The study aim was to evaluate whether the
Mineralocorticoid Receptors (MR) antagonist eplerenone,
effects circulating microparticles originated from apoptotic
and activated endothelial cells (EMP) in Chronic Heart
Failure (CHF) patients.
Methods: The study population consisted of 152
consecutive patients with CHF who underwent
angiography or PCI between April 2010 and June 2014,
and post-myocardial infarction subjects. All subjects
enrolled in the study were divided into two cohorts:
eplerenone treated (n=45) or placebo (n=107) for 52
weeks. Patients were treated with optimal dose of
eplerenone (25-50 mg daily) adjusted to plasma potassium.
All biomarkers were determined at the beginning
(baseline) and at the termination of the study. Endothelial
derived Microparticles (EMPs) were phenotyped by flow
cytometry using a High-Definition Fluorescence Activated
Cell Sorter.
Results: At baseline, there was not difference in EMPs
between groups. Eplerenone treatment reduced EMPs
(CD144+/ CD31+/annexin V+ and CD31+/annexin V+)
when compared with placebo. But activated CD62E+ EMP
numbers were significantly increased by 24.3%.
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The Effect of Eplerenone on Circulating Microparticle Numbers in Patients with Chronic Heart Failure
Alexander E Berezin*1, Alexander A Kremzer2, Tatyana A Samura2, Tatyana A Berezina3, Peter Kruzliak4
Corresponding Author: Alexander E Berezin
Received: Apr 16, 2015
Accepted: Apr 28, 2015
Published: Apr 30, 2015
Views: 5
DOI: 10.14437
Abstract
Alexander E Berezin (2015), The Effect of Eplerenone on Circulating Microparticle Numbers in Patients with Chronic
Heart Failure. Aperito J Drug Design Pharmacol 2:112
Copyright:
Copyright: © 2015 AJDDP. This is an open-access article distributed under the terms of the Creative Commons Attribution License, Version 3.0, which permits
unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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