Vulnerability to atrial fibrillation and flutter was examined in 11 alcohol abusers who did not have cardiomyopathy or manifest heart failure. Atrial extrastimulation was done with rapid pacing (drive cycle length 500 ms) to facilitate induction of atrial vulnerability, seen in four alcohol abusers. The remaining seven were retested 30 minutes after drinking 60 to 120 ml of 86 proof whiskey (ethanol blood levels were 49 to 101 mg/100 ml but pulmonary capillary wedge pressure remained normal in all) and atrial fibrillation or flutter was induced in three of the drinkers. Three nondrinkers, symptomatic with sinus bradycardia but not in heart failure, were found not to be vulnerable to atrial fibrillation or flutter, but flutter was induced in two of the three after drinking whiskey. Whiskey did not alter atrial functional refractory periods (mean +/- standard error of the mean 297 +/- 14 to 290 +/- 12 ms) or widen the dispersion among three disparate right atrial sites (57 +/- 13 to 47 +/- 12 ms). Thus, whiskey enhanced vulnerability to atrial fibrillation and flutter in patients without heart failure or cardiomyopathy, substantiating the "holiday heart" syndrome.

SUMMARY Abnormal atrial refractoriness was examined as a cause of atrial fibrillation/flutter (AFF) in patients with bradycardia. Refractory periods at three disparate right atrial sites were compared in 17 patients with sinus node dysfunction (SND) and 16 controls. Atrial pacing shortened refractory periods, but failed to decrease dispersion of refractoriness significantly. During sinus rhythm, duration and dispersion of refractoriness were greater in SND patients than in controls. These differences persisted with atrial pacing. For example, at the paced rate, dispersion of effective refractory periods in SND patients was greater than in controls (62.9 ± 34 vs 36.6 ± 21 msec,p < 0.01). Six SND patients had AFF, but they did not have greater dispersion than other SND patients, or unusually short or long refractory periods. Thus, prolonged and nonuniform refractoriness were features of SND. Abnormal refractoriness in SND reflected atrial disease and persisted with pacing. These abnormalities were not unique to patients with AFF.EARLY ATRIAL EXTRASYSTOLES are critical to the initiation of atrial fibrillation and flutter (AFF).1, 2 According to one theory, AFF results from nonuniform recovery of excitability3 4 and nonhomogeheous spread of the early excitation.5 Thus, AFF results when there is dispersion of atrial refractoriness. Because slower heart rates have been shown to increase the normal dispersion of canine atrial refractoriness,6 bradycardia should predispose to ectopic atrial rhythms.7 A clinical model of this theory would be the bradycardia-tachycardia sequences in some patients with sinus node dysfunction (SND).6 9 HIowever, faster heart rates curtail atrial refractoriness in man, exposing the vulnerable zone to excitation.'0 Thus, vulnerability to AFF from early extrasystoles could reflect a shortened refractory period rather than dispersion of refractory periods. Alternative explanations for atrial tachycardias include enhanced automaticity or tachycardias triggered from afterpotentials." These mechanisms suggest that faster, not slower heart rates, predispose to AFF.In this investigation we assess atrial refractoriness in patients with SND to delineate the role of bradycardia in determining dispersion of refractoriness and arrhythmia in man. In this preliminary investigation, measurements were limited to the right atrium of patients without obvious hemodynamic abnormalities.

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