Short-term Changes in Gal 3 Circulating Levels After Acute Myocardial Infarction

Background and Aims Galectin 3 (Gal 3) is a β-galactoside-binding lectin known to play a part in inflammation, adverse remodeling and fibrosis. Gal 3 seems to be linked to atherogenesis and Coronary Artery Disease (CAD), but less is known about the relationship between Gal 3 and acute myocardial inf...

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Published in:Archives of medical research 2016-10, Vol.47 (7), p.521-525
Main Authors: Bivona, Giulia, Bellia, Chiara, Lo Sasso, Bruna, Agnello, Luisa, Scazzone, Concetta, Novo, Giuseppina, Ciaccio, Marcello
Format: Article
Language:English
Subjects:
Aged
AMI
Biomarkers - blood
CAD
Coronary Artery Disease - blood
Coronary Artery Disease - physiopathology
Female
Galectin 3
Galectin 3 - blood
Humans
Inflammation
Internal Medicine
Male
Middle Aged
Myocardial Infarction - blood
Myocardial Infarction - physiopathology
Plaque
Time Factors
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container_issue 7
container_start_page 521
container_title Archives of medical research
container_volume 47
creator Bivona, Giulia
Bellia, Chiara
Lo Sasso, Bruna
Agnello, Luisa
Scazzone, Concetta
Novo, Giuseppina
Ciaccio, Marcello
description Background and Aims Galectin 3 (Gal 3) is a β-galactoside-binding lectin known to play a part in inflammation, adverse remodeling and fibrosis. Gal 3 seems to be linked to atherogenesis and Coronary Artery Disease (CAD), but less is known about the relationship between Gal 3 and acute myocardial infarction (AMI). The aim of the present study is to assess circulating levels of Gal 3 after AMI and to evaluate short-term changes of the biomarker within 5 days from the acute event. Methods Two hundred fifteen confirmed AMI patients (125 STEMI, M/F = 2.8; mean age: 65.4 ± 13.8 years) were enrolled in the present study; two blood samples were collected from each patient: first, within 1 h from admission to the Emergency Area (T1) and then upon discharge (T2). Results Kinetics of Gal 3 during AMI show that the marker boosts during the acute event (T1) and then decreases from baseline, being significantly lower at T2 (18 [14.2–25] vs. 16.8 [12.7–23.4]; p  = 0.006). Gal 3 levels were correlated to hsTnI and eGFR on admission ( r  = 0.2; p
doi_str_mv 10.1016/j.arcmed.2016.12.009
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Gal 3 seems to be linked to atherogenesis and Coronary Artery Disease (CAD), but less is known about the relationship between Gal 3 and acute myocardial infarction (AMI). The aim of the present study is to assess circulating levels of Gal 3 after AMI and to evaluate short-term changes of the biomarker within 5 days from the acute event. Methods Two hundred fifteen confirmed AMI patients (125 STEMI, M/F = 2.8; mean age: 65.4 ± 13.8 years) were enrolled in the present study; two blood samples were collected from each patient: first, within 1 h from admission to the Emergency Area (T1) and then upon discharge (T2). Results Kinetics of Gal 3 during AMI show that the marker boosts during the acute event (T1) and then decreases from baseline, being significantly lower at T2 (18 [14.2–25] vs. 16.8 [12.7–23.4]; p  = 0.006). Gal 3 levels were correlated to hsTnI and eGFR on admission ( r  = 0.2; p &lt;0.001 and r  = −0.25; p &lt;0.001, respectively). Linear regression analysis confirms an association between Gal 3 and ejection fraction ( r2  = 0.037; p  = 0.005). Conclusions Gal 3 is reasonably supposed to be a part of those mechanisms leading to formation, destabilization and rupture of plaque; however, the usefulness of Gal 3 as a biomarker in CAD/AMI is far from being elucidated.