Elsevier

Heart Rhythm

Volume 16, Issue 2, February 2019, Pages 251-259
Heart Rhythm

Clinical
Imaging/Mapping
Moderate alcohol consumption is associated with atrial electrical and structural changes: Insights from high-density left atrial electroanatomic mapping

https://doi.org/10.1016/j.hrthm.2018.10.041Get rights and content

Background

Regular alcohol intake is an important modifiable risk factor associated with atrial fibrillation (AF) and left atrial (LA) dilation.

Objective

The purpose of this study was to determine the impact of different degrees of alcohol consumption on atrial remodeling using high-density electroanatomic mapping.

Methods

We enrolled 75 patients before AF ablation to undergo high-density LA mapping (CARTO, Biosense Webster) using a multipolar catheter. The Confidense algorithm was used to create maps during distal coronary sinus pacing at 600 ms. Bipolar voltage and complex atrial activity were assessed, and isochronal activation maps were created to determine global conduction velocity (CV). Patients were classified as lifelong nondrinkers, mild drinkers (2–7 drinks/week), or moderate drinkers (8–21 drinks/week).

Results

High-density electroanatomic mapping (mean 1016 ± 445 points per patient) was performed on 25 lifelong nondrinkers, 25 mild drinkers (4.4 ± 2.3 drinks/week), and 25 moderate drinkers (14.0 ± 4.2 drinks/week). Moderate drinkers had significantly lower mean global bipolar voltages (1.53 ± 0.62 mV vs 1.89 ± 0.45 mV; P = .02), slower CV (33.5 ± 14.4 cm/s vs 41.7 ± 12.1 cm/s; P = .04), and a higher proportion of complex atrial potentials (7.8% ± 4.7% vs 4.5% ± 2.7%; P = .004) compared to nondrinkers. Global voltage and CV did not differ significantly in mild drinkers, but there was a significant increase in global complex potentials (6.6% ± 4.6%; P = .04) and regional low-voltage zones (<0.5 mV) in the septum and lateral wall (P <.05) compared with nondrinkers.

Conclusion

Regular moderate alcohol consumption, but not mild consumption, is an important modifiable risk factor for AF associated with lower atrial voltage and conduction slowing. These electrical and structural changes may explain the propensity to AF in regular drinkers.

Introduction

Excessive alcohol consumption has emerged as a potentially modifiable risk factor for atrial fibrillation (AF).1 Both binge drinking and habitual alcohol consumption have been implicated in electrical and structural changes involving the left atrium (LA). Acute electrophysiological effects of excessive alcohol include shortening of atrial refractoriness and slowing of intra-atrial conduction.2 More recently, binge drinking has been found to activate c-Jun N-terminal kinase (JNK), leading to sarcoplasmic reticulum calcium mishandling3 and causing contractile dysfunction related to oxidative stress, mitochondrial damage, and cardiac steatosis,4 thereby increasing susceptibility to “holiday heart syndrome.”

Observational studies suggest that regular alcohol consumption, even at moderate levels, may increase AF risk. A meta-analysis of 7 studies involving 859,420 patients and 12,554 AF cases demonstrated an 8% increase in incident AF for each additional daily standard drink.5 Whereas alcoholic cardiomyopathy is well described in the ventricle for those consuming >80 g/d for >10 years,6 the thinner-walled atrium may be more susceptible to toxicity at lower doses. Compared to abstainers, those consuming even 1 drink per day have been reported to have a higher prevalence of atrial “low-voltage zones”.7 There is a dose-related relationship between regular alcohol consumption and LA enlargement, with each additional 10 g associated with a 0.16-mm increase in LA size.8

Despite the association between regular alcohol intake and AF, detailed human electrophysiological studies describing the nature of alcohol-related atrial remodeling are lacking. We aimed to determine the impact of regular alcohol consumption on electrical and structural changes in the LA in patients with a history of AF using high-density electroanatomic mapping before AF ablation.

Section snippets

Patient population

This multicenter cross-sectional study was conducted from March 2016 to May 2018 at 2 hospitals. We recruited 75 patients with paroxysmal or persistent AF willing to consent to high-density LA mapping during initial AF ablation using the CARTO (Biosense Webster, Diamond Bar, CA) 3-dimensional electroanatomic mapping system. The study was approved by Alfred Health and Melbourne Health Human Research Ethics Committees, and all patients provided written informed consent.

Patients self-reported

Patient characteristics

Before AF ablation, 75 patients (69% male; mean age 58.7 ± 9.1 years; median CHA2DS2-VASc score 1) underwent high-density LA mapping during CS pacing. There were 25 lifelong nondrinkers, 25 mild drinkers (4.4 ± 2.3 drinks/week), and 25 moderate drinkers (14.0 ± 4.2 drinks/week). Representative voltage and propagation maps for the 3 groups are shown in Figure 1.

Baseline characteristics for all 3 groups are listed in Table 1. The 3 groups had a similar profile with respect to age, gender, AF

Discussion

This cross-sectional study of patients with a history of AF and relatively low prevalence of other comorbidities reports the electrical and structural changes in the atrium associated with long-term alcohol consumption. The key findings are as follows.

  • 1.

    Regular moderate drinkers (average ∼14 drinks/week) had significantly lower global atrial voltage, proportion of low voltage, and slower CVs.

  • 2.

    Moderate alcohol consumption, together with older age and female gender, was a stronger multivariate

Conclusion

Regular moderate alcohol consumption, but not mild consumption, is associated with lower atrial voltage and conduction slowing. These electrical and structural changes may in part explain the propensity to AF in regular drinkers and may represent an important modifiable risk factor for AF.

References (30)

Cited by (60)

  • Alcohol and Arrhythmias

    2023, JACC: Clinical Electrophysiology
View all citing articles on Scopus

Dr Voskoboinik is supported by NHMRC/NHF postgraduate scholarships and Baker Institute Bright Sparks scholarships. Prof Kalman is supported by an NHMRC practitioner fellowship. Dr McLellan is supported by a Heart Foundation postdoctoral fellowship. Prof Kalman is on the advisory board of Biosense Webster; and reports receiving research and fellowship support from Biosense Webster, Boston Scientific, St. Jude Medical, and Medtronic.

1

Drs Voskoboinik and Wong are joint first authors.

View full text