Abstract
For many years it has been recognized that sympathetic nervous stimulation can influence the development of cardiac arrhythmias in both normal and abnormal hearts, during ischemic and nonischemic states, and that β-adrenergic—receptor blockade or surgical interruption of the stellate ganglia can prevent these arrhythmias. The mechanism by which the autonomic nervous system precipitates or prevents the arrhythmias is not known. In this issue of the Journal, Meredith et al.1 provide information about the association between sympathetic stimulation and ventricular arrhythmias, demonstrating an almost fivefold increase in cardiac norepinephrine spillover in patients with reduced left ventricular function who had had . . .