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The effect of long-term amiodarone administration on myocardial fibrosis and evolution of left ventricular remodeling in a porcine model of ischemic cardiomyopathy

Amiodarone is effective in suppressing arrhythmias in heart failure patients. We investigated the effect of long-term amiodarone administration on myocardial fibrosis and left ventricular (LV) remodeling in a porcine model of ischemic cardiomyopathy. Eighteen infarcted farm pigs were randomized to r...

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Autores principales: Zagorianou, Anastasia, Marougkas, Meletios, Drakos, Stavros G., Diakos, Nikolaos, Konstantopoulos, Panagiotis, Perrea, Despina N., Anastasiou-Nana, Maria, Malliaras, Konstantinos
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer International Publishing 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5023647/
https://www.ncbi.nlm.nih.gov/pubmed/27652141
http://dx.doi.org/10.1186/s40064-016-3249-3
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author Zagorianou, Anastasia
Marougkas, Meletios
Drakos, Stavros G.
Diakos, Nikolaos
Konstantopoulos, Panagiotis
Perrea, Despina N.
Anastasiou-Nana, Maria
Malliaras, Konstantinos
author_facet Zagorianou, Anastasia
Marougkas, Meletios
Drakos, Stavros G.
Diakos, Nikolaos
Konstantopoulos, Panagiotis
Perrea, Despina N.
Anastasiou-Nana, Maria
Malliaras, Konstantinos
author_sort Zagorianou, Anastasia
collection PubMed
description Amiodarone is effective in suppressing arrhythmias in heart failure patients. We investigated the effect of long-term amiodarone administration on myocardial fibrosis and left ventricular (LV) remodeling in a porcine model of ischemic cardiomyopathy. Eighteen infarcted farm pigs were randomized to receive long-term amiodarone administration for 3 months (n = 9) or conventional follow-up (n = 9). Evolution of LV remodeling over 3 months post-myocardial infarction was examined at tissue level (myocyte size, myocardial fibrosis and vascular density assessed by whole-field digital histopathology), organ level (LV structure and function assessed by echocardiography), and systemic level (BNP and MMP-9 levels). Long-term administration of the standard anti-arrhythmic doses of amiodarone was not associated with adverse effects on myocardial fibrosis and other features of adverse cardiac remodeling. This favorable safety profile suggests that long-term anti-arrhythmic therapy with amiodarone warrants further clinical investigation in the subpopulation of heart failure patients with significantly increased burden of arrhythmias.
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spelling pubmed-50236472016-09-20 The effect of long-term amiodarone administration on myocardial fibrosis and evolution of left ventricular remodeling in a porcine model of ischemic cardiomyopathy Zagorianou, Anastasia Marougkas, Meletios Drakos, Stavros G. Diakos, Nikolaos Konstantopoulos, Panagiotis Perrea, Despina N. Anastasiou-Nana, Maria Malliaras, Konstantinos Springerplus Research Amiodarone is effective in suppressing arrhythmias in heart failure patients. We investigated the effect of long-term amiodarone administration on myocardial fibrosis and left ventricular (LV) remodeling in a porcine model of ischemic cardiomyopathy. Eighteen infarcted farm pigs were randomized to receive long-term amiodarone administration for 3 months (n = 9) or conventional follow-up (n = 9). Evolution of LV remodeling over 3 months post-myocardial infarction was examined at tissue level (myocyte size, myocardial fibrosis and vascular density assessed by whole-field digital histopathology), organ level (LV structure and function assessed by echocardiography), and systemic level (BNP and MMP-9 levels). Long-term administration of the standard anti-arrhythmic doses of amiodarone was not associated with adverse effects on myocardial fibrosis and other features of adverse cardiac remodeling. This favorable safety profile suggests that long-term anti-arrhythmic therapy with amiodarone warrants further clinical investigation in the subpopulation of heart failure patients with significantly increased burden of arrhythmias. Springer International Publishing 2016-09-15 /pmc/articles/PMC5023647/ /pubmed/27652141 http://dx.doi.org/10.1186/s40064-016-3249-3 Text en © The Author(s) 2016 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
spellingShingle Research
Zagorianou, Anastasia
Marougkas, Meletios
Drakos, Stavros G.
Diakos, Nikolaos
Konstantopoulos, Panagiotis
Perrea, Despina N.
Anastasiou-Nana, Maria
Malliaras, Konstantinos
The effect of long-term amiodarone administration on myocardial fibrosis and evolution of left ventricular remodeling in a porcine model of ischemic cardiomyopathy
title The effect of long-term amiodarone administration on myocardial fibrosis and evolution of left ventricular remodeling in a porcine model of ischemic cardiomyopathy
title_full The effect of long-term amiodarone administration on myocardial fibrosis and evolution of left ventricular remodeling in a porcine model of ischemic cardiomyopathy
title_fullStr The effect of long-term amiodarone administration on myocardial fibrosis and evolution of left ventricular remodeling in a porcine model of ischemic cardiomyopathy
title_full_unstemmed The effect of long-term amiodarone administration on myocardial fibrosis and evolution of left ventricular remodeling in a porcine model of ischemic cardiomyopathy
title_short The effect of long-term amiodarone administration on myocardial fibrosis and evolution of left ventricular remodeling in a porcine model of ischemic cardiomyopathy
title_sort effect of long-term amiodarone administration on myocardial fibrosis and evolution of left ventricular remodeling in a porcine model of ischemic cardiomyopathy
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5023647/
https://www.ncbi.nlm.nih.gov/pubmed/27652141
http://dx.doi.org/10.1186/s40064-016-3249-3
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