Relationship of activin A levels with clinical presentation, extent, and severity of coronary artery disease
We aimed to evaluate the relationship of serum activin A levels with risk factors, clinical presentation, biochemical marker levels, extent, and severity of atherosclerotic coronary artery disease (CAD). In total, 310 CAD patients [92 with ST-segment elevation myocardial infarction (STEMI), 111 with...
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Veröffentlicht in: | Anatolian journal of cardiology 2017-12, Vol.18 (6), p.402-409 |
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description | We aimed to evaluate the relationship of serum activin A levels with risk factors, clinical presentation, biochemical marker levels, extent, and severity of atherosclerotic coronary artery disease (CAD).
In total, 310 CAD patients [92 with ST-segment elevation myocardial infarction (STEMI), 111 with non-STEMI (NSTEMI), and 107 with unstable angina (UA)] and 207 healthy subjects (controls) were enrolled. Activin A levels in all participants were measured using ELISA. Angiographic measurements were performed in patients and not in the healthy subjects.
Activin A levels were higher in all patient groups than in controls (patients vs. controls, p=0.041; NSTEMI vs. UA, p=0.744; STEMI vs. UA, p=0.172; NSTEMI vs. STEMI, p=0.104). According to the cut-off value of activin A level, patients with high and low activin A levels had a similar distribution of clinical and biochemical variables but the prevalence of severe stenosis was observed in groups with high activin A levels. Our results revealed that activin A levels did not decrease as thrombolysis in myocardial infarction (risk score increased (p=0.590). The area under the ROC curve for activin A levels in patients was 0.590±0.047 (95% CI: 0.439-0.591, p=0.193). In multiple analysis of the overall population, male gender (ß=-0.260; 95% CI: -617.39 to -110.04; p=0.005) was an independent predictor of activin A levels.
This study indicated that activin A can not be a predictive marker in CAD and is not associated with extensive and severe CAD. In contrast, the increase in activin A levels in patients, especially in patients with different clinical groups of acute coronary syndromes, suggested its involvement in atherosclerosis. |
doi_str_mv | 10.14744/AnatolJCardiol.2017.7935 |
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In total, 310 CAD patients [92 with ST-segment elevation myocardial infarction (STEMI), 111 with non-STEMI (NSTEMI), and 107 with unstable angina (UA)] and 207 healthy subjects (controls) were enrolled. Activin A levels in all participants were measured using ELISA. Angiographic measurements were performed in patients and not in the healthy subjects.
Activin A levels were higher in all patient groups than in controls (patients vs. controls, p=0.041; NSTEMI vs. UA, p=0.744; STEMI vs. UA, p=0.172; NSTEMI vs. STEMI, p=0.104). According to the cut-off value of activin A level, patients with high and low activin A levels had a similar distribution of clinical and biochemical variables but the prevalence of severe stenosis was observed in groups with high activin A levels. Our results revealed that activin A levels did not decrease as thrombolysis in myocardial infarction (risk score increased (p=0.590). The area under the ROC curve for activin A levels in patients was 0.590±0.047 (95% CI: 0.439-0.591, p=0.193). In multiple analysis of the overall population, male gender (ß=-0.260; 95% CI: -617.39 to -110.04; p=0.005) was an independent predictor of activin A levels.
