In 17 controls, and 17 patients with sinus nodal dysfunction, an electrophysiologic study was made of sinus nodal function and atrioventricular nodal conduction in the basal state. The study was then repeated in all patients after atropine. The heart rate, mean sinus cycle length, variations of sinus cycle length, sinus node recovery times, sinuatrial conduction time, AH interval, and atrioventricular nodal Wenckebach threshold were significantly different in patients from those of controls. All these parameters changed significantly in patients after atropine, and were comparable to those of controls except for the atrioventricular nodal Wenckebach threshold. Atropine failed to increase the heart rate beyond 90 beats per minute in 10 of 17 patients (sensitivity of 59%) or by at least 30% above the resting heart rate only in 4 of them (sensitivity of 24%). The variations of sinus cycle length, and their standardized value, could detect sinus nodal dysfunction with sensitivities of 59 and 47%, respectively. From our results, we conclude that there is parasympathetic overactivity in patients with sinus nodal dysfunction. Because of their very low sensitivities, the atropine test and variations of sinus cycle length were not useful in identifying sinus nodal dysfunction noninvasively. The normal response of the heart rate to atropine does not exclude sinus nodal dysfunction, but atropine may help to differentiate abnormalities intrinsic and extrinsic to the sinus node during the electrophysiologic study.
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