Effects of procainamide on refractoriness, conduction, and excitable gap in canine atrial reentrant tachycardia.

The effects of procainamide were studied in a model of atrial flutter around the tricuspid valve in seven open chest, chloralose-anesthetized dogs (31 +/- 3 kg). A Y-shaped incision in the intercaval area extending to the right atrial appendage was made and five bipolar electrodes were sutured on the atrial epicardium around the tricuspid valve. Reentry tachycardia was induced in the absence and presence of drug by burst pacing. Procainamide (15 mg/kg bolus followed by 0.075 mg/kg/min infusion) produced stable plasma levels (38 +/- 9 microM) during the study. At a pacing cycle length of 200 msec, mean (+/- SD) diastolic threshold at the five sites increased from 1.6 +/- 1.5 to 2.0 +/- 1.7 mA and mean atrial effective refractory period from 125 +/- 9 to 140 +/- 16 msec on drug (P less than 0.05). Procainamide prolonged the cycle length of atrial flutter from 144 +/- 10 to 160 +/- 13 msec and slowed conduction velocity during atrial flutter around the tricuspid valve from 73 +/- 6 to 66 +/- 6 cm/sec (P less than 0.05). A reset response curve was determined by introducing premature stimuli during atrial flutter. Procainamide prolonged effective refractory period during atrial flutter from 101 +/- 13 to 116 +/- 17 msec but did not change the duration of the excitable gap (38 +/- 9 vs 40 +/- 18 msec). Although the reset response curve was predominantly increasing, in six of seven experiments there was present a flat portion at long coupling intervals approaching the atrial flutter cycle length that comprised 23% +/- 10% of the excitable gap.(ABSTRACT TRUNCATED AT 250 WORDS)