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Relationship of activin A levels with clinical presentation, extent, and severity of coronary artery disease

OBJECTIVE: 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). METHODS: In total, 310 CAD patients [92 with ST-segment elevation myocardial infarcti...

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Autores principales: Bouzidi, Nadia, Betbout, Fethi, Maatouk, Faouzi, Gamra, Habib, Miled, Abdelhedi, Ferchichi, Salima
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Kare Publishing 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6282897/
https://www.ncbi.nlm.nih.gov/pubmed/29256875
http://dx.doi.org/10.14744/AnatolJCardiol.2017.7935
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author Bouzidi, Nadia
Betbout, Fethi
Maatouk, Faouzi
Gamra, Habib
Miled, Abdelhedi
Ferchichi, Salima
author_facet Bouzidi, Nadia
Betbout, Fethi
Maatouk, Faouzi
Gamra, Habib
Miled, Abdelhedi
Ferchichi, Salima
author_sort Bouzidi, Nadia
collection PubMed
description OBJECTIVE: 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). METHODS: 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. RESULTS: 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 (β=–0.260; 95% CI: –617.39 to –110.04; p=0.005) was an independent predictor of activin A levels. CONCLUSION: 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.
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spelling pubmed-62828972018-12-10 Relationship of activin A levels with clinical presentation, extent, and severity of coronary artery disease Bouzidi, Nadia Betbout, Fethi Maatouk, Faouzi Gamra, Habib Miled, Abdelhedi Ferchichi, Salima Anatol J Cardiol Original Investigation OBJECTIVE: 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). METHODS: 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. RESULTS: 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 (β=–0.260; 95% CI: –617.39 to –110.04; p=0.005) was an independent predictor of activin A levels. CONCLUSION: 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. Kare Publishing 2017-06 2017-12-07 /pmc/articles/PMC6282897/ /pubmed/29256875 http://dx.doi.org/10.14744/AnatolJCardiol.2017.7935 Text en Copyright: © 2017 Turkish Society of Cardiology http://creativecommons.org/licenses/by-nc-sa/4.0 This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License
spellingShingle Original Investigation
Bouzidi, Nadia
Betbout, Fethi
Maatouk, Faouzi
Gamra, Habib
Miled, Abdelhedi
Ferchichi, Salima
Relationship of activin A levels with clinical presentation, extent, and severity of coronary artery disease
title Relationship of activin A levels with clinical presentation, extent, and severity of coronary artery disease
title_full Relationship of activin A levels with clinical presentation, extent, and severity of coronary artery disease
title_fullStr Relationship of activin A levels with clinical presentation, extent, and severity of coronary artery disease
title_full_unstemmed Relationship of activin A levels with clinical presentation, extent, and severity of coronary artery disease
title_short Relationship of activin A levels with clinical presentation, extent, and severity of coronary artery disease
title_sort relationship of activin a levels with clinical presentation, extent, and severity of coronary artery disease
topic Original Investigation
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6282897/
https://www.ncbi.nlm.nih.gov/pubmed/29256875
http://dx.doi.org/10.14744/AnatolJCardiol.2017.7935
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