Electrophysiologic effects of procainamide on sinus function in patients with and without sinus node disease.

To compare the effects of procainamide on sinus node (SN) function in the presence (seven patients) and absence (nine patients) of SN dysfunction, sinus cycle length (SCL), maximal corrected sinus recovery time (maximal CRST), paced cycle length yielding peak SN suppression (PCLp), and indirect sinoatrial conduction time (SACT) were determined before and after intravenous administration of 10 to 15 mg/kg procainamide in each patient. Plasma procainamide concentration was in the therapeutic range in all patients. The mean SCL did not change significantly in either group (-24 +/- 58 and -73 +/- 171 msec for patients with normal and abnormal SN function, respectively). The maximal CSRT shortened 136 +/- 112 msec (p less than 0.01) in the group with normal SN function (nine of nine patients)( but tended to lengthen 85 +/- 95 msec (p less than 0.10) in the group with SN dysfunction (six of seven patients). PCLp shortened in only two of nine of the normal group but tended (NS) to shorten in five of seven patients with SN dysfunction. We conclude that in the absence of SN disease, procainamide does not adversely affect SN function. In apparent contrast in patients with SN dysfunction, procainamide tended (NS) to prolong CSRT and seemed (NS) to enhance conduction in the sinoatrial junction (PCLp and SACT both declined). The occasional lengthening of CSRT implies that procainamide might prolong post-tachycardia pauses and thus could worsen symptoms in certain patients with the bradycardia-tachycardia syndrome.