Holiday Heart Syndrome: A Literature Review

Holiday Heart Syndrome (HHS) is a condition characterised by the development of atrial fibrillation (AF) and other tachyarrhythmias following episodes of binge drinking in individuals without pre-existing cardiac disease. As the binge drinking rate rises worldwide, it is increasingly important to understand the pathophysiology, epidemiology, and clinical significance of this syndrome. The objective of this literature review is to synthesise current evidence on the relationship between binge alcohol drinking and AF, exploring the underlying mechanisms and risk factors associated with HHS. A literature review was conducted using PubMed and Cochrane databases up to August 2024. Articles were selected based on predefined inclusion criteria, focusing on studies assessing the impact of acute alcohol intake on AF incidence. Studies evaluating chronic alcohol consumption, literature reviews, case series, and publications in languages other than English were excluded. A total of 11 studies met the inclusion criteria, comprising cohort and case-control studies. The findings consistently demonstrated a strong association between binge drinking and AF onset. Epidemiological evidence suggests that an increased incidence of new AF cases in individuals without structural heart disease can be attributed to alcohol consumption. Mechanistic insights identify several pathophysiological processes that contribute to the development of HHS, including autonomic dysregulation, ion channel modifications, and transient atrial structural changes. Acute alcohol consumption leads to increased sympathetic activity and reduced vagal tone, increasing heart rate variability and predisposing individuals to AF. Furthermore, alcohol has been shown to increase the activity of T-type calcium channels, which contributes to atrial ectopy and electrical instability. Structural alterations, such as reduced left atrial emptying fraction, have also been observed in binge drinkers, further supporting the link between alcohol and arrhythmogenesis. The evidence reviewed underscores the significant arrhythmogenic risk of binge drinking. While some studies suggest a J-shaped relationship between alcohol intake and AF risk, binge drinking consistently appears as a major trigger. However, variability in study populations and methodologies necessitates further research to establish safe consumption thresholds and interventions. Most studies relied on self-reported alcohol intake, with inconsistent screening methods, and physiological assessments included electrocardiogram monitoring and blood alcohol level measurements. This review highlights the significant role of binge drinking in the pathogenesis of HHS, stressing the need for targeted public health interventions and personalised patient counselling. Future research should prioritise longitudinal studies to improve risk assessment models and clarify the long-term cardiovascular impacts of alcohol-induced AF. Clinicians are encouraged to routinely screen for alcohol use, particularly in patients with a history of arrhythmias, to help prevent recurrent episodes and minimise associated complications.