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Holiday Heart Syndrome

  • Author: Adam S Budzikowski, MD, PhD, FHRS; Chief Editor: Jeffrey N Rottman, MD  more...
 
Updated: Dec 31, 2015
 

Background

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.[1]

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.[2]

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.[3] The most common rhythm disorder is atrial fibrillation, which usually converts to normal sinus rhythm within 24 hours.[4] Holiday heart syndrome should be particularly considered as a diagnosis in patients without structural heart disease and with new-onset atrial fibrillation.[5] 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.[6]

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Pathophysiology

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.[7] 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[8] and humans being similarly affected, while the dog atria appear unaffected.[9]

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.[12] 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.[13]

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.

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Epidemiology

Frequency

United States

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.[14] 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.

International

Worldwide prevalence is not well documented. Prevalence is presumably increased in countries with higher rates of alcohol ingestion and alcoholism.

Mortality/Morbidity

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.

Race

Evidence regarding race is unavailable.

Sex

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.

Age

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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Contributor Information and Disclosures
Author

Adam S Budzikowski, MD, PhD, FHRS Assistant Professor of Medicine, Division of Cardiovascular Medicine, Electrophysiology Section, State University of New York Downstate Medical Center, University Hospital of Brooklyn

Adam S Budzikowski, MD, PhD, FHRS is a member of the following medical societies: European Society of Cardiology, Heart Rhythm Society

Disclosure: Received consulting fee from Boston Scientific for speaking and teaching; Received honoraria from St. Jude Medical for speaking and teaching; Received honoraria from Zoll for speaking and teaching.

Coauthor(s)

Richard H Smith, MD Director of Echocardiography, Long Island Heart Associates

Richard H Smith, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians-American Society of Internal Medicine, American Medical Association

Disclosure: Nothing to disclose.

James P Daubert, MD Professor of Medicine, Cardiology Division, Duke University School of Medicine

James P Daubert, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American Heart Association, Heart Rhythm Society

Disclosure: Partner received equity interest from Medtronic for none; Received honoraria from Boston Scientific for speaking and teaching; Received consulting fee from CV Therapeutics for consulting; Received consulting fee from Cryocor for consulting.

Howard S Weiss, DO Associate Medical Director, St Peter's Hospital Sleep Center

Howard S Weiss, DO is a member of the following medical societies: American Medical Association, American Osteopathic Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Steven J Compton, MD, FACC, FACP, FHRS Director of Cardiac Electrophysiology, Alaska Heart Institute, Providence and Alaska Regional Hospitals

Steven J Compton, MD, FACC, FACP, FHRS is a member of the following medical societies: American College of Physicians, American Heart Association, American Medical Association, Heart Rhythm Society, Alaska State Medical Association, American College of Cardiology

Disclosure: Nothing to disclose.

Chief Editor

Jeffrey N Rottman, MD Professor of Medicine, Department of Medicine, Division of Cardiovascular Medicine, University of Maryland School of Medicine; Cardiologist/Electrophysiologist, University of Maryland Medical System and VA Maryland Health Care System

Jeffrey N Rottman, MD is a member of the following medical societies: American Heart Association, Heart Rhythm Society

Disclosure: Nothing to disclose.

References
  1. Tonelo D, Providencia R, Goncalves L. Holiday heart syndrome revisited after 34 years. Arq Bras Cardiol. 2013 Aug. 101(2):183-9. [Medline]. [Full Text].

  2. Ettinger PO, Wu CF, De La Cruz C, et al. Arrhythmias and the "Holiday Heart": alcohol-associated cardiac rhythm disorders. Am Heart J. 1978 May. 95(5):555-62. [Medline].

  3. Kosior DA, Filipiak KJ, Stolarz P, Opolski G. Paroxysmal atrial fibrillation following marijuana intoxication: a two-case report of possible association. Int J Cardiol. 2001 Apr. 78(2):183-4. [Medline]. [Full Text].

  4. Thornton JR. Atrial fibrillation in healthy non-alcoholic people after an alcoholic binge. Lancet. 1984 Nov 3. 2(8410):1013-5. [Medline].

  5. Koskinen P, Kupari M, Leinonen H, Luomanmaki K. Alcohol and new onset atrial fibrillation: a case-control study of a current series. Br Heart J. 1987 May. 57(5):468-73. [Medline].

  6. Uyarel H, Ozdol C, Gencer AM, Okmen E, Cam N. Acute alcohol intake and QT dispersion in healthy subjects. J Stud Alcohol. Jul 2005. 66:555-8. [Medline].

  7. Laposata EA, Lange LG. Presence of nonoxidative ethanol metabolism in human organs commonly damaged by ethanol abuse. Science. 1986 Jan 31. 231(4737):497-9. [Medline].

  8. Nadareishvili KSh, Meskhishvili II, Kakhiani DD, Ormrtsadze GL, Khvedelidze MT, Chitanava ET. Effects of low ethanol doses on heart rhythm in rabbits. Bull Exp Biol Med. Sept 2004. 138:271-5. [Medline]. [Full Text].

  9. Fenelon G, Balbao CE, Fernandes R, et al. Characterization of the acute cardiac electrophysiologic effects of ethanol in dogs. Alcohol Clin Exp Res. 2007 Sep. 31(9):1574-80. [Medline].

  10. Romani AM. Effect of acute and prolonged alcohol administration on Mg(2+) homeostasis in cardiac cells. Alcohol. 2015 May. 49 (3):265-73. [Medline].

  11. Nguyen H, Romani A. Effect of Alcohol Administration on Mg2+ Homeostasis in H9C2 Cells. J Cardiovasc Dis Diagn. 2014 Oct 23. 2 (6):179. [Medline].

  12. Aasebo W, Erikssen J, Jonsbu J, Stavem K. ECG changes in patients with acute ethanol intoxication. Scand Cardiovasc J. Apr 2007. 41:79-84. [Medline]. [Full Text].

  13. Greenspon AJ, Schaal SF. The "holiday heart": electrophysiologic studies of alcohol effects in alcoholics. Ann Intern Med. 1983 Feb. 98(2):135-9. [Medline].

  14. Lowenstein SR, Gabow PA, Cramer J, et al. The role of alcohol in new-onset atrial fibrillation. Arch Intern Med. 1983 Oct. 143(10):1882-5. [Medline].

 
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