This study indicated that activin A can not be a predictive marker in CAD and is not associated with extensive and severe CAD. In contrast, the increase in activin A levels in patients, especially in patients with different clinical groups of acute coronary syndromes, suggested its involvement in atherosclerosis.</description><identifier>ISSN: 2149-2263</identifier><identifier>EISSN: 2149-2271</identifier><identifier>DOI: 10.14744/AnatolJCardiol.2017.7935</identifier><identifier>PMID: 29256875</identifier><language>eng</language><publisher>Turkey: Kare Publishing</publisher><subject>Cardiovascular disease ; Coronary vessels ; Electrocardiography ; Heart attacks ; Original Investigation</subject><ispartof>Anatolian journal of cardiology, 2017-12, Vol.18 (6), p.402-409</ispartof><rights>Copyright Aves Yayincilik Ltd. STI. Dec 2017</rights><rights>Copyright: © 2017 Turkish Society of Cardiology 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c451t-a97fb79c62a701d68e29b3b57a2edfa74e4b243ba708f187d9bd5546c7cacf553</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6282897/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6282897/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29256875$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bouzidi, Nadia</creatorcontrib><creatorcontrib>Betbout, Fethi</creatorcontrib><creatorcontrib>Maatouk, Faouzi</creatorcontrib><creatorcontrib>Gamra, Habib</creatorcontrib><creatorcontrib>Miled, Abdelhedi</creatorcontrib><creatorcontrib>Ferchichi, Salima</creatorcontrib><title>Relationship of activin A levels with clinical presentation, extent, and severity of coronary artery disease</title><title>Anatolian journal of cardiology</title><addtitle>Anatol J Cardiol</addtitle><description>We aimed to evaluate the relationship of serum activin A levels with risk factors, clinical presentation, biochemical marker levels, extent, and severity of atherosclerotic coronary artery disease (CAD).
In total, 310 CAD patients [92 with ST-segment elevation myocardial infarction (STEMI), 111 with non-STEMI (NSTEMI), and 107 with unstable angina (UA)] and 207 healthy subjects (controls) were enrolled. Activin A levels in all participants were measured using ELISA. Angiographic measurements were performed in patients and not in the healthy subjects.
Activin A levels were higher in all patient groups than in controls (patients vs. controls, p=0.041; NSTEMI vs. UA, p=0.744; STEMI vs. UA, p=0.172; NSTEMI vs. STEMI, p=0.104). According to the cut-off value of activin A level, patients with high and low activin A levels had a similar distribution of clinical and biochemical variables but the prevalence of severe stenosis was observed in groups with high activin A levels. Our results revealed that activin A levels did not decrease as thrombolysis in myocardial infarction (risk score increased (p=0.590). The area under the ROC curve for activin A levels in patients was 0.590±0.047 (95% CI: 0.439-0.591, p=0.193). In multiple analysis of the overall population, male gender (ß=-0.260; 95% CI: -617.39 to -110.04; p=0.005) was an independent predictor of activin A levels.
This study indicated that activin A can not be a predictive marker in CAD and is not associated with extensive and severe CAD. In contrast, the increase in activin A levels in patients, especially in patients with different clinical groups of acute coronary syndromes, suggested its involvement in atherosclerosis.</description><subject>Cardiovascular disease</subject><subject>Coronary vessels</subject><subject>Electrocardiography</subject><subject>Heart attacks</subject><subject>Original Investigation</subject><issn>2149-2263</issn><issn>2149-2271</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpdkVFrFDEUhYNYbKn9CxLxxYfuOslMJsmLsCzaKoVCqc_hTuaOm5JN1iS7tf_ebFsX69NNuOcczuUj5D1r5qyTXfdpEaBE_30JaXTRz3nD5FzqVrwiJ5x1esa5ZK8P7749Jmc53zVN1bWKsf4NOeaai15JcUL8DXooLoa8chsaJwq2uJ0LdEE97tBneu_KilrvgrPg6SZhxlAeLecUf5f6OacQRpqrPLnysA-xMcUA6YFCKljH6DJCxrfkaAKf8ex5npIfX7_cLi9nV9cX35aLq5ntBCsz0HIapLY9B9mwsVfI9dAOQgLHcQLZYTfwrh3qVk1MyVEPoxBdb6UFOwnRnpLPT7mb7bDG0daOCbzZJLeupUwEZ15ugluZn3Fneq640rIGfHwOSPHXFnMxa5cteg8B4zYbpqWSTDHFq_TDf9K7uE2hnmd4w5kUrJX7RvpJZVPMOeF0KMMa84jVvMRq9ljNHmv1vvv3moPzL8T2DwI_pUY</recordid><startdate>20171201</startdate><enddate>20171201</enddate><creator>Bouzidi, Nadia</creator><creator>Betbout, Fethi</creator><creator>Maatouk, Faouzi</creator><creator>Gamra, Habib</creator><creator>Miled, Abdelhedi</creator><creator>Ferchichi, Salima</creator><general>Kare