Differential response to right and left ansae subclaviae stimulation of early afterdepolarizations and ventricular tachycardia induced by cesium in dogs.

Abstract

Early afterdepolarizations (EADs) are depolarizing potentials that occur before complete repolarization. They may be important in the acquired and possibly the idiopathic long QT syndrome and associated ventricular tachycardia (VT). The purpose of these experiments was to study in 20 open-chest dogs the effects of sympathetic stimulation on EADs and VT produced with cesium chloride (84 mg/kg i.v.) alone or combined with left (LAS), right (RAS), or bilateral (BAS) ansae subclaviae stimulation (2 Hz, 4 msec, 2 mA). We compared the EAD amplitude and area as a percentage of monophasic action potential amplitude and area, respectively, recorded simultaneously with contact electrodes from right (RV) and left ventricular (LV) endocardium and recorded the prevalence of VT induction during each intervention. Both LAS and BAS produced left ventricular EADs with larger amplitudes and areas than did RAS or cesium alone. BAS and LAS produced larger EADs recorded from the LV than from the RV. Cesium produced VT in six of 20 dogs, RAS in three of 20, BAS in 12 of 20, and LAS in 16 of 20. Norepinephrine (0.1-1.5 micrograms/kg/min) caused VT in all dogs by producing a dose-related increase in EAD amplitude that was similar in RV and LV, suggesting that the response of RV and LV EADs to catecholamine stimulation was not intrinsically different. During stimulation of left ansae subclaviae at increasing frequencies (1, 2, 4, and 6 Hz), EADs were significantly larger in LV than in RV at all stimulus frequencies, and the amplitude of EADs in both ventricles increased with increasing stimulus frequencies. Based on the increased LV amplitude and area of cesium chloride-induced EADs during LAS and BAS, with EAD amplitude dependent on the frequency of LAS but with an equal RV and LV EAD amplitude during norepinephrine infusion, it is possible that more norepinephrine released into the LV during LAS and BAS compared with RAS causes larger amplitude LV EADs that reach threshold to cause VT more often. Thus, quantitative differences between the effects of left and right stellate ganglia stimulation rather than qualitative differences or imbalance may account for the arrhythmogenic potential of the left stellate ganglion.