The association between levels of tissue inhibitor of metalloproteinase-1 with acute heart failure and left ventricular dysfunction in patients with ST elevation myocardial infarction treated by primary percutaneous coronary intervention
Tissue inhibitors of metalloproteinase (TIMPs) bind to active matrix metalloproteinase (MMPs), and thereby inhibit their proteolytic activity. We investigated the role of polymorphisms in the gene for TIMP-1 and serum levels of TIMP-1 in association with postmyocardial infarction (MI), left ventricu...
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| Veröffentlicht in: | Genetic testing and molecular biomarkers 2012-10, Vol.16 (10), p.1172-1178 |
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| creator | Goldbergova, Monika Pavkova Parenica, Jiri Jarkovsky, Jiri Kala, Petr Poloczek, Martin Manousek, Jan Kluz, Krystyna Kubkova, Lenka Littnerova, Simona Tesak, Martin Toman, Ondrej Pavek, Nikolas Cermakova, Zdenka Tomandl, Josef Vasku, Anna Spinar, Jindrich |
| description | Tissue inhibitors of metalloproteinase (TIMPs) bind to active matrix metalloproteinase (MMPs), and thereby inhibit their proteolytic activity. We investigated the role of polymorphisms in the gene for TIMP-1 and serum levels of TIMP-1 in association with postmyocardial infarction (MI), left ventricular (LV) dysfunction, and symptoms of acute heart failure (AHF) in patients treated with primary percutaneous coronary intervention.
In total, 556 patients with STEMI were evaluated. Levels of TIMP-1 were measured at admission and 24 h after MI onset. The TIMP-1 exon 5 SNP rs4898 (F124F with T>C) located at X chromosome was assayed.
TIMP-1 levels were higher for men with AHF as well as for men with LV dysfunction (ejection fraction [EF] |
| doi_str_mv | 10.1089/gtmb.2012.0120 |
| format | Article |
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In total, 556 patients with STEMI were evaluated. Levels of TIMP-1 were measured at admission and 24 h after MI onset. The TIMP-1 exon 5 SNP rs4898 (F124F with T>C) located at X chromosome was assayed.
TIMP-1 levels were higher for men with AHF as well as for men with LV dysfunction (ejection fraction [EF]<40%). According to multivariate analysis, the TIMP-1 level was a factor with an independent negative relationship to EF and AHF in men. An independent relationship between exon 5 TIMP-1 gene polymorphism and EF, AHF or TIMP-1 level was not documented.
These results provide evidence that a higher level of circulating TIMP-1 is independently associated with worse EF and AHF.</description><identifier>ISSN: 1945-0265</identifier><identifier>EISSN: 1945-0257</identifier><identifier>DOI: 10.1089/gtmb.2012.0120</identifier><identifier>PMID: 22971139</identifier><language>eng</language><publisher>United States: Mary Ann Liebert, Inc</publisher><subject>Adult ; Aged ; Exons ; Female ; Heart Failure - blood ; Heart Failure - genetics ; Humans ; Male ; Middle Aged ; Myocardial Infarction - blood ; Myocardial Infarction - genetics ; Myocardial Infarction - therapy ; Original ; Percutaneous Coronary Intervention - methods ; Polymorphism, Genetic ; Tissue Inhibitor of Metalloproteinase-1 - blood ; Tissue Inhibitor of Metalloproteinase-1 - genetics ; Ventricular Dysfunction, Left - blood ; Ventricular Dysfunction, Left - genetics</subject><ispartof>Genetic testing and molecular biomarkers, 2012-10, Vol.16 (10), p.1172-1178</ispartof><rights>Copyright 2012, Mary Ann Liebert, Inc. 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c423t-1fc3c412690d2f1155b455dc7dee76ad53b13db025d9131999aa9622ed59c1f83</citedby><cites>FETCH-LOGICAL-c423t-1fc3c412690d2f1155b455dc7dee76ad53b13db025d9131999aa9622ed59c1f83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,315,781,785,886,27929,27930</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22971139$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Goldbergova, Monika Pavkova</creatorcontrib><creatorcontrib>Parenica, Jiri</creatorcontrib><creatorcontrib>Jarkovsky, Jiri</creatorcontrib><creatorcontrib>Kala, Petr</creatorcontrib><creatorcontrib>Poloczek, Martin</creatorcontrib><creatorcontrib>Manousek, Jan</creatorcontrib><creatorcontrib>Kluz, Krystyna</creatorcontrib><creatorcontrib>Kubkova, Lenka</creatorcontrib><creatorcontrib>Littnerova, Simona</creatorcontrib><creatorcontrib>Tesak, Martin</creatorcontrib><creatorcontrib>Toman, Ondrej</creatorcontrib><creatorcontrib>Pavek, Nikolas</creatorcontrib><creatorcontrib>Cermakova, Zdenka</creatorcontrib><creatorcontrib>Tomandl, Josef</creatorcontrib><creatorcontrib>Vasku, Anna</creatorcontrib><creatorcontrib>Spinar, Jindrich</creatorcontrib><title>The association between levels of tissue inhibitor of metalloproteinase-1 with acute heart failure and left ventricular dysfunction in patients with ST elevation myocardial infarction treated by primary percutaneous coronary intervention</title><title>Genetic testing and molecular biomarkers</title><addtitle>Genet Test Mol Biomarkers</addtitle><description>Tissue inhibitors of metalloproteinase (TIMPs) bind to active matrix metalloproteinase (MMPs), and thereby inhibit their proteolytic activity. We investigated the role of polymorphisms in the gene for TIMP-1 and serum levels of TIMP-1 in association with postmyocardial infarction (MI), left ventricular (LV) dysfunction, and symptoms of acute heart failure (AHF) in patients treated with primary percutaneous coronary intervention.
