Premature Atrial Stimulation for Evaluation of Sinoatrial Conduction in Man

Recent interest in the pathophysiology of sinus node dysfunction has stimulated the development of techniques that would provide a means of quantitating disturbances of sinoatrial conduction and sinus node automati-city in this group of patients [3, 6, 7, 8, 10, 11, 14, 15, 18, 20, 23, 25, 28, 30]. Such information might be useful not only in the understanding of the underlying pathophysiology but might also provide some insight into the mechanism(s) by which cardioactive agents depress sinus node function. A lack of such knowledge undoubtedly contributes to our empiricism in the selection of safe pharmacologic agents for use in these patients. One such example is the effects of digitalis in patients with sick sinus syndrome. Greenwood and Finkelstein in a review of the literature stated that 22% of all reported instances of sinoatrial (SA) block were due to digitalis excess [9]. It would not be unreasonable to assume that digitalis would cause SA block in a large number of patients with sinus node dysfunction, yet, except for the occasional patient with sinus node dysfunction [16], most of these patients tolerate digitalis remarkably well [6]. Another such example relates to the effects of quinidine and procainamide in patients with the bradycardia-tachycardia syndrome. Short reported on the markedly depressant effect of these drugs in his patients [24].