David Conen, MD @mcmasteru @PHRIresearch #AtrialFibrillation #CardiovascularDisease #Research Alcohol Consumption, At...

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David Conen, MD from the Population Health Research Institute and McMaster University, discusses Alcohol consumption, atrial fibrillation, and cardiovascular disease: finding the right balance.

Link To Study -
https://academic.oup.com/eurheartj/advance-article/doi/10.1093/eurheartj/ehaa955/6090247

Atrial fibrillation (AF) is associated with an increased risk of death and cardiovascular complications and has been described as one of the 21st century cardiovascular epidemics.1 AF pathogenesis is complex, but many risk factors for AF have been described previously, explaining the attributable risk of about 50 percent of the population.1-4 Enhancing our understanding of risk factors. Indeed, only oral anticoagulation has so far been undeniably shown to boost difficult results once AF.5 has been established by a patient.

Excessive alcohol intake is a significant modifiable risk factor that predisposes to AF. 6,7 The development of AF has been related to both acute and increased habitual drinking. As is apparent in the Holiday Heart Syndrome, acute alcohol intake has a direct impact on the heart, contributing to atrial tachyarrhythmias.8,9 Chronic alcohol consumption is also associated with an elevated risk of AF.6,7 In the Women's Health Study, women who drank > 2 alcoholic drinks per day had a 60% higher risk of AF incident after the multivariable change, while lower amounts did n.



In this issue of the Journal, in a very broad dataset, Csengeri et al.10 discussed the relationship between alcohol consumption and incident AF. Five prospective community-based cohorts totaling 107,845 individuals free of AF at baseline were combined by Csengeri et al.10, of whom 5854 developed new-onset AF over a median follow-up of 13.9 years. From patient self-report, alcohol intake was determined at baseline, while incident AF was determined from hospitalization data through ICD codes or comorbidities reported on death certificates. The median age was 47.8 years, 48.3 percent were men and 3 g/day was the median intake of alcohol. Consumption of 1 alcoholic beverage (defined as 12 g of alcohol) per day was correlated with a 16 percent increased risk of incident AF in Cox regression models stratified by sex and cohort [hazard ratio 1.16, 95 percent confidence interval (CI) 1.11–1.22, P < 0.001]. Importantly, at very low alcohol consumption levels, there was a substantial association between alcohol and increased AF risk. Even an average 3 g/day intake was closely correlated with the risk of AF (HR 1.04, 95% CI 1.02-1.05). Adjustment for other AF risk factors has not substantially attenuated this relationship. It is important to remember, while not mentioned in the manuscript, that the absolute risk of AF was likely low in participants who drank low to moderate amounts of alcohol.



The authors found a J-shaped association between alcohol intake and heart failure events, with the lowest risk reported at alcohol levels of up to 20 g per day. The relationship between alcohol- and time-dependent heart failure (HF) was not important when evaluating the intermediate function of incident heart failure in developing AF from alcohol intake. Finally, N-terminal pro-B-type natriuretic peptide (NT-proBNP) and high-sensitivity troponin-I (hsTnI) were weakly associated with alcohol intake and the association between alcohol and AF for these biomarkers was not attenuated.



There are some strengths in the current study 10. Harmonization of the outcome and covariates across five cohorts allowed the authors to conduct standardized studies with very broad sample size and great power to define important associations between alcohol intake and AF, including the lower alcohol consumption range where the probability of AF incident is expected to be minimal. This research, therefore, offers strong evidence that even very low alcohol levels (i.e. < 1 drink per day) remain substantially correlated with an increased risk of new-onset AF.



There are drawbacks to the Csengeri et al.10 analysis. First, from hospitalization results, AF episodes were not adjudicated and relied on the international classification of diseases (ICD codes), which may have contributed to bias in misclassification. In addition, AF instances that did not result in hospital presentation or were listed on death certificates may not have been reported. Second, the link between binge drinking and incident AF could not be investigated in this review. Third, absolute risks of AF associated with low levels of alcohol intake were not reported in the study. This important problem must also be taken into account when considering the potentially beneficial associations with other cardiovascular outcomes of moderate alcohol intake.11-14 Finally, the research was not intended to shed more light on the mechanisms that link habitual alcohol consumption and AF production. Although the authors explored the potential role of NT-proBNP and hsTnI in this relationship, only a minority of patients had biomarker data available, and only at baseline. The effects of alcohol on atrial electrophysiology are likely to rely on many variables, including changes in atrial repolarization, vagal sound, and direct myocardial injury and fibrosis.9 More studies are required to investigate how alcohol affects atrial electrophysiology across these possible pathways.



In conclusion, the current Article10 makes a significant contribution to our understanding of the relationship between alcohol intake and AF incidence, especially with the lower alcohol consumption continuum. There was a substantial association between alcohol and AF, and even small amounts of alcohol were associated with an increased, albeit small, risk of AF incidence. Together with a recent randomized study showing that a decrease in alcohol intake resulted in a decrease in AF recurrence,15 these data indicate that reducing alcohol intake may be relevant for AF prevention and management. Importantly, any decrease in low-to-moderate alcohol consumption to potentially prevent AF needs to be balanced with the potentially beneficial association of low amounts of alcohol with other cardiovascular findings (Graphical abstract).11-14 More research is needed for the net clinical advantage of consuming low amounts of alcohol, preferably in adequately powered randomized studies. Until then, each person has to make their own best-educated decision as to whether it is worthwhile and healthy to consume up to 1 alcoholic drink per day.