polymorphism of PAI-1 was tested with polymerase chain reaction and reverse hybridization. 4G allele carriers (4G/4G and 4G/5G genotypes) of PAI-1 were less frequent in patients than in controls (69.6 vs. 83.6%,
P
= 0.007). 4G carriership of the polymorphism of PAI-1 was associated with lower risk for acute MI (odds ratio 0.45, 95% confidence interval 0.23–0.88,
P
= 0.02) after adjusting for major cardiovascular risk factors. Patients possessing the 4G allele had higher PAI-1 plasma levels (32.2 ± 25 vs. 22.2 ± 11.3 ng/ml,
P
= 0.006) but lower lipoprotein(a) levels (10.1 [2.1–29.9] vs. 15.3 [8.2–57.1] mg/dl,
P
= 0.03) compared to 5G/5G homozygotes. Our data indicate that the 4G allele of the PAI-1 4G/5G polymorphism is less frequent among survivors of MI at very young age compared with matched controls. |
doi_str_mv | 10.1007/s11239-009-0398-z |
format | article |
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P
= 0.007). 4G carriership of the polymorphism of PAI-1 was associated with lower risk for acute MI (odds ratio 0.45, 95% confidence interval 0.23–0.88,
P
= 0.02) after adjusting for major cardiovascular risk factors. Patients possessing the 4G allele had higher PAI-1 plasma levels (32.2 ± 25 vs. 22.2 ± 11.3 ng/ml,
P
= 0.006) but lower lipoprotein(a) levels (10.1 [2.1–29.9] vs. 15.3 [8.2–57.1] mg/dl,
P
= 0.03) compared to 5G/5G homozygotes. Our data indicate that the 4G allele of the PAI-1 4G/5G polymorphism is less frequent among survivors of MI at very young age compared with matched controls.</description><identifier>ISSN: 0929-5305</identifier><identifier>EISSN: 1573-742X</identifier><identifier>DOI: 10.1007/s11239-009-0398-z</identifier><identifier>PMID: 19844663</identifier><language>eng</language><publisher>Boston: Springer US</publisher><subject>Adult ; Alleles ; Cardiology ; Female ; Hematology ; Homozygote ; Humans ; Lipoprotein(a) - blood ; Male ; Medicine ; Medicine & Public Health ; Myocardial Infarction - blood ; Myocardial Infarction - genetics ; Myocardial Infarction - mortality ; Plasminogen Activator Inhibitor 1 - blood ; Plasminogen Activator Inhibitor 1 - genetics ; Polymorphism, Genetic ; Retrospective Studies ; Risk Factors</subject><ispartof>Journal of thrombosis and thrombolysis, 2010-05, Vol.29 (4), p.497-502</ispartof><rights>Springer Science+Business Media, LLC 2009</rights><rights>Springer Science+Business Media, LLC 2010</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c370t-f2cb16ba1bf08cedc3cdf7bdf9bda78bdbc239c80342afb8c8b199270a760b223</citedby><cites>FETCH-LOGICAL-c370t-f2cb16ba1bf08cedc3cdf7bdf9bda78bdbc239c80342afb8c8b199270a760b223</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19844663$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rallidis, Loukianos S.</creatorcontrib><creatorcontrib>Gialeraki, Argyri</creatorcontrib><creatorcontrib>Merkouri, Efrosyni</creatorcontrib><creatorcontrib>Liakos, George</creatorcontrib><creatorcontrib>Dagres, Nikolaos</creatorcontrib><creatorcontrib>Sionis, Dimitrios</creatorcontrib><creatorcontrib>Travlou, Anthi</creatorcontrib><creatorcontrib>Lekakis, John</creatorcontrib><creatorcontrib>Kremastinos, Dimitrios T.</creatorcontrib><title>Reduced carriership of 4G allele of plasminogen activator inhibitor-1 4G/5G polymorphism in very young survivors of myocardial infarction</title><title>Journal of thrombosis and thrombolysis</title><addtitle>J Thromb Thrombolysis</addtitle><addtitle>J Thromb Thrombolysis</addtitle><description>There are limited and controversial data regarding the impact of 4G/5G polymorphism of the plasminogen activator inhibitor-1 (PAI-1) gene in the pathogenesis of premature myocardial infarction (MI). We explored whether 4G/5G polymorphism of the PAI-1 gene is associated with the development of MI ≤ 35 years of age. We recruited 201 consecutive patients who had survived their first acute MI ≤ 35 years of age (mean age = 32.2 ± 3.4 years). The control group consisted of 140 healthy individuals matched with cases for age and sex, without a family history of premature coronary heart disease. 4G/5G polymorphism of PAI-1 was tested with polymerase chain reaction and reverse hybridization. 4G allele carriers (4G/4G and 4G/5G genotypes) of PAI-1 were less frequent in patients than in controls (69.6 vs. 83.6%,
