Medicine, via pristina

Medicine, via pristina

Holiday Heart Syndrome 

1. Knuuti J, Wijns W, Saraste A, Capodanno D, Barbato E, Funck-Brentano C, et al. 2019 ESC Guidelines for the diagnosis and management of chronic coronary syndromes. Eur Heart J. 2020;41(3):407-477.
PMID: 31504439
DOI: https://doi.org/10.1093/eurheartj/ehz425


2. Fihn SD, Gardin JM, Abrams J, Berra K, Blankenship JC, Dallas AP, et al. 2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS guideline for the diagnosis and management of patients with stable ischemic heart disease. J Am Coll Cardiol. 2012;60(24):e44-e164.
PMID: 23182125
DOI: https://doi.org/10.1016/j.jacc.2012.07.013


3. Khan MA, Hashim MJ, Mustafa H, Baniyas MY, Al Suwaidi SKBM, AlKatheeri R, et al. Global epidemiology of ischemic heart disease: Results from the Global Burden of Disease Study. Cureus. 2020;12(7):e9349.
PMID: 32742886
DOI: 10.7759/cureus.9349


4. Ibanez B, James S, Agewall S, Antunes MJ, Bucciarelli-Ducci C, Bueno H, et al. 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. Eur Heart J. 2018;39(2):119-177.
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5. Amsterdam EA, Wenger NK, Brindis RG, Casey DE Jr, Ganiats TG, Holmes DR Jr, et al. 2014 AHA/ACC guideline for the management of patients with non–ST-elevation acute coronary syndromes. J Am Coll Cardiol. 2014;64(24):e139-e228.
PMID: 25260716
DOI: https://doi.org/10.1016/j.jacc.2014.09.017

Background 

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. 

 

Classification/Types 

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). 

 

Pathophysiology 

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. 

 

Epidemiology 

  • 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. 

 


Etiology
 

I) Primary Causes: 

  • Binge drinking (defined as >5 drinks in men or >4 in women on a single occasion). 

  • Excessive alcohol consumption over weekends or holidays. 


II) Contributing Factors:
 

  • Sleep deprivation 

  • Emotional stress 

  • Heavy meals 

  • Stimulant use (e.g., nicotine, caffeine) 

  • Underlying predisposition to arrhythmias (e.g., subtle conduction abnormalities) 

 


Clinical Presentation
 

I) History (Symptoms): 

  • Sudden-onset palpitations 

  • Lightheadedness, dizziness 

  • Dyspnea or chest tightness 

  • Fatigue 

  • History of heavy drinking within 24–72 hours 


II) Physical Exam (Signs):
 

  • Irregularly irregular rhythm (classic for AF) 

  • Tachycardia 

  • Normal or slightly elevated blood pressure 

  • Absence of structural heart findings on exam 

 


Differential Diagnosis (DDx)
 

  • 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) 

 


Diagnostic Tests
 

Initial Work-Up: 

  • 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. 


Advanced Testing:
 

  • Holter Monitor: For frequent palpitations or recurrent AF episodes. 

  • Event Monitor: For infrequent, unexplained symptoms. 

  • Toxicology screen: In selected cases with suspected polysubstance use. 

 


Treatment
 

I) Acute Management: 

  • 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. 


II) Chronic Management:
 

  • 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. 

 

Medications 

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 

 

Device Therapy 

  • 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. 

 


Patient Education, Screening, Vaccines
 

  • Educate on the arrhythmogenic potential of binge drinking

  • Encourage alcohol moderation or abstinence
  • Emphasize hydration and electrolyte balance

  • Screen for coexisting conditions (e.g., hypertension, OSA). 

  • Recommend influenza and pneumococcal vaccines for cardiac risk patients. 

 


Consults/Referrals
 

  • 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. 

 


Follow-Up
 

Short-Term: 

  • Reassess within 1–2 weeks post-episode. 

  • Holter or event monitoring if recurrence suspected. 

  • Monitor response to lifestyle changes and medical therapy. 


Long-Term:
 

  • Prevent recurrence with sustained alcohol avoidance. 

  • Evaluate for underlying cardiac conditions if episodes persist. 

  • Consider annual ECG and periodic rhythm monitoring. 

 

Prognosis 

  • 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. 

 

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