The association of alcohol abuse, especially binge drinking, and atrial fibrillation, recently termed "holiday heart," has been recognized for some time. The effects of alcohol on atrial fibrillation, however, have not been studied. Accordingly, measurements of hemodynamics and duration of electrically induced atrial fibrillation were made in alpha-chloralose anesthetized dogs during the 30 min before and during a 30-min intravenous infusion of 1.7 g/kg of ethanol (25%, v/v), which produced an average infusion concentration of 254 +/- 21 mg/dl. Average cardiac output, left ventricular (LV) peak dp/dt, and pulmonary artery mean pressure did not change, whereas LV systolic (116 +/- 8 to 107 +/- 9 mm Hg, p less than 0.05) and aortic mean (95 +/- 7 to 87 +/- 9 mmHg, p less than 0.05) pressures decreased. Heart rate and atrioventricular conduction in sinus rhythm, and atrial and ventricular activity in atrial fibrillation also did not change. Despite a decrease in arterial pH, duration of atrial fibrillation decreased (356 +/- 143 to 93 +/- 38 sec, p less than 0.05). Moreover, at 15 min, when average ethanol concentration was 208 +/- 20 mg/dl, and aortic mean pressure (95 +/- 7 to 85 +/- 8 mm Hg, p less than 0.05), pulmonary artery mean pressure (16 +/- 2 to 14 +/- 2 mm Hg, p less than 0.05), and LV peak dp/dt (1563 +/- 143 to 1285 +/- 167 mm Hg-sec-1, p less than 0.05) were reduced, duration of atrial fibrillation was less than control (356 +/- 143 to 114 +/- 56 sec, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Although the inotropic and dromotropic effects of cardiac glycosides in atrial fibrillation (AF) are well recognized, their action on AF itself is not clear. Accordingly, to determine whether cardiac glycosides prolong AF, the duration of electrically induced AF, atrioventricular conduction, and left ventricular function were assessed for 30 minutes before and for 30 minutes following intravenous administration of acetyl strophanthidin (AS), 20 micrograms/kg, in neurally intact, beta-blocked, and beta-blocked and vagotomized dogs. In the intact dog, AS, 20 micrograms/kg, increased peak dp/dt by 132 +/- 35 mmHg.sec-1, p less than 0.05, and slowed ventricular response by 16 +/- 7 min-1, p less than 0.05, but had a variable effect on AF duration. While the increased left ventricular peak dp/dt persisted for 15 minutes after AS, an increased duration of AF was evident only at 20 minutes, when the effects of AS on left ventricular (LV) inotropy were no longer apparent. Moreover, the subset of dogs that did not demonstrate prolongation of average duration of AF after AS had a greater increment of peak dp/dt than those that showed prolongation, 237 +/- 52 versus 53 +/- 31 mmHg.sec-1, p less than 0.05. An additional 20 micrograms/kg, which produced ventricular extrasystoles, prolonged AF duration when compared to both control and 30-minute measurements. Acetyl strophanthidin, 20 micrograms/kg, had a variable effect on duration of AF with beta-blockade but prolonged duration by 114 +/- 34%, p less than 0.05, with both vagotomy and beta-blockade.(ABSTRACT TRUNCATED AT 250 WORDS)