Document Detail


Ivabradine protects against ventricular arrhythmias in acute myocardial infarction in the rat.
MedLine Citation:
PMID:  24590965     Owner:  NLM     Status:  In-Data-Review    
Abstract/OtherAbstract:
Ventricular arrhythmias are an important cause of mortality in the acute myocardial infarction (MI). To elucidate effect of ivabradine, pure heart rate (HR) reducing drug, on ventricular arrhythmias within 24 h after non-reperfused MI in the rat. ECG was recorded for 24 h after MI in untreated and ivabradine treated rats and episodes of ventricular tachycardia/fibrillation (VT/VF) were identified. Forty-five minutes and twenty-four hours after MI epicardial monophasic action potentials (MAPs) were recorded, cardiomyocyte Ca(2+) handling was assessed and expression and function of ion channels were studied. Ivabradine reduced average HR by 17%. Combined VT/VF incidence and arrhythmic mortality were higher in MI versus MI + Ivabradine rats. MI resulted in (1) increase of Ca(2+) sensitivity of ryanodine receptors 24 h after MI; (2) increase of HCN4 expression in the left ventricle (LV) and funny current (IF ) in LV cardiomyocytes 24 h after MI, and (3) dispersion of MAP duration both 45 min and 24 h after MI. Ivabradine partially prevented all these three potential proarrhythmic effects of MI. Ivabradine is antiarrhythmic in the acute MI in the rat. Potential mechanisms include prevention of: diastolic Ca(2+) -leak from sarcoplasmic reticulum, upregulation of IF current in LV and dispersion of cardiac repolarization. Ivabradine could be an attractive antiarrhythmic agent in the setting of acute MI. J. Cell. Physiol. 229: 813-823, 2014. © 2013 Wiley Periodicals, Inc.
Authors:
Urszula Mackiewicz; Joseph Y Gerges; Sandy Chu; Monika Duda; Halina Dobrzynski; Bohdan Lewartowski; Michał Mączewski
Related Documents :
17598815 - Myocardial infarction: contemporary management strategies.
15298045 - Relation of circulating interleukin-6 to left ventricular remodeling in patients with r...
15166945 - Abo locus o1 allele and risk of myocardial infarction.
19808375 - Loss of angiotensin-converting enzyme 2 accelerates maladaptive left ventricular remode...
19181935 - Endogenous testosterone attenuates neointima formation after moderate coronary balloon ...
7760375 - Differential expression of tni and tnt isoforms in rabbit heart during the perinatal pe...
Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Journal of cellular physiology     Volume:  229     ISSN:  1097-4652     ISO Abbreviation:  J. Cell. Physiol.     Publication Date:  2014 Jun 
Date Detail:
Created Date:  2014-03-04     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0050222     Medline TA:  J Cell Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  813-23     Citation Subset:  IM    
Copyright Information:
© 2013 Wiley Periodicals, Inc.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Stable Genetic Alterations of ?-Catenin and ROR2 Regulate the Wnt Pathway, Affect the Fate of MSCs.
Next Document:  The Research Domain Criteria: moving the goalposts to change the game.