Holiday Heart Syndrome

Updated: May 30, 2018
  • Author: Lawrence Rosenthal, MD, PhD, FACC, FHRS; Chief Editor: Jose M Dizon, MD  more...
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In 1978, Philip Ettinger and coinvestigators coined the term holiday heart syndrome (HHS) as "an acute cardiac rhythm and/or conduction disturbance associated with heavy ethanol consumption in a person without other clinical evidence of heart disease..." [1] The initial recognition of the syndrome was a result of their study evaluating 32 separate dysrhythmic episodes in 24 patients who were admitted to the hospital for their condition. [1] These patients consumed alcohol heavily and regularly; in addition, they took part in a weekend or holiday drinking binge immediately prior to evaluation. In their series, the most common cardiac rhythm disturbances were supraventricular tachyarrhythmias and atrial fibrillation. Typically, this resolved rapidly with spontaneous recovery during subsequent abstinence from alcohol use. [1]

It is relevant to note that chronic consumption of large quantities of alcohol (In the context of this article, alcohol refers specifically to ethanol) has long been recognized to induce an alcoholic cardiomyopathy. Clinically similar to idiopathic dilated cardiomyopathy, alcoholic cardiomyopathy is a major form of secondary dilated cardiomyopathy in the western world. (See the Medscape Drugs and Diseases articles Alcoholic Cardiomyopathy and Dilated Cardiomyopathy.) With this change in cardiac structure and decline in function, there exists the substrate for atrial and ventricular arrhythmias. [2]  

In the modern era, the term HHS has primarily been used to refer to acute cardiac rhythm disturbances related to acute alcohol consumption (ie, binge drinking), regardless of the underlying cardiac disease. [3] This is supported by the fact that the effect of alcohol on the induction of arrhythmias is dose dependent, and it is independent of preexisting cardiovascular diseases or heart failure. [4]   Even modest alcohol intake can be identified as a trigger in some patients with paroxysmal atrial fibrillation. [3, 5]  Although less rigorously studied, it should be noted that other substances associated with binge drinking certainly may contribute. As such, similar reports have indicated that recreational use of marijuana may have corresponding effects. [6]

The most common rhythm disorder with HHS is atrial fibrillation. [7, 8] HHS should be considered as a diagnosis in patients without structural heart disease and with new-onset atrial fibrillation. [9]  



Several mechanisms are theorized to be responsible for the arrhythmogenicity of alcohol. They may be characterized into two broad groups: direct effects on the myocardium and alcohol's effect on traditional risk factors for atrial fibrillation.

With regard to direct effects on the atrial myocardium, alcohol causes a autonomic nervous system imbalance. Alcohol increases sympathetic nervous system (SNS) activity (and its related increased secretion of epinephrine and norepinephrine), with resultant effects including an increased release of calcium into the myocytes from the sarcoplasmic reticulum. [3, 10] Increased SNS activity is further evidenced by a marked increase in the incidence of sinus tachycardia and reduced respiratory sinus arrhythmia during acute alcohol intoxication. [11] Consequently, the parasympathetic nervous system (PNS) is activated as well, with an increased intermittent vagal tone, which has been shown to also shorten the atrial refractory period and preciptate atrial fibrillation. [10] Note that the risk of atrial fibrillation persists into the "hangover" and/or withdrawal phase, which corresponds with an increased sympathetic tone. [3]

Other direct effects on the myocardium are perhaps less well studied. They include the effects of alcohol's primary metabolite acetaldehyde, which is associated with local inflammation and oxidative stress. [10]  Alcohol itself can also directly decrease the myocyte sodium current and can affect intracellular pH, ether causing acidosis with low doses or alkalosis with higher doses. Interestingly, these effects may be species specific, with rabbits [12] and humans being similarly affected, whereas canine atria appear unaffected. [13]  Research indicates that cardiac cells exposed to ethanol doses of 0.1% or greater undergo extrusion of magnesium (Mg2+), possibly owing to ethanol oxidation by cytochrome P-450 2E1; whether this contributes to alcoholic cardiomyopathy is not known. [14, 15]

A more recent study revealed that binge alcohol consumption activates the stress kinase JNK (c-Jun N-terminal kinase) (JNK2), which subsequently phosphorylates (and activates) the CaMKII protein, thereby enhancing CaMKII-driven mishandling of sarcoplasmic reticulum calcium—which prompts aberrant calcium waves and enhances susceptibility to atrial arrhythmia. [8] Conversely, CaMKII inhibition eliminates binge alcohol-evoked arrhythmic activities.

In another recent study involving isolated human atrial and murine atrial or ventricular cardiomyocytes, investigators indicated sarcoplasmic reticulum calcium leak as well as disordered excitation-contraction coupling as the basis for the arrhythmogenic and negative inotropic effects (reduced systolic calcium release) of acute ethanol exposure. [16] The investigators noted that production of reactive oxygen species (ROS) via nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX2) and oxidative activation of CaMKII appeared have key roles in the mechanism of action.

