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MicroRNA 208 in Atrial Fibrillation | OMICS International | Abstract
ISSN: 2155-9880

Journal of Clinical & Experimental Cardiology
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Research Article

MicroRNA 208 in Atrial Fibrillation

Arlo Radtke1, Thorsten Hanke1, Junfeng Yan1, Beate Godau2, Jens Cordes2, Vishal Nigam3, Hans H Sievers1 and Salah A Mohamed1*
1Department of Cardiac and Thoracic Vascular Surgery, Medical Centre Schleswig-Holstein, Campus Luebeck, Luebeck, Germany
2Clinic of Urology, Medical Centre Schleswig-Holstein, Campus Luebeck, Germany
3Department of Paediatrics (Cardiology), University of California San Diego, USA
Corresponding Author : Salah A Mohamed
Department of Cardiac and Thoracic Vascular Surgery
University Clinic of Schleswig-Holstein Campus Luebeck
Ratzeburger Allee 160, 23538 Luebeck, USA
Tel: +494515006425
Fax: +494515002051
E-mail: [email protected]
Received May 21, 2014; Accepted June 24, 2014; Published July 05, 2014
Citation: Radtke A, Hanke T, Yan J, Godau B, Cordes J, et al. (2014) MicroRNA 208 in Atrial Fibrillation. J Clin Exp Cardiolog 5:325. doi:10.4172/2155-9880.1000325
Copyright: © 2014 Radtke A, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Abstract

MicroRNAs (miRNAs) are critical regulators of most major cellular processes and seem to play a vital role in the pathogenesis of numerous diseases including atrial fibrillation, the most commonly encountered cardiac rhythm disorder. Among the several miRNAs that appear to be involved in pathogenesis of atrial fibrillation, miRNA 208a is linked to fibrosis and proper cardiac conduction.

We quantified the expression levels of miRNA 208a in left atrial appendage tissue of patients with paroxysmal (n=2), persistent (n=10), and long-standing persistent (n=7) arrhythmia using quantitative PCR. In paroxysmal atrial fibrillation, miRNA 208a was expressed moderately, whereas the expression was enhanced in persistent atrial fibrillation and significantly reduced in long-standing persistent atrial fibrillation. The difference between persistent and long-standing persistent atrial fibrillation was significant at p=0.02.

The findings from our study suggest a decline in miRNA 208a expression with ongoing arrhythmia, possibly preceded by a rise in expression from paroxysmal to persistent atrial fibrillation or even long-standing persistent. The significant changes in miRNA 208a expression over the course of the disease may be used as an additional diagnostic tool to monitor the progression of atrial fibrillation.

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