The effects of caffeine on the inducibility of atrial fibrillation
Abdul Rashid, Mujahid Hines, Benjamin J Scherlag, William S Yamanashi, William Lovallo, Abdul Rashid, Mujahid Hines, Benjamin J Scherlag, William S Yamanashi, William Lovallo
Abstract
Introduction: There 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 material: Caffeine (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 microg/mL. To simulate focal AF, premature stimulation from the right superior pulmonary vein was delivered at 2x, 4x, and 10x threshold at a rate of 180/min (S(1)-S(2) = 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 (S(1)-S(2)) minus the shortest S(1)-S(2), which induced AF. The cumulative WOV is the sum of the individually determined WOV.
Results: At 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 <or= .003-.02).
Conclusion: These 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).
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Source: PubMed