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Heart Rhythm. 2019 Nov 19. pii: S1547-5271(19)31026-4. doi: 10.1016/j.hrthm.2019.11.014. [Epub ahead of print]

Effect of acute and chronic ethanol on atrial fibrillation vulnerability in rats.

Author information

1
Division of Cardiology, Cardiovascular Research Institute, University of California San Francisco, San Francisco, California, USA.
2
Division of Cardiology, Electrophysiology Section, University of California San Francisco, San Francisco, California, USA.
3
Division of Cardiology, Cardiovascular Research Institute, University of California San Francisco, San Francisco, California, USA; Division of Cardiology, Electrophysiology Section, University of California San Francisco, San Francisco, California, USA.
4
Division of Cardiology, Cardiovascular Research Institute, University of California San Francisco, San Francisco, California, USA; Division of Cardiology, Electrophysiology Section, University of California San Francisco, San Francisco, California, USA; Cardiac Electrophysiology and Cardiovascular Research Institute, University of California San Francisco. 505 Parnassus Avenue, Room M-1182, Box 0124, San Francisco, California, USA. Electronic address: jeffrey.olgin@ucsf.edu.

Abstract

BACKGROUND:

Even though ethanol consumption has been associated with risk of atrial fibrillation (AF), little is known about how ethanol affects atrial electrophysiology.

OBJECTIVES:

to study electrophysiologic effect of ethanol on rat atrial fibrillation.

METHODS:

Atrial optical mapping was performed on male Long Evans rat hearts with escalating concentrations of ethanol (0, 1, 2, and 3 mM). In addition, patch clamp recordings on isolated atrial myocytes were performed. In chronic ethanol study, rats were divided into control and chronic ethanol groups (20% ethanol in drinking water for 6 months). Atrial optical mapping, histology, immunohistochemistry and RT-PCR were performed in chronic rats.

RESULTS:

Acute ethanol perfusion increased AF vulnerability (0% at 0mM, 0% at 1mM, 57.1% at 2mM and 100% at 3mM) in a dose related response. Ethanol infusion decreased conduction velocities (CV) in both atria, shortened effective refractory periods (ERP) only in the right atria with increased in dispersion of refractoriness; action potential duration at 50% and 90% repolarization from right atrial myocytes were shortened with corresponding increase of sustained potassium current. Chronic ethanol consumption increased AF inducibility (10%, control vs. 95.2%, chronic ethanol). CVs in both atria were significantly decreased; ERP of right atrium was shortened, and dispersion of ERP was increased. Expression (mRNA) of KCNQ1 and connexin-40 were increased, but KCNA5 was decreased in the right atrium of rats exposed to chronic ethanol.

CONCLUSION:

Acute and chronic exposure to ethanol increases AF vulnerability by slowing CV, shortening right atrial ERP and increasing dispersion of ERP.

KEYWORDS:

atrial fibrillation vulnerability; effective refractory period; ethanol; optical mapping; patch clamping; potassium current

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