Publishing</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>EDSIH</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PADUT</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20171201</creationdate><title>Relationship of activin A levels with clinical presentation, extent, and severity of coronary artery disease</title><author>Bouzidi, Nadia ; Betbout, Fethi ; Maatouk, Faouzi ; Gamra, Habib ; Miled, Abdelhedi ; Ferchichi, Salima</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c451t-a97fb79c62a701d68e29b3b57a2edfa74e4b243ba708f187d9bd5546c7cacf553</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Cardiovascular disease</topic><topic>Coronary vessels</topic><topic>Electrocardiography</topic><topic>Heart attacks</topic><topic>Original Investigation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bouzidi, Nadia</creatorcontrib><creatorcontrib>Betbout, Fethi</creatorcontrib><creatorcontrib>Maatouk, Faouzi</creatorcontrib><creatorcontrib>Gamra, Habib</creatorcontrib><creatorcontrib>Miled, Abdelhedi</creatorcontrib><creatorcontrib>Ferchichi, Salima</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Turkey Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Research Library China</collection><collection>Publicly Available Content Database</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>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Anatolian journal of cardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bouzidi, Nadia</au><au>Betbout, Fethi</au><au>Maatouk, Faouzi</au><au>Gamra, Habib</au><au>Miled, Abdelhedi</au><au>Ferchichi, Salima</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Relationship of activin A levels with clinical presentation, extent, and severity of coronary artery disease</atitle><jtitle>Anatolian journal of cardiology</jtitle><addtitle>Anatol J Cardiol</addtitle><date>2017-12-01</date><risdate>2017</risdate><volume>18</volume><issue>6</issue><spage>402</spage><epage>409</epage><pages>402-409</pages><issn>2149-2263</issn><eissn>2149-2271</eissn><abstract>We aimed to evaluate the relationship of serum activin A levels with risk factors, clinical presentation, biochemical marker levels, extent, and severity of atherosclerotic coronary artery disease (CAD).
In total, 310 CAD patients [92 with ST-segment elevation myocardial infarction (STEMI), 111 with non-STEMI (NSTEMI), and 107 with unstable angina (UA)] and 207 healthy subjects (controls) were enrolled. Activin A levels in all participants were measured using ELISA. Angiographic measurements were performed in patients and not in the healthy subjects.
Activin A levels were higher in all patient groups than in controls (patients vs. controls, p=0.041; NSTEMI vs. UA, p=0.744; STEMI vs. UA, p=0.172; NSTEMI vs. STEMI, p=0.104). According to the cut-off value of activin A level, patients with high and low activin A levels had a similar distribution of clinical and biochemical variables but the prevalence of severe stenosis was observed in groups with high activin A levels. Our results revealed that activin A levels did not decrease as thrombolysis in myocardial infarction (risk score increased (p=0.590). The area under the ROC curve for activin A levels in patients was 0.590±0.047 (95% CI: 0.439-0.591, p=0.193). In multiple analysis of the overall population, male gender (ß=-0.260; 95% CI: -617.39 to -110.04; p=0.005) was an independent predictor of activin A levels.
This study indicated that activin A can not be a predictive marker in CAD and is not associated with extensive and severe CAD. In contrast, the increase in activin A levels in patients, especially in patients with different clinical groups of acute coronary syndromes, suggested its involvement in atherosclerosis.</abstract><cop>Turkey</cop><pub>Kare Publishing</pub><pmid>29256875</pmid><doi>10.14744/AnatolJCardiol.2017.7935</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Cardiovascular disease Coronary vessels Electrocardiography Heart attacks Original Investigation |
title | Relationship of activin A levels with clinical presentation, extent, and severity of coronary artery disease |
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