Epinephrine-induced reversal of verapamil's electrophysiologic and therapeutic effects in patients with paroxysmal supraventricular tachycardia.

Abstract

The purpose of our study was to determine whether an infusion of epinephrine reverses the electrophysiologic effects of verapamil and whether reversal of verapamil's effects on the induction of paroxysmal supraventricular tachycardia (PSVT) by epinephrine during electropharmacologic testing is predictive of stress-related recurrences of PSVT during long-term treatment with verapamil. The infusion rates of epinephrine used in this study were 25 and 50 ng/kg/min, which previously have been demonstrated to result in plasma epinephrine concentrations in the range that occurs during a variety of stresses in humans. The subjects of this study were 17 patients with recurrent PSVT who underwent an electrophysiologic study in the control state and after at least 2 days of treatment with 240-480 mg/day verapamil. After assessing the response to verapamil, epinephrine was infused and testing was repeated. Verapamil significantly slowed atrioventricular conduction and prolonged refractoriness in the atrium and atrioventricular node. The effects of the two infusion rates of epinephrine were generally similar in magnitude and, therefore, the results were pooled. Epinephrine partially or completely reversed all of verapamil's electrophysiologic effects. Verapamil suppressed the induction of sustained PSVT in 15 patients. Epinephrine facilitated the induction of PSVT in seven of these 15 patients. All 15 patients were treated on a long-term basis with verapamil. The eight patients in whom epinephrine did not facilitate the induction of PSVT had no recurrences of PSVT during 9-18 months of follow-up. In contrast, there were multiple recurrences of PSVT in six of the seven patients in whom epinephrine had facilitated the induction of PSVT, and in five of these patients the episodes of PSVT occurred exclusively during exertion or emotional stress. These five patients then were treated with verapamil and 50 mg/day atenolol. Three patients could not tolerate this combination; however, the remaining two patients had no further recurrences of PSVT. In conclusion, physiologic doses of epinephrine attenuate the electrophysiologic effects of verapamil and may reverse verapamil's effects on the induction of PSVT during electropharmacologic testing. Reversal by epinephrine of verapamil's effects on the induction of PSVT may accurately identify patients who are likely to experience stressrelated recurrences of PSVT and who may benefit from treatment with a f-blocker during long-term therapy with verapamil. (Circulation 1989;79:783-790) A physiologic increase in circulating epinephrine has been demonstrated to shorten atrial and atrioventricular (AV) nodal refractoriness and to accelerate AV nodal From

Effects of Isoproterenol and Amiodarone on the Double Potential Interval After Ablation of the Cavotricuspid Isthmus

“…Sympathetic activation by isoproterenol or epinephrine has been demonstrated to reverse the pharmacologic effects of several antiarrhythmic drugs, including verapamil, quinidine, procainamide, and flecainide 8–13 . Because amiodarone is a β‐adrenergic antagonist, 14 its electrophysiologic effects in the ventricle have been found to be more resistant to sympathetic activation than the effects of other drugs 15,16 .…”