Cocaine abuse has markedly increased over the past decade having reached epidemic levels in Western countries [1][2][3][4] . Cocaine intoxication is associated with a significant morbidity and mortality and is a frequent cause of drug-related sudden death 2,3 . Most evidence suggests that cocaineinduced sudden death results from its cardiovascular consequences, particularly ventricular arrhythmias 1 . However, the mechanisms involved in the genesis of these arrhythmias remain incompletely understood. Although cocaineinduced arrhythmias may be associated with myocardial ischemia or infarction 3,5 , cocaine may be arrhythmogenic in the absence of an ischemic event 1 . In addition to its powerful indirect sympathomimetic actions 1-4 (promoted by blockade of presynaptic reuptake of norepinephrine and dopamine), high doses of cocaine exert significant local anesthetic effects that could promote conduction disturbances and reentrant arrhythmias 1,3,6,7 . Nevertheless, experimental studies evaluating cocaine's effects on programmed electrical stimulation-induced arrhythmias have had conflicting results, with cocaine either increasing or having a neutral effect on inducibility of ventricular arrhythmias 6,[8][9][10][11] . Further, although supraventricular tachyarrhythmias, including atrial tachycardia, atrial flutter, and atrial fibrillation, can also occur in the setting of cocaine abuse 1,3,[12][13][14] , limited data are is available assessing the impact of the drug on inducibility of atrial arrhythmias.Therefore, we sought to characterize the actions of high plasma concentrations of cocaine on atrial and ventricular electrophysiology and arrhythmia inducibility in a canine preparation with normal hearts. MethodsBeagle dogs (n=12; weight, 9-13 kg) were divided into 2 groups: cocaine (n=8) and sham control (n=4). The study protocol was approved by the research committee of the Objective -To characterize the cardiac electrophysiologic effects of cocaine. Methods -In 8 dogs (9-13 kg), electrophysiologic parameters and programmed stimulation were undertaken using transvenous catheters at baseline, and after cocaine intravenous infusion (12 mg/kg bolus followed by 0.22 mg/ kg/min for 25 minutes).Results -Cocaine plasma levels (n=5) rose to 6.73± 0.56 µg/mL. Cocaine did not affect sinus cycle length and arterial pressure. Cocaine prolonged P wave duration (54±6 vs 73±4 ms, P<0.001), PR interval (115±17 vs 164±15 ms, P<0.001), QRS duration (62±10 vs 88±14 ms, P<0.001), and QTc interval (344±28 vs 403±62 ms, P=0.03) but not JT interval (193±35 vs 226±53 ms, NS). Cocaine prolonged PA (9±6 vs 23±8 ms, P<0.001), AH (73±16 vs 92±15 ms; P=0.03), and HV (35±5 vs 45±3ms; P<0.001) intervals and Wenckebach point (247±26 vs 280±28 ms, P=0.04). An increase occurred in atrial (138±8 vs 184± 20 ms; P<0.001) and ventricular (160±15 vs 187±25 ms; P=0.03)