Analysis of electrocardiograms (ECGs) performed following the resolution of arrhythmias in patients who have consumed a large quantity of alcohol shows significant prolongation of the PR, QRS, and QT intervals compared to that of patients who experienced arrhythmias in the absence of alcohol consumption. [1, 17]

The arrhythmogenicity of alcohol has also been examined in the electrophysiology (EP) laboratory. In a study that evaluated 14 patients with a history of significant alcohol consumption, initially, the atrial and ventricular extrastimulus technique induced nonsustained ventricular tachycardia in a patient, nonsustained atrial fibrillation in another patient, paired ventricular responses in a third patient, and no response in the remaining 11 patients. [18] Following administration of alcohol, 10 of the 14 patients developed sustained or nonsustained tachyarrhythmias in response to the extrastimulus technique, with significant prolongation of His-ventricular conduction. [18]  In another study, ingestion of whiskey resulted in no change in the atrial refractory period but facilitated induction of atrial flutter in individuals who were chronic drinkers and those who were nondrinkers. [2, 19]  This evidence strongly suggests that alcohol possesses proarrhythmic properties. These seem to be more pronounced in patients with larger P-wave dispersion.

Although ventricular repolarization abnormalities on surface ECG were described, whether ventricular myocardium responds similarly to ethanol is uncertain. One case of ventricular fibrillation was described in a patient with heavy alcohol ingestion, but an electrophysiologic study (EPS) revealed only inducibility of atrial fibrillation with rapid ventricular response but no ventricular arrhythmias. Alcohol-induced atrioventricular block has been reported as a rare event that can occur at relatively low serum alcohol levels. [20] Investigators suggest that the mechanism for conduction slowing and block may be partly due to an exaggerated partial inhibition of calcium and, potentially, sodium currents in conductive tissue structures as result of elevated vagal tone. Impaired gap junction function may also play a role. [20]

With regard to alcohol's effect on traditional risk factors, one of the best studied is alcohol and its ability to exacerbate the severity of obstructive sleep apnea (OSA). OSA has clearly been associated with incident atrial fibrillation. [3] Alcohol consumption has been shown to increase the severity of sleep apnea, or the apnea-hypopnea index (AHI) through a variety of mechanisms. [21]  In addition, it is clear that alcohol consumption (perhaps via activation of the SNS), increases systolic and diastolic blood pressure. [22]  Furthermore, alcohol is also associated with worsening hypertension, obesity, and cardiomyopathy. [3] Although these risk factors are associated more with the long-term risk for development of atrial fibrillation, they are worth mentioning.



United States data

The frequency with which cardiac arrhythmias can be attributed to alcohol use is unclear owing to differing data. One study showed alcohol as the causative agent in 35% of cases of new-onset atrial fibrillation and in 63% of cases in patients younger than 65 years. [23] Conversely, another study showed revealed 5%-10% of all new episodes of atrial fibrillation were attributable to alcohol use. [9]

The frequency of alcohol-related disturbance depends on the population studied. For example, when considering patients hospitalized for alcohol-related rhythm disturbances, atrial fibrillation and atrial flutter appear to be most common arrhythmias. [1, 3] When considering an otherwise healthy, asymptomatic outpatient population, sinus tachycardia appears to be the most common arrhythmia. [24]  

International data

The first large prospective study regarding arrhythmias and alchohol was performed in Munich at Octoberfest in 2015. [24] This study was unique when compared to prior studies in that the study population was an otherwise healthy outpatient population at a festival during acute alcohol consumption. The most common arrhythmia was sinus tachycardia (25.9%); atrial fibrillation (and/or atrial flutter) was seen in 0.8%. When all arrhythmias were considered together, an increasing blood alcohol concentration was associated with an increased incidence of arrhythmia.



The prognosis of holiday heart syndrome (HHS) depends on the presence of any underlying heart disease. Long-term alcohol use increases the risk of cardiomyopathy, arrhythmia, and chronic liver disease.

Note that although the majority (>90%) of cases of alcohol-related atrial fibrillation self-terminate, approximately 20%-30% will recur within 12 months. [11] When considering the type of atrial fibrillation, moderate to heavy alcohol consumption was the strongest risk factor for progression from paroxysmal atrial fibrillation to persistent atrial fibrillation. [25]


A study showed that males who consume more than 27 standard drinks per week have a higher risk of death, stroke, or systemic thromboembolism. [26] The same study demonstrated that females consuming over 20 standard drinks per week were at a higher risk of stroke or systemic thromboembolism. [26] However, contradictory evidence was seen in another study that demonstrated consumption of greater than 14 standard drinks per week was associated with a lower stroke risk. [3] This highlights the fact that the relationship between atrial fibrillation and thrombogenesis is still not well understood.

Note that the incidence of atrial fibrillation, as a function of alcohol ingestion, clearly increases in a linear and dose-dependent fashion. A separate issue is that modest alcohol consumption has been shown to be beneficial. As such, there is a U-shaped curve relating to alcohol consumption and overall cardiovascular mortality. [3] Stated another way: With the available data, there is no dose of alcohol that should be considered "protective" for atrial fibrillation, whereas there is clearly a range of alcohol dosage that is protective with regard to overall cardiovascular disease. [3]