Effects of procainamide on strength-interval relations in normal and chronically infarcted canine myocardium

Abstract

The effects of procainamide on strength-interval relations in normal and chronically infarcted canine myocardium were determined in nine adult mongrel dogs susceptible to sustained ventricular tachyarrhythmias. The dogs were studied at 3 to 30 days after two stage occlusion and reperfusion of the mid left anterior descending coronary artery. Unipolar cathodal stimulation (pulse duration 2 ms, drive cycle length 300 ms) was used to evaluate excitability and refractoriness at a total of 19 normal and 22 infarct sites both before and 15 to 30 minutes after intravenous infusion of procainamide, 20 to 25 mg/kg body weight. The electrophysiologic effects of procainamide were evaluated at the time of the plateau phase of procainamide's antiarrhythmic activity in this model. At normal sites, procainamide had only a minimal effect on the mean diastolic excitability threshold (increased from a mean [± standard deviation]of 0.07 ± 0.02 to 0.08 ± 0.02 mA [probability (p) = not significant (NS)], the mean effective refractory period (increased from 137 ± 10 to 139 ± 11 ms [p = NS]) and the mean ventricular refractory period at twice diastolic threshold (increased from 156 ± 12 to 163 ± 16 ms [p <0.01]). At infarct sites, the mean diastolic excitability threshold was similarly unchanged after procainamide (from 0.57 ± 1.13 to 0.57 ± 1.09 mA [p = NS]), but both the mean effective refractory period (from 142 ± 17 to 159 ± 27 ms [p <0.001]) and the mean ventricular refractory period at twice diastolic threshold (from 166 ± 25 to 187 ± 33 ms [p <0.001]) were moderately prolonged. In addition, dispersion of refractoriness between normal and infarct sites as well as within areas of infarcted myocardium was often either unchanged or increased rather than decreased by procainamide. Thus, the antiarrhythmic activity of procainamide in this canine model of chronic myocardial infarction was not explained by an effect on the excitability or refractoriness of normal myocardium, by changes in the diastolic excitability of infarcted tissue or by an effect on the dispersion of refractoriness. The most prominent effect of procainamide was to decrease the excitability of abnormal myocardium during the relative refractory period and to prolong the refractoriness of abnormal myocardium.