Atrial fibrillation (AF) is the most common arrhythmia in humans, and it is estimated that 1 in 4 individuals over the age of 40 will eventually develop AF [1]. AF is linked to various significant health complications, including dementia, stroke, heart failure, and reduced exercise tolerance [[2], [3], [4]]. Alcohol is the most widely consumed drug in western countries [5] and is known to have long-term adverse effects on the cardiovascular system, including atrial fibrosis, atrial dilation and AF [[6], [7], [8], [9]]. While the majority of research on this topic has focused on chronic or long-term consequences of alcohol consumption and AF, limited research has been conducted on the acute physiological cardiovascular alterations associated with alcohol consumption.

We recently demonstrated that acute alcohol consumption was associated with a heightened risk of a discrete AF episode hours later [10]. But the mechanisms underlying such a near-term relationship remain largely unknown. We found in our randomized, double-blinded, controlled clinical trial called the HOw ALcohol InDuces Atrial TachYarrhythmias (HOLIDAY) that an alcohol infusion titrated to 0.08% blood alcohol concentration (and not a volume and osmolality-matched placebo) shortened the atrial effective refractory period (AERP) specifically in the pulmonary veins [11] Contrary to prior findings in animal models that showed a reduction in conduction velocities upon alcohol exposure [12], no differences in conduction times were observed. However, measurements could only be conducted where catheters were positioned, and only a surface electrocardiogram can provide insights into more global electrophysiologic effects. Therefore, we sought to assess the acute ECG changes associated with the administration of a known concentration of alcohol in the HOLIDAY study.