</description><identifier>ISSN: 0188-4409</identifier><identifier>EISSN: 1873-5487</identifier><identifier>DOI: 10.1016/j.arcmed.2016.12.009</identifier><identifier>PMID: 28262193</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Aged ; AMI ; Biomarkers - blood ; CAD ; Coronary Artery Disease - blood ; Coronary Artery Disease - physiopathology ; Female ; Galectin 3 ; Galectin 3 - blood ; Humans ; Inflammation ; Internal Medicine ; Male ; Middle Aged ; Myocardial Infarction - blood ; Myocardial Infarction - physiopathology ; Plaque ; Time Factors</subject><ispartof>Archives of medical research, 2016-10, Vol.47 (7), p.521-525</ispartof><rights>IMSS</rights><rights>2016 IMSS</rights><rights>Copyright © 2016 IMSS. Published by Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c417t-880938377dcbfa95c531c85e6c57764e98119f1e1b4c1036efa58f8b885888323</citedby><cites>FETCH-LOGICAL-c417t-880938377dcbfa95c531c85e6c57764e98119f1e1b4c1036efa58f8b885888323</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27922,27923</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28262193$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bivona, Giulia</creatorcontrib><creatorcontrib>Bellia, Chiara</creatorcontrib><creatorcontrib>Lo Sasso, Bruna</creatorcontrib><creatorcontrib>Agnello, Luisa</creatorcontrib><creatorcontrib>Scazzone, Concetta</creatorcontrib><creatorcontrib>Novo, Giuseppina</creatorcontrib><creatorcontrib>Ciaccio, Marcello</creatorcontrib><title>Short-term Changes in Gal 3 Circulating Levels After Acute Myocardial Infarction</title><title>Archives of medical research</title><addtitle>Arch Med Res</addtitle><description>Background and Aims Galectin 3 (Gal 3) is a β-galactoside-binding lectin known to play a part in inflammation, adverse remodeling and fibrosis. Gal 3 seems to be linked to atherogenesis and Coronary Artery Disease (CAD), but less is known about the relationship between Gal 3 and acute myocardial infarction (AMI). The aim of the present study is to assess circulating levels of Gal 3 after AMI and to evaluate short-term changes of the biomarker within 5 days from the acute event. Methods Two hundred fifteen confirmed AMI patients (125 STEMI, M/F = 2.8; mean age: 65.4 ± 13.8 years) were enrolled in the present study; two blood samples were collected from each patient: first, within 1 h from admission to the Emergency Area (T1) and then upon discharge (T2). Results Kinetics of Gal 3 during AMI show that the marker boosts during the acute event (T1) and then decreases from baseline, being significantly lower at T2 (18 [14.2–25] vs. 16.8 [12.7–23.4]; p  = 0.006). Gal 3 levels were correlated to hsTnI and eGFR on admission ( r  = 0.2; p &lt;0.001 and r  = −0.25; p &lt;0.001, respectively). Linear regression analysis confirms an association between Gal 3 and ejection fraction ( r2  = 0.037; p  = 0.005). Conclusions Gal 3 is reasonably supposed to be a part of those mechanisms leading to formation, destabilization and rupture of plaque; however, the usefulness of Gal 3 as a biomarker in CAD/AMI is far from being elucidated.</description><subject>Aged</subject><subject>AMI</subject><subject>Biomarkers - blood</subject><subject>CAD</subject><subject>Coronary Artery Disease - blood</subject><subject>Coronary Artery Disease - physiopathology</subject><subject>Female</subject><subject>Galectin 3</subject><subject>Galectin 3 - blood</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Internal Medicine</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Myocardial Infarction - blood</subject><subject>Myocardial Infarction - physiopathology</subject><subject>Plaque</subject><subject>Time Factors</subject><issn>0188-4409</issn><issn>1873-5487</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><recordid>eNqFkcFq3DAQhkVpabZJ3qAUHXuxq5Fka3wpLEuaBra0kOQstPI40dZrp5Id2LevzCaXXnoaxHz_jPiGsY8gShBQf9mXLvoDtaXMrxJkKUTzhq0AjSoqjeYtWwlALLQWzRn7kNJeCIG6Nu_ZmURZS2jUiv26fRzjVEwUD3zz6IYHSjwM_Nr1XPFNiH7u3RSGB76lZ-oTX3cZ5Ws_T8R_HEfvYhsyezN0-TdTGIcL9q5zfaLLl3rO7r9d3W2-F9uf1zeb9bbwGsxUIIpGoTKm9bvONZWvFHisqPaVMbWmBgGaDgh22oNQNXWuwg53iBUiKqnO2efT3Kc4_pkpTfYQkqe-dwONc7LZgzaojV5QfUJ9HFOK1NmnGA4uHi0Iu7i0e3tyaReXFqTNLnPs08uGebf0XkOv8jLw9QRkMfQcKNrkAw2e2hDJT7Ydw_82_DvA92EI3vW_6UhpP85xyA4t2JQD9na553JOqJWQsqnVX7SQmfY</recordid><startdate>20161001</startdate><enddate>20161001</enddate><creator>Bivona, Giulia</creator><creator>Bellia, Chiara</creator><creator>Lo Sasso, Bruna</creator><creator>Agnello, Luisa</creator><creator>Scazzone, Concetta</creator><creator>Novo, Giuseppina</creator><creator>Ciaccio, Marcello</creator><general>Elsevier 