α-2 adrenergic antagonism enhances risk of ventricular tachycardia during acute ischemia

Abstract

Objective. In this study we tested the hypothesis that α-2 adrenergic antagonism could facilitate induction of previously non-inducible ventricular tachycardia (VT) during acute ischemia. Previous reports suggest that VT during ischemia may be modulated by α-2 adrenergic agonists. Design. The left anterior descending artery was occluded after instrumentation of the ischemic risk zone with 21 multipolar plunge needles, each recording 6 bipolar electrograms. Three dimensional mapping characterized the mechanism of VT induced with extrastimuli. Results. Of 16 non-inducible dogs included, eight which were given the α-2 adrenergic antagonist yohimbine all had inducible VT, while all eight in the control group remained non-inducible (p <0.05). Six of the VTs were of focal Purkinje origin. The cycle length of the VT was 119±4 ms. Mean arterial pressure (81±8 to 82±8 mmHg, p =ns), ventricular effective refractory period (146±6 to 144±5 ms, p =ns) and ischemic zone size (55±6% vs. 61±4%, p =0.45) were not altered by yohimbine indicating minimal central or pre-junctional effects of the drug. Conclusions. Yohimbine facilitates induction of VT, especially those with focal Purkinje fiber origin, suggestive of an effect mediated through antagonism of post-junctional α-2 adrenoceptors on Purkinje fibers.