P
= 0.007). 4G carriership of the polymorphism of PAI-1 was associated with lower risk for acute MI (odds ratio 0.45, 95% confidence interval 0.23–0.88,
P
= 0.02) after adjusting for major cardiovascular risk factors. Patients possessing the 4G allele had higher PAI-1 plasma levels (32.2 ± 25 vs. 22.2 ± 11.3 ng/ml,
P
= 0.006) but lower lipoprotein(a) levels (10.1 [2.1–29.9] vs. 15.3 [8.2–57.1] mg/dl,
P
= 0.03) compared to 5G/5G homozygotes. Our data indicate that the 4G allele of the PAI-1 4G/5G polymorphism is less frequent among survivors of MI at very young age compared with matched controls.</description><subject>Adult</subject><subject>Alleles</subject><subject>Cardiology</subject><subject>Female</subject><subject>Hematology</subject><subject>Homozygote</subject><subject>Humans</subject><subject>Lipoprotein(a) - blood</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Myocardial Infarction - blood</subject><subject>Myocardial Infarction - genetics</subject><subject>Myocardial Infarction - mortality</subject><subject>Plasminogen Activator Inhibitor 1 - blood</subject><subject>Plasminogen Activator Inhibitor 1 - genetics</subject><subject>Polymorphism, Genetic</subject><subject>Retrospective Studies</subject><subject>Risk Factors</subject><issn>0929-5305</issn><issn>1573-742X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><recordid>eNp1kc9qGzEQxkVJaRy3D9BLEbn0tI3-7FqrYwitEwgUSgu9CUkr2Qra1UbyGjZvkLfuODYEAgUJjZjffDPMh9BnSr5RQsRVoZRxWRECl8u2enqHFrQRvBI1-3uGFkQyWTWcNOfoopQHAqAk7AM6p7Kt69WKL9DzL9dN1nXY6pyDy2UbRpw8rtdYx-iiO3zGqEsfhrRxA9Z2F_Z6lzIOwzaYAFFFAb9q1nhMce5THreh9JDGe5dnPKdp2OAy5X3Yp1wOev2coF0XdATK6wySafiI3nsdi_t0epfoz4_vv29uq_uf67ub6_vKckF2lWfW0JXR1HjSwuCW284L03lpOi1a0xkLO7Et4TXT3rS2NVRKJogWK2IY40v09ag75vQ4ubJTfSjWxagHl6aiBOeyaUXdAHn5hnxIUx5gOMUY6L-cJaJHyOZUSnZejTn0Os-KEnVwSR1dUrB8dXBJPUHNl5PwZHrXvVacbAGAHYECqWHj8mvn_6v-A7Q9oNM</recordid><startdate>20100501</startdate><enddate>20100501</enddate><creator>Rallidis, Loukianos S.</creator><creator>Gialeraki, Argyri</creator><creator>Merkouri, Efrosyni</creator><creator>Liakos, George</creator><creator>Dagres, Nikolaos</creator><creator>Sionis, Dimitrios</creator><creator>Travlou, Anthi</creator><creator>Lekakis, John</creator><creator>Kremastinos, Dimitrios T.</creator><general>Springer US</general><general>Springer Nature B.V</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>3V.</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20100501</creationdate><title>Reduced carriership of 4G allele of plasminogen activator inhibitor-1 4G/5G polymorphism in very young survivors of myocardial infarction</title><author>Rallidis, Loukianos S. ; Gialeraki, Argyri ; Merkouri, Efrosyni ; Liakos, George ; Dagres, Nikolaos ; Sionis, Dimitrios ; Travlou, Anthi ; Lekakis, John ; Kremastinos, Dimitrios T.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c370t-f2cb16ba1bf08cedc3cdf7bdf9bda78bdbc239c80342afb8c8b199270a760b223</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Adult</topic><topic>Alleles</topic><topic>Cardiology</topic><topic>Female</topic><topic>Hematology</topic><topic>Homozygote</topic><topic>Humans</topic><topic>Lipoprotein(a) - blood</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Myocardial Infarction - blood</topic><topic>Myocardial Infarction - genetics</topic><topic>Myocardial Infarction - mortality</topic><topic>Plasminogen Activator Inhibitor 1 - blood</topic><topic>Plasminogen Activator Inhibitor 1 - genetics</topic><topic>Polymorphism, Genetic</topic><topic>Retrospective Studies</topic><topic>Risk Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rallidis, Loukianos S.