In total, 556 patients with STEMI were evaluated. Levels of TIMP-1 were measured at admission and 24 h after MI onset. The TIMP-1 exon 5 SNP rs4898 (F124F with T>C) located at X chromosome was assayed.
TIMP-1 levels were higher for men with AHF as well as for men with LV dysfunction (ejection fraction [EF]<40%). According to multivariate analysis, the TIMP-1 level was a factor with an independent negative relationship to EF and AHF in men. An independent relationship between exon 5 TIMP-1 gene polymorphism and EF, AHF or TIMP-1 level was not documented.
These results provide evidence that a higher level of circulating TIMP-1 is independently associated with worse EF and AHF.</description><subject>Adult</subject><subject>Aged</subject><subject>Exons</subject><subject>Female</subject><subject>Heart Failure - blood</subject><subject>Heart Failure - genetics</subject><subject>Humans</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Myocardial Infarction - blood</subject><subject>Myocardial Infarction - genetics</subject><subject>Myocardial Infarction - therapy</subject><subject>Original</subject><subject>Percutaneous Coronary Intervention - methods</subject><subject>Polymorphism, Genetic</subject><subject>Tissue Inhibitor of Metalloproteinase-1 - blood</subject><subject>Tissue Inhibitor of Metalloproteinase-1 - genetics</subject><subject>Ventricular Dysfunction, Left - blood</subject><subject>Ventricular Dysfunction, Left - genetics</subject><issn>1945-0265</issn><issn>1945-0257</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFUsuKFDEULURxxtGtS8nSTbV5VKo7G0EGXzDgwnYdUsnNVCSVtEmqh_5o_8GU1Ta6MhBuuI9zzg2naV4SvCF4J97cl2nYUEzopl78qLkmouMtpnz7-PLu-VXzLOfvGPcd2_VPmytKxZYQJq6bn_sRkMo5aqeKiwENUB4AAvJwBJ9RtKi4nGdALoxucCWmJTdBUd7HQ4oFXFAZWoIeXBmR0nMBNIJKBVnl_JwqfDAVzhZ0hFCS07NXCZlTtnPQvzldQIfKXqt5Rfm6R1AFrIqmU9QqGad8bbQqrTMlgSpg0HBCh-QmlWqEVNlVgDhnpGOKYcm6UCAtzHXqefPEKp_hxTneNN8-vN_ffmrvvnz8fPvurtUdZaUlVjPdEdoLbKglhPOh49zorQHY9spwNhBmhvrLRhBGhBBKiZ5SMFxoYnfspnm74h7mYQKjl72Vl2ehMion_60EN8r7eJSs63eEdBXg9RkgxR8z5CInlzV4v24nKyvvKaNC_L-1nl1PMV9QN2urTjHnBPaiiGC52EkudpKLneRipzrw6u89Lu1__MN-AdAm0BU</recordid><startdate>201210</startdate><enddate>201210</enddate><creator>Goldbergova, Monika Pavkova</creator><creator>Parenica, Jiri</creator><creator>Jarkovsky, Jiri</creator><creator>Kala, Petr</creator><creator>Poloczek, Martin</creator><creator>Manousek, Jan</creator><creator>Kluz, Krystyna</creator><creator>Kubkova, Lenka</creator><creator>Littnerova, Simona</creator><creator>Tesak, Martin</creator><creator>Toman, Ondrej</creator><creator>Pavek, Nikolas</creator><creator>Cermakova, Zdenka</creator><creator>Tomandl, Josef</creator><creator>Vasku, Anna</creator><creator>Spinar, Jindrich</creator><general>Mary Ann Liebert, Inc</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>7X8</scope><scope>7QO</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>5PM</scope></search><sort><creationdate>201210</creationdate><title>The association between levels of tissue inhibitor of metalloproteinase-1 with acute heart failure and left ventricular dysfunction in patients with ST elevation myocardial infarction treated by primary percutaneous coronary intervention</title><author>Goldbergova, Monika Pavkova ; Parenica, Jiri ; Jarkovsky, Jiri ; Kala, Petr ; Poloczek, Martin ; Manousek, Jan ; Kluz, Krystyna ; Kubkova, Lenka ; Littnerova, Simona ; Tesak, Martin ; Toman, Ondrej ; Pavek, Nikolas ; Cermakova, Zdenka ; Tomandl, Josef ; Vasku, Anna ; Spinar, Jindrich</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c423t-1fc3c412690d2f1155b455dc7dee76ad53b13db025d9131999aa9622ed59c1f83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Exons</topic><topic>Female</topic><topic>Heart Failure - blood</topic><topic>Heart Failure - genetics</topic><topic>Humans</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Myocardial Infarction - blood</topic><topic>Myocardial Infarction - genetics</topic><topic>Myocardial Infarction - therapy</topic><topic>Original</topic><topic>Percutaneous Coronary Intervention - methods</topic><topic>Polymorphism, Genetic</topic><topic>Tissue Inhibitor of Metalloproteinase-1 - blood</topic><topic>Tissue Inhibitor of Metalloproteinase-1 - genetics</topic><topic>Ventricular Dysfunction, Left - blood</topic><topic>Ventricular Dysfunction, Left - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Goldbergova, Monika Pavkova</creatorcontrib><creatorcontrib>Parenica, Jiri</creatorcontrib><creatorcontrib>Jarkovsky, Jiri</creatorcontrib><creatorcontrib>Kala, Petr</creatorcontrib><creatorcontrib>Poloczek, Martin</creatorcontrib><creatorcontrib>Manousek, Jan</creatorcontrib><creatorcontrib>Kluz, Krystyna</creatorcontrib><creatorcontrib>Kubkova, Lenka</creatorcontrib><creatorcontrib>Littnerova, Simona</creatorcontrib><creatorcontrib>Tesak, Martin</creatorcontrib><creatorcontrib>Toman, Ondrej</creatorcontrib><creatorcontrib>Pavek, Nikolas</creatorcontrib><creatorcontrib>Cermakova, Zdenka</creatorcontrib><creatorcontrib>Tomandl, Josef</creatorcontrib><creatorcontrib>Vasku, Anna</creatorcontrib><creatorcontrib>Spinar, Jindrich</creatorcontrib><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><collection>Biotechnology Research Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Genetic testing and molecular biomarkers</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Goldbergova, Monika Pavkova</au><au>Parenica, Jiri</au><au>Jarkovsky, Jiri</au><au>Kala, Petr</au><au>Poloczek, Martin</au><au>Manousek, Jan</au><au>Kluz, Krystyna</au><au>Kubkova, Lenka</au><au>Littnerova, Simona</au><au>Tesak, Martin</au><au>Toman, Ondrej</au><au>Pavek, Nikolas</au><au>Cermakova, Zdenka</au><au>Tomandl, Josef</au><au>Vasku, Anna</au><au>Spinar, Jindrich</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The association between levels of tissue inhibitor of metalloproteinase-1 with acute heart failure and left ventricular dysfunction in patients with ST elevation myocardial infarction treated by primary percutaneous coronary intervention</atitle><jtitle>Genetic testing and molecular biomarkers</jtitle><addtitle>Genet Test Mol Biomarkers</addtitle><date>2012-10</date><risdate>2012</risdate><volume>16</volume><issue>10</issue><spage>1172</spage><epage>1178</epage><pages>1172-1178</pages><issn>1945-0265</issn><eissn>1945-0257</eissn><abstract>Tissue inhibitors of metalloproteinase (TIMPs) bind to active matrix metalloproteinase (MMPs), and thereby inhibit their proteolytic activity. We investigated the role of polymorphisms in the gene for TIMP-1 and serum levels of TIMP-1 in association with postmyocardial infarction (MI), left ventricular (LV) dysfunction, and symptoms of acute heart failure (AHF) in patients treated with primary percutaneous coronary intervention.
In total, 556 patients with STEMI were evaluated. Levels of TIMP-1 were measured at admission and 24 h after MI onset. The TIMP-1 exon 5 SNP rs4898 (F124F with T>C) located at X chromosome was assayed.
TIMP-1 levels were higher for men with AHF as well as for men with LV dysfunction (ejection fraction [EF]<40%). According to multivariate analysis, the TIMP-1 level was a factor with an independent negative relationship to EF and AHF in men. An independent relationship between exon 5 TIMP-1 gene polymorphism and EF, AHF or TIMP-1 level was not documented.
These results provide evidence that a higher level of circulating TIMP-1 is independently associated with worse EF and AHF.</abstract><cop>United States</cop><pub>Mary Ann Liebert, Inc</pub><pmid>22971139</pmid><doi>10.1089/gtmb.2012.0120</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Genetic testing and molecular biomarkers, 2012-10, Vol.16 (10), p.1172-1178 |
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| language | eng |
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| source | MEDLINE; Alma/SFX Local Collection |
| subjects | Adult Aged Exons Female Heart Failure - blood Heart Failure - genetics Humans Male Middle Aged Myocardial Infarction - blood Myocardial Infarction - genetics Myocardial Infarction - therapy Original Percutaneous Coronary Intervention - methods Polymorphism, Genetic Tissue Inhibitor of Metalloproteinase-1 - blood Tissue Inhibitor of Metalloproteinase-1 - genetics Ventricular Dysfunction, Left - blood Ventricular Dysfunction, Left - genetics |
| title | The association between levels of tissue inhibitor of metalloproteinase-1 with acute heart failure and left ventricular dysfunction in patients with ST elevation myocardial infarction treated by primary percutaneous coronary intervention |
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