A daily alcoholic drink for women or two for men might be good for heart health, compared to drinking more or not drinking at all.
But while there is some evidence that drinking in moderation might prevent heart attacks, now a randomized, double-blinded clinical study of 100 heart patients has added a new wrinkle to the contours of the debate over alcohol and heart disease.
UC San Francisco researchers found that alcohol has an immediate effect on the heart in patients with atrial fibrillation (AFib), the most common life-threatening heart-rhythm disorder.
In the study, published online January 27, 2021 in the Journal of the American College of Cardiology: Clinical Electrophysiology, electrical properties that drive the muscles of the heart to contract changed immediately in patients who were randomly assigned to an infusion of alcohol maintained at the lower limit of legal intoxication, compared to an equal number of control subjects who instead received a placebo infusion.
According to senior study author Gregory Marcus, MD, professor of medicine in the Division of Cardiology at UCSF, “The acute impact of exposure to alcohol is a reduction in the time needed for certain heart muscle cells in the left atrium to recover after being electrically activated and to be ready to activated again, particularly in the pulmonary veins that empty into the left atrium.”
“Although epidemiological studies have found an association between self-reported alcohol consumption and the development of an atrial fibrillation diagnosis, ours is the first study to point to a mechanism through which a lifestyle factor can acutely change the electrical properties of the heart to increase the chance of an arrhythmia,” Marcus said.
The same changes caused by alcohol infusion in the study have earlier been associated with episodes of AFib in previous computer models and animal studies, he said.
In AFib the orderly pumping of blood through the atria, the heart’s upper chambers, is disrupted. Pumping normally is driven by regular waves of electrical signal conduction along well travelled circuits that form in the heart between cells in the muscle tissue, but in AFib electrical properties change within the atria and electrical signals travel chaotically through the chambers’ muscles, all of which can themselves conduct and perpetuate waves of electrical activation.
The number of people in the U.S. with AFib is approaching 12 million, and the condition leads to 454,000 hospitalizations yearly, according to the Centers for Disease Control with Prevention. AFib contributes to about 158,000 U.S. deaths each year and is a leading cause of stroke, as blood clots can form inside fibrillation-prone atria.
The study patients were all undergoing a scheduled, standard “catheter ablation” procedure, the most effective method to suppress atrial fibrillation episodes. This procedure targets elimination of the electrical connection between the pulmonary veins and the left atrium, the same area noted to be affected exposure to alcohol in the current study.
Preparation for ablation surgery already required placement of catheters and electrodes in the heart chambers to monitor and pace the heart and destroy targeted tissue. For the study, investigators measured the refractory period needed by cells to recover before they could transmit electrical signals again, as well as the speed of signal conduction from one point to another within the heart. They also applied a stimulus to greatly increase the likelihood of inducing a transient AFib episode.
The speed of electrical conduction through the upper chambers did not change significantly in the study, but in comparison to placebo, alcohol infusion resulted in an average reduction of 12-milliseconds in the refractory period for tissue in the pulmonary vein, and also reduced the refractory period in significantly more sites throughout the atria. During the procedure, the number of induced AFib episodes did not differ significantly between alcohol and placebo infusion groups.
“We were able to induce AFib in large numbers of patients in both groups, but our artificial methods of inducing AFib may have overwhelmed any observable differences between the groups,” Marcus said. “Alternatively, it may be that there is a delay between the change in electrical properties caused by alcohol and the increased likelihood of triggering AFib.”
“Patients should be aware that alcohol can have immediate effects that are expected to increase risk for arrhythmias,” Marcus concludes.
Atrial fibrillation (AF) is an arrhythmia with a major impact on public health due to its increasing prevalence in ageing populations and its association with adverse outcomes, including stroke and heart failure (HF), with more than a doubling of mortality risk.1,2 The effect of alcohol on AF risk has remained ambiguous.
For diseases predisposing to AF such as coronary artery disease3 or HF4,5 low to moderate alcohol consumption seems to be related to a lower incidence, while higher levels of consumption are associated with an increased risk.6 The reported associations with AF range from null associations at lower regular alcohol intake,5,7 rather linearly increasing in large meta-analyses8,9 to a more J-shaped relation in women.1 In particular, the association at low levels of alcohol consumption is less clear.
From a pathophysiological perspective, alcohol may exhibit direct effects on arrhythmogenesis as observed for the holiday heart syndrome.10–13 Acute alcohol consumption induces autonomic imbalance reflected by sinus tachycardia, predisposing to arrhythmia.10 Electrolyte disturbance and alterations of the acid-base balance are further pro-arrhythmic triggers. Chronic alcohol consumption is known to be correlated with changes in cardiac structure and function including cardiomyopathy.4,11–13
Habitual alcohol intake has been related to atrial remodelling as an intermediate AF phenotype in the community.12,13 At the same time, alcohol intake is also associated with the most prevalent risk factors of AF. Increased alcohol intake is accompanied by higher frequency of hypertension and obesity.14
In younger individuals with low-risk factor burden and heart disease, acute excessive alcohol consumption was not associated with higher AF burden.10 Furthermore, alcohol consumption is predictive of incident HF, which itself is a risk factor for new-onset AF4,6 and may help explain known associations.