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></search><sort><creationdate>20161001</creationdate><title>Short-term Changes in Gal 3 Circulating Levels After Acute Myocardial Infarction</title><author>Bivona, Giulia ; Bellia, Chiara ; Lo Sasso, Bruna ; Agnello, Luisa ; Scazzone, Concetta ; Novo, Giuseppina ; Ciaccio, Marcello</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c417t-880938377dcbfa95c531c85e6c57764e98119f1e1b4c1036efa58f8b885888323</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Aged</topic><topic>AMI</topic><topic>Biomarkers - blood</topic><topic>CAD</topic><topic>Coronary Artery Disease - blood</topic><topic>Coronary Artery Disease - physiopathology</topic><topic>Female</topic><topic>Galectin 3</topic><topic>Galectin 3 - blood</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Internal Medicine</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Myocardial Infarction - blood</topic><topic>Myocardial Infarction - physiopathology</topic><topic>Plaque</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bivona, Giulia</creatorcontrib><creatorcontrib>Bellia, Chiara</creatorcontrib><creatorcontrib>Lo Sasso, Bruna</creatorcontrib><creatorcontrib>Agnello, Luisa</creatorcontrib><creatorcontrib>Scazzone, Concetta</creatorcontrib><creatorcontrib>Novo, Giuseppina</creatorcontrib><creatorcontrib>Ciaccio, Marcello</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><jtitle>Archives of medical research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bivona, Giulia</au><au>Bellia, Chiara</au><au>Lo Sasso, Bruna</au><au>Agnello, Luisa</au><au>Scazzone, Concetta</au><au>Novo, Giuseppina</au><au>Ciaccio, Marcello</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Short-term Changes in Gal 3 Circulating Levels After Acute Myocardial Infarction</atitle><jtitle>Archives of medical research</jtitle><addtitle>Arch Med Res</addtitle><date>2016-10-01</date><risdate>2016</risdate><volume>47</volume><issue>7</issue><spage>521</spage><epage>525</epage><pages>521-525</pages><issn>0188-4409</issn><eissn>1873-5487</eissn><abstract>Background and Aims Galectin 3 (Gal 3) is a β-galactoside-binding lectin known to play a part in inflammation, adverse remodeling and fibrosis. Gal 3 seems to be linked to atherogenesis and Coronary Artery Disease (CAD), but less is known about the relationship between Gal 3 and acute myocardial infarction (AMI). The aim of the present study is to assess circulating levels of Gal 3 after AMI and to evaluate short-term changes of the biomarker within 5 days from the acute event. Methods Two hundred fifteen confirmed AMI patients (125 STEMI, M/F = 2.8; mean age: 65.4 ± 13.8 years) were enrolled in the present study; two blood samples were collected from each patient: first, within 1 h from admission to the Emergency Area (T1) and then upon discharge (T2). Results Kinetics of Gal 3 during AMI show that the marker boosts during the acute event (T1) and then decreases from baseline, being significantly lower at T2 (18 [14.2–25] vs. 16.8 [12.7–23.4]; p  = 0.006). Gal 3 levels were correlated to hsTnI and eGFR on admission ( r  = 0.2; p &lt;0.001 and r  = −0.25; p &lt;0.001, respectively). Linear regression analysis confirms an association between Gal 3 and ejection fraction ( r2  = 0.037; p  = 0.005). Conclusions Gal 3 is reasonably supposed to be a part of those mechanisms leading to formation, destabilization and rupture of plaque; however, the usefulness of Gal 3 as a biomarker in CAD/AMI is far from being elucidated.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>28262193</pmid><doi>10.1016/j.arcmed.2016.12.009</doi><tpages>5</tpages></addata></record>
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subjects Aged
AMI
Biomarkers - blood
CAD
Coronary Artery Disease - blood
Coronary Artery Disease - physiopathology
Female
Galectin 3
Galectin 3 - blood
Humans
Inflammation
Internal Medicine
Male
Middle Aged
Myocardial Infarction - blood
Myocardial Infarction - physiopathology
Plaque
Time Factors
title Short-term Changes in Gal 3 Circulating Levels After Acute Myocardial Infarction
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