کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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2969376 | 1178907 | 2006 | 5 صفحه PDF | دانلود رایگان |

IntroductionThere is widespread belief that caffeine consumption is linked to atrial arrhythmias; however, there is a relative lack of systematic evidence to support the assertion. The purpose of this study was to investigate whether caffeine, in doses equivalent to daily use in the general population, alter the propensity for atrial fibrillation (AF) in an experimental model comparing normal and simulated predisposition to AF.Methods and MaterialCaffeine (caffeine Na benzoate, 50:50 mixture) was administered intravenously at 1, 3, and 5 mg/kg doses in dogs producing serum levels of 2 to 4, 5 to 7, and 8 to 10 μg/mL. To simulate focal AF, premature stimulation from the right superior pulmonary vein was delivered at 2×, 4×, and 10× threshold at a rate of 180/min (S1-S2 = 330 milliseconds) without and then with low-level stimulation of ganglionated plexi (GP) at the entrance of the right superior pulmonary vein. The window of vulnerability (WOV), a measure of the propensity for AF inducibility, was determined by the longest coupling interval of the premature beat (S1-S2) minus the shortest S1-S2, which induced AF. The cumulative WOV is the sum of the individually determined WOV.ResultsAt each serum level of caffeine, the cumulative WOV was lower without rather than with GP stimulation compared with control. The cumulative WOV for both the stimulated, that is, predisposed to AF, and nonstimulated, that is, normal groups, exhibited a significantly lower average as compared with that exhibited by the control group (P ≤ .003-.02).ConclusionThese findings suggest that the presence of caffeine may result in an unexpected reduction in the propensity for AF in healthy individuals and in those with a predisposition for AF (enhanced AF inducibility caused by the stimulation of the GP).
Journal: Journal of Electrocardiology - Volume 39, Issue 4, October 2006, Pages 421–425