Circulating cardiac biomarkers are quantitative measures which shed light on current cardiac pathophysiology. Troponin reflects myocardial injury, while N-terminal pro-B-type natriuretic peptide (NT-proBNP) indicates often chronic, subclinical wall stress.15 A recent study demonstrated that both biomarkers showed distinct patterns in relation to alcohol consumption.15 Whereas troponin concentrations decreased with higher alcohol consumption, NT-proBNP increased.15 Whether this pattern is related to AF risk remains to be shown.
A strong controversy remains for the relation of alcohol consumption with AF in individuals with low alcohol consumption. Therefore, we examined the association of alcohol consumption with incident AF while accounting for classical risk factors, HF and cardiac biomarkers across European cohorts.
The present study comprises five community-based cohorts from the Monica Risk, Genetics, Archiving and Monograph (MORGAM) (https://www.thl.fi/morgam/)/ Biomarker for Cardiovascular Risk Assessment across Europe (BiomarCaRE) (http://biomarcare.eu/) projects with available information on AF status at baseline and follow-up (DAN-MONICA, FINRISK, Moli-sani, Tromsø, and Northern Sweden), totalling 107 845 individuals with baseline examinations between 1982 and 2010.
We excluded 7753 individuals with self-reported and/or physician-diagnosed history of AF/atrial flutter and/or prior ICD-8-9- or -10 coding for AF/atrial flutter from the analyses. Details on enrolment and follow-up procedures by study are provided in the Supplementary material online. In total, 100 092 participants free of AF at baseline entered our analyses.
Where appropriate, we stratified cohorts by the period of recruitment and study area, as shown in Supplementary material online, Table S1. Cohort stratification was possible because we did not observe an interaction for association of alcohol and incident AF by cohort.
Local Ethics Committees have approved all participating studies. Participants signed written informed consent. The authors had full access to the data and take responsibility for its integrity. All authors have read and agreed to the manuscript as written.
Risk factors and follow-up
Risk factor information was available from the baseline visits. Information on body mass index (BMI), hypertension, systolic blood pressure, diabetes, total cholesterol, current smoking, anti-hypertensive medication, history of HF, myocardial infarction or stroke, employment status, education level, and habitual alcohol intake were collected and measured locally.
These data were centrally harmonized by the MORGAM project16 and defined AF in a way consistent with previous risk prediction algorithms.14
Average alcohol consumption was assessed in gram per day and categorized according to the World Health Organization average volume drinking categories.17 The quantity of average alcohol consumption in gram per day was a harmonized variable derived from different questionnaires across cohorts as a component of local food frequency questionnaires. Participants were asked to indicate how often they consumed beer, wine, and spirits as well as the drinking pattern.
For the calculation of the amount of alcohol consumed, it was assumed that 120 mL of wine, 330 mL of beer, or 40 mL of spirits contained 12 g of ethanol.5
Continuous alcohol variables were average alcohol consumption in gram per day and alcohol in gram per day consumed from beer, spirits, and wine, respectively. These continuous variables were right winsorized at the level of 98.9% for the analysis. We further examined categorical variables. Drinking pattern had six categories: lifelong abstainer (reference group), ex-drinker, less than once a week, 1–2, 3–5, and 6–7 days/week.
We created a new categorical variable from initial average alcohol consumption in gram per day by subdividing the population into seven groups as defined5: former drinker, never drinker (reference group), occasional drinker (<1 g/day), 1–12 g/day (<1 drink/day), 12.1–24 g/day (>1 drink/day), 24.1–48 g/day (2–4 drinks/day) and more than 48 g/day.
The ‘never drinker’ group comprised those who consume 0 g of alcohol and who were lifelong abstainers. Individuals with missing values for alcohol variables were excluded from the analyses. Analyses using the continuous variables had the reference level at 0 g/day.
Meta-analyses have shown that former drinkers have sustained higher risk of cardiovascular diseases and higher mortality even compared with never drinkers. The interpretation of findings in this group remains difficult. Therefore, we excluded former drinkers with 0 g in average daily alcohol consumption from the group of non-drinkers.18
Analyses using categorical variables comprise the category of former drinkers. The reference of these analyses is the category of never drinkers.
The outcome diagnosis of AF and HF was based on questionnaire information, national hospital discharge registry data including data on ambulatory visits and comorbidities available from causes of death registry data to identify incident AF or HF. Atrial fibrillation was defined as either of AF/atrial flutter. Further information on the definition of the outcome of AF is provided in the Supplementary material online. The last available follow-up was between 2010 and 2011 in different cohorts.
reference link: https://academic.oup.com/eurheartj/advance-article/doi/10.1093/eurheartj/ehaa953/6090248