TY - JOUR

T1 - Mechanisms and Therapeutic Opportunities in Atrial Fibrillation in Relationship to Alcohol Use and Abuse

AU - Linz, Benedikt

AU - Hertel, Julie Norup

AU - Jespersen, Thomas

AU - Linz, Dominik

N1 - Publisher Copyright: © 2022 The Authors

PY - 2022

Y1 - 2022

N2 - Excessive drinking has detrimental effects on the cardiovascular system. Atrial fibrillation (AF) after alcohol binge drinking, also named “holiday heart syndrome,” is well established. However, chronic lower levels of alcohol intake also may increase AF risk. In this review, we aim to provide a comprehensive overview of the epidemiology and pathophysiology by which alcohol may be responsible for AF and discuss whether alcohol abstinence is required for optimal rhythm control as well as to maintain sinus rhythm in patients with AF. The pathophysiologic mechanisms responsible for the relationship between alcohol consumption and AF may include both direct and chronic effects increasing AF burden. Acute effects may include arrhythmogenic changes (such as shortening in atrial refractoriness, slowing in conduction velocity, and increased atrial ectopy) and an autonomic imbalance. Chronic changes contributing to the development of an arrhythmogenic substrate involve atrial structural and functional remodelling processes due to atrial dilation, elevated pressures, and fibrosis formation. In addition, alcohol consumption contributes to developing concomitant AF risk factors such as obesity, sleep-disordered breathing, and hypertension. Alcohol abstinence is associated with a reduction in AF recurrence and overall burden and moreover improves AF risk factor development such as obesity, hypertension, sleep apnea, and AF-related consequences such as stroke. In conclusion, alcohol consumption is associated with atrial arrhythmia and a wide range of cardiovascular comorbidities. Although further evidence is needed, current knowledge indicates that there might not be a safe level of alcohol consumption that does not increase AF risk.

AB - Excessive drinking has detrimental effects on the cardiovascular system. Atrial fibrillation (AF) after alcohol binge drinking, also named “holiday heart syndrome,” is well established. However, chronic lower levels of alcohol intake also may increase AF risk. In this review, we aim to provide a comprehensive overview of the epidemiology and pathophysiology by which alcohol may be responsible for AF and discuss whether alcohol abstinence is required for optimal rhythm control as well as to maintain sinus rhythm in patients with AF. The pathophysiologic mechanisms responsible for the relationship between alcohol consumption and AF may include both direct and chronic effects increasing AF burden. Acute effects may include arrhythmogenic changes (such as shortening in atrial refractoriness, slowing in conduction velocity, and increased atrial ectopy) and an autonomic imbalance. Chronic changes contributing to the development of an arrhythmogenic substrate involve atrial structural and functional remodelling processes due to atrial dilation, elevated pressures, and fibrosis formation. In addition, alcohol consumption contributes to developing concomitant AF risk factors such as obesity, sleep-disordered breathing, and hypertension. Alcohol abstinence is associated with a reduction in AF recurrence and overall burden and moreover improves AF risk factor development such as obesity, hypertension, sleep apnea, and AF-related consequences such as stroke. In conclusion, alcohol consumption is associated with atrial arrhythmia and a wide range of cardiovascular comorbidities. Although further evidence is needed, current knowledge indicates that there might not be a safe level of alcohol consumption that does not increase AF risk.

UR - http://www.scopus.com/inward/record.url?scp=85133730652&partnerID=8YFLogxK

U2 - 10.1016/j.cjca.2022.04.009

DO - 10.1016/j.cjca.2022.04.009

M3 - Review

C2 - 35436533

AN - SCOPUS:85133730652

VL - 38

SP - 1352

EP - 1363

JO - Canadian Journal of Cardiology

JF - Canadian Journal of Cardiology

SN - 0828-282X

IS - 9

ER -