Holiday Heart Syndrome
- Author: Adam S Budzikowski, MD, PhD, FHRS; Chief Editor: Jeffrey N Rottman, MD more...
Alcohol consumed in large quantities for many years has long been recognized to induce an alcoholic cardiomyopathy. Clinically identical to idiopathic dilated cardiomyopathy, alcoholic cardiomyopathy is a major form of secondary dilated cardiomyopathy in the Western world. (See Medscape Reference 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. However, only within the past 20-25 years has the arrhythmogenic potential of short-term alcohol consumption been elucidated in patients without clinically evident heart failure.
In 1978, Ettinger et al conducted a study evaluating 32 separate dysrhythmic episodes in 24 patients. These patients consumed alcohol heavily and regularly; in addition, they took part in a weekend or holiday drinking binge immediately prior to evaluation. Based on the results of this study, the term holiday heart syndrome was coined. It was defined as an acute cardiac rhythm and/or conduction disturbance, most commonly supraventricular tachyarrhythmia, associated with heavy ethanol consumption in a person without other clinical evidence of heart disease. Typically, this resolved rapidly with spontaneous recovery during subsequent abstinence from alcohol use.
Holiday heart syndrome now most commonly refers to the association between alcohol use and rhythm disturbances, particularly supraventricular tachyarrhythmias in apparently healthy people. Similar reports have indicated that recreational use of marijuana may have similar effects. The most common rhythm disorder is atrial fibrillation, which usually converts to normal sinus rhythm within 24 hours. Holiday heart syndrome should be particularly considered as a diagnosis in patients without structural heart disease and with new-onset atrial fibrillation. Although the syndrome can recur, its clinical course is benign, and specific antiarrhythmic therapy is usually not indicated. Interestingly, even modest alcohol intake can be identified as a trigger in some patients with paroxysmal atrial fibrillation.
Several mechanisms are theorized to be responsible for the arrhythmogenicity of alcohol. These include an increased secretion of epinephrine and norepinephrine, increased sympathetic output, a rise in the level of plasma free fatty acids, and an indirect effect through acetaldehyde, the primary metabolite of alcohol, or fatty acid ethyl esters, a cardiac alcohol metabolite. Alcohol can also directly decrease 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 and humans being similarly affected, while the dog atria appear unaffected.
Research indicates that cardiac cells exposed to ethanol doses of 0.1% or greater undergo extrusion of Mg2+, possibly owing to ethanol oxidation by cytochrome P-450 2E1; whether this contributes to alcoholic cardiomyopathy is not known.[10, 11]
Analysis of ECGs performed following resolution of arrhythmias in patients who have consumed a large quantity of alcohol show significant prolongation of the PR, QRS, and QT intervals compared with patients who experienced arrhythmias in the absence of alcohol consumption. The arrhythmogenicity of alcohol has also been examined in the electrophysiology laboratory.
One study evaluated 14 patients with a history of significant alcohol consumption. Initially, the atrial and ventricular extrastimulus technique induced nonsustained ventricular tachycardia in 1 patient, nonsustained atrial fibrillation in 1 patient, paired ventricular responses in 1 patient, and no response in the remaining 11 patients. 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.
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. 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.
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. Conversely, another study showed only about 5-10% of all new episodes of atrial fibrillation to be explainable by alcohol use.
Atrial fibrillation is the most common rhythm disturbance associated with alcohol consumption. Atrial flutter, isolated ventricular premature beats, isolated atrial premature beats, junctional tachycardia, and various other rhythm disturbances may occur with less frequency.
Worldwide prevalence is not well documented. Prevalence is presumably increased in countries with higher rates of alcohol ingestion and alcoholism.
Regular consumption of alcohol in modest amounts does not seem to have the same potential to cause arrhythmias as alcohol consumed in heavy amounts. In fact, it has been shown in a sample of patients whose usual daily alcohol intake exceeds 6 drinks that the risk of developing atrial fibrillation, atrial flutter, and atrial premature beats is at least twice that of patients who drink alcohol at least monthly but who on average consume less than a single drink daily.
Evidence regarding race is unavailable.
An increased incidence of the holiday heart syndrome has not been clearly documented in males; however, this can be inferred as males have a higher incidence of atrial fibrillation and alcoholism.
Although atrial fibrillation increases with age, it is unclear if holiday heart syndrome is more common in elderly patients, since this age group is more likely to have structural heart disease.
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