</creatorcontrib><creatorcontrib>Gialeraki, Argyri</creatorcontrib><creatorcontrib>Merkouri, Efrosyni</creatorcontrib><creatorcontrib>Liakos, George</creatorcontrib><creatorcontrib>Dagres, Nikolaos</creatorcontrib><creatorcontrib>Sionis, Dimitrios</creatorcontrib><creatorcontrib>Travlou, Anthi</creatorcontrib><creatorcontrib>Lekakis, John</creatorcontrib><creatorcontrib>Kremastinos, Dimitrios T.</creatorcontrib><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>Neurosciences Abstracts</collection><collection>Health & Medical Collection (Proquest)</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</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)</collection><collection>ProQuest Central</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</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>MEDLINE - Academic</collection><jtitle>Journal of thrombosis and thrombolysis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rallidis, Loukianos S.</au><au>Gialeraki, Argyri</au><au>Merkouri, Efrosyni</au><au>Liakos, George</au><au>Dagres, Nikolaos</au><au>Sionis, Dimitrios</au><au>Travlou, Anthi</au><au>Lekakis, John</au><au>Kremastinos, Dimitrios T.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Reduced carriership of 4G allele of plasminogen activator inhibitor-1 4G/5G polymorphism in very young survivors of myocardial infarction</atitle><jtitle>Journal of thrombosis and thrombolysis</jtitle><stitle>J Thromb Thrombolysis</stitle><addtitle>J Thromb Thrombolysis</addtitle><date>2010-05-01</date><risdate>2010</risdate><volume>29</volume><issue>4</issue><spage>497</spage><epage>502</epage><pages>497-502</pages><issn>0929-5305</issn><eissn>1573-742X</eissn><abstract>There are limited and controversial data regarding the impact of 4G/5G polymorphism of the plasminogen activator inhibitor-1 (PAI-1) gene in the pathogenesis of premature myocardial infarction (MI). We explored whether 4G/5G polymorphism of the PAI-1 gene is associated with the development of MI ≤ 35 years of age. We recruited 201 consecutive patients who had survived their first acute MI ≤ 35 years of age (mean age = 32.2 ± 3.4 years). The control group consisted of 140 healthy individuals matched with cases for age and sex, without a family history of premature coronary heart disease. 4G/5G polymorphism of PAI-1 was tested with polymerase chain reaction and reverse hybridization. 4G allele carriers (4G/4G and 4G/5G genotypes) of PAI-1 were less frequent in patients than in controls (69.6 vs. 83.6%,
P
= 0.007). 4G carriership of the polymorphism of PAI-1 was associated with lower risk for acute MI (odds ratio 0.45, 95% confidence interval 0.23–0.88,
P
= 0.02) after adjusting for major cardiovascular risk factors. Patients possessing the 4G allele had higher PAI-1 plasma levels (32.2 ± 25 vs. 22.2 ± 11.3 ng/ml,
P
= 0.006) but lower lipoprotein(a) levels (10.1 [2.1–29.9] vs. 15.3 [8.2–57.1] mg/dl,
P
= 0.03) compared to 5G/5G homozygotes. Our data indicate that the 4G allele of the PAI-1 4G/5G polymorphism is less frequent among survivors of MI at very young age compared with matched controls.</abstract><cop>Boston</cop><pub>Springer US</pub><pmid>19844663</pmid><doi>10.1007/s11239-009-0398-z</doi><tpages>6</tpages></addata></record> |
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subjects | Adult Alleles Cardiology Female Hematology Homozygote Humans Lipoprotein(a) - blood Male Medicine Medicine & Public Health Myocardial Infarction - blood Myocardial Infarction - genetics Myocardial Infarction - mortality Plasminogen Activator Inhibitor 1 - blood Plasminogen Activator Inhibitor 1 - genetics Polymorphism, Genetic Retrospective Studies Risk Factors |
title | Reduced carriership of 4G allele of plasminogen activator inhibitor-1 4G/5G polymorphism in very young survivors of myocardial infarction |
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