Changes in spontaneous sinus node rate as an estimate of cardiac autonomic tone during stable and unstable ventricular tachycardia

Abstract

Changes in sinus node rate were measured as an estimate of reflex control of cardiac autonomic tone during 32 episodes of stable ventricular tachycardia (without loss of consciousness) and 21 episodes of unstable ventricular tachycardia (loss of consciousness requiring electrical cardioversion) in 32 patients without retrograde ventriculoatrial conduction. Sinus node rate was measured before induction of ventricular tachycardia (at 5 s intervals during tachycardia) and 5 s after termination of ventricular tachycardia. It increased from 85 ± 12 beats/min to a maximum of 109 ± 25 beats/min during stable ventricular tachycardia (p < 0.001) and from 82 ± 15 beats/min to a maximum of 105 ± 34 beats/min during unstable ventricular tachycardia (p < 0.001).During unstable ventricular tachycardia, the increase in sinus rate was more abrupt and was followed by a sharp decrease beginning before termination of the tachycardia and resulting in a slower rate after termination (56 ± 15 beats/min) than before tachycardia (p < 0.001). Stable ventricular tachycardia resulted in a continuous increase of sinus node rate, which remained higher after termination (102 ± 15 beats/min) than before tachycardia (p < 0.001). Autonomic mechanisms responsible for changes in sinus rate were evaluated by reinducing the ventricular tachycardia after beta-adrenergic blockade by propranolol in 10 patients. Intravenous propranolol (mean dose 11 ± 4 mg) had no effect on the magnitude of increase in sinus rate (+18 ± 6 beats/min before and +17 ± 7 beats/min after propranolol).It is concluded that 1) induced ventricular tachycardia is accompanied by an increase in sinus node rate, which is not altered by beta-blockade, suggesting that sympathetic activation is not a predominant mechanism; and 2) changes in sinus node rate are different during stable and unstable ventricular tachycardia. The latter differences may be due to differences in the autonomic reflexes elicited by the two arrhythmias.