What is the pathophysiology of alcohol arrhythmia in holiday heart syndrome (HHS)?

Updated: May 30, 2018
  • Author: Lawrence Rosenthal, MD, PhD, FACC, FHRS; Chief Editor: Jose M Dizon, MD  more...
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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.

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