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Holiday Heart Syndrome (HHS) refers to acute cardiac arrhythmias, most commonly atrial fibrillation (AF), that occur in healthy individuals following binge alcohol consumption, particularly during weekends or holidays. First described in 1978, HHS typically presents in individuals without structural heart disease and resolves with alcohol abstinence. The syndrome underscores the arrhythmogenic effects of acute alcohol ingestion, often unrecognized by patients or providers.
By Rhythm Abnormality:
Paroxysmal Atrial Fibrillation: Most frequent presentation; typically self-limiting.
Atrial Flutter or Supraventricular Tachycardia: Less common.
Ventricular Premature Complexes (PVCs) or Non-sustained Ventricular Tachycardia: Occasionally observed.
By Trigger:
Alcohol-induced: Most classic trigger.
Combined triggers: Alcohol plus dehydration, stress, electrolyte imbalance, or stimulant use (e.g., caffeine, energy drinks).
Acute ethanol ingestion can provoke arrhythmias through several mechanisms:
Direct myocardial irritability due to ethanol and its metabolite acetaldehyde.
Autonomic imbalance, with increased sympathetic and decreased vagal tone.
Electrolyte disturbances, especially hypokalemia and hypomagnesemia.
Volume shifts and dehydration, leading to heightened cardiac excitability.
These changes transiently impair atrial conduction, facilitating the development of atrial fibrillation even in structurally normal hearts.
Most common in young to middle-aged adults without prior cardiac disease.
Increased incidence around holidays (e.g., New Year’s, Christmas, weekends).
Estimated to contribute to holiday-related emergency room visits for AF.
Men are more frequently affected than women.
Binge drinking (defined as >5 drinks in men or >4 in women on a single occasion).
Excessive alcohol consumption over weekends or holidays.
Sleep deprivation
Emotional stress
Heavy meals
Stimulant use (e.g., nicotine, caffeine)
Underlying predisposition to arrhythmias (e.g., subtle conduction abnormalities)
Sudden-onset palpitations
Lightheadedness, dizziness
Dyspnea or chest tightness
Fatigue
History of heavy drinking within 24–72 hours
Irregularly irregular rhythm (classic for AF)
Tachycardia
Normal or slightly elevated blood pressure
Absence of structural heart findings on exam
Paroxysmal AF due to structural heart disease
Hyperthyroidism-induced arrhythmia
Anxiety or panic attacks
Supraventricular tachycardia (SVT)
Sinus tachycardia due to stimulant use
Acute coronary syndrome (ACS)
12-lead ECG: Confirms atrial fibrillation, flutter, or other arrhythmia.
Electrolyte panel, magnesium, phosphorus: Check for alcohol-induced derangements.
Liver function tests: May show transaminitis due to alcohol use.
Thyroid function tests: Rule out thyrotoxicosis as alternative cause.
Echocardiogram: Assess for structural or valvular heart disease.
Holter Monitor: For frequent palpitations or recurrent AF episodes.
Event Monitor: For infrequent, unexplained symptoms.
Toxicology screen: In selected cases with suspected polysubstance use.
Rate control: Beta-blockers (e.g., metoprolol) or nondihydropyridine calcium channel blockers (e.g., diltiazem).
Rhythm control: Electrical or pharmacologic cardioversion if hemodynamically unstable or persistent AF.
Electrolyte correction: Replete potassium and magnesium.
Observation: Many cases spontaneously revert to sinus rhythm within 24–48 hours of alcohol cessation.
Patient counseling: Abstinence from alcohol; avoidance of binge drinking.
Anticoagulation: Based on CHA₂DS₂-VASc score if AF persists or recurs.
Antiarrhythmics: Considered in recurrent cases with EP evaluation.
Lifestyle modifications: Weight loss, blood pressure control, sleep hygiene.
Drug Class | Examples | Notes |
Beta-blockers | Metoprolol, atenolol | First-line for rate control in AF |
CCBs (non-DHP) | Diltiazem, verapamil | Alternative for rate control |
Antiarrhythmics | Flecainide, amiodarone | For rhythm control; use only under EP guidance |
Anticoagulants | DOACs, warfarin | Based on stroke risk in persistent/recurrent AF |
Electrolyte repletion | K⁺, Mg²⁺ | Correct promptly if low to reduce arrhythmia risk |
Holter monitor: For patients with frequent or uncertain episodes.
Event monitor: For rare but symptomatic recurrences.
No permanent device therapy is typically required, unless AF becomes recurrent and symptomatic.
Educate on the arrhythmogenic potential of binge drinking.
Emphasize hydration and electrolyte balance.
Screen for coexisting conditions (e.g., hypertension, OSA).
Recommend influenza and pneumococcal vaccines for cardiac risk patients.
Cardiology: For initial AF evaluation or recurrent episodes.
Electrophysiology: If ablation or antiarrhythmic therapy is being considered.
Addiction Medicine: For patients with alcohol use disorder.
Primary Care: For ongoing lifestyle counseling and cardiovascular risk management.
Reassess within 1–2 weeks post-episode.
Holter or event monitoring if recurrence suspected.
Monitor response to lifestyle changes and medical therapy.
Prevent recurrence with sustained alcohol avoidance.
Evaluate for underlying cardiac conditions if episodes persist.
Consider annual ECG and periodic rhythm monitoring.
Excellent in isolated cases with alcohol abstinence.
High recurrence risk if binge drinking continues.
Increased stroke risk if atrial fibrillation becomes recurrent or chronic.
Early diagnosis and patient education dramatically improve outcomes.
HMD is a beacon of medical education, committed to forging a global network of physicians, medical students, and allied healthcare professionals.