ELECTROPHYSIOLOGIC EFFECTS OF A CLASS-I ANTIARRHYTHMIC AGENT, CIBENZOLINE, ON THE REFRACTORINESS AND CONDUCTION OF THE HUMAN ATRIUM IN-VIVO

We investigated the effects of a class I antiarrhythmic drug, cibenzol ine, on human atrial muscle in vivo. Electrophysiologic measurements w ere performed in 44 patients (mean age 49 +/- 15 years), before and af ter an intravenous infusion of cibenzoline 1.4 mg/kg in 5 min. Extrast imuli at a basic cycle length (BCL) of 500 ms were delivered from the right atrial appendage. The effective refractory period of the right a trium (ERP-A), the conduction time from the high right atrium to the c oronary sinus, maximum conduction delay (Max, CD), repetitive atrial f iring zone (RAFZ), fragmented atrial activity zone (FAAZ), and conduct ion delay zone (CDZ) were measured. Patients were divided into two gro ups according to whether repetitive atrial firing (RAF) was induced (g roup A, n = 18) or not (group B, n = 26). Cibenzoline increased ERP-A from 198 +/- 25 to 214 +/- 26 ms (p < 0.05) and decreased Max. CD from 55 +/- 23 to 43 +/- 19 ms (p < 0.05). There were significant decrease s in the RAFZ (10 +/- 17 to 4 +/- 10 ms, p < 0.05), the FAAZ (20 +/- 2 5 to 12 +/- 18, ms p < 0.05), and the CDZ (41 +/- 21 to 32 +/- 19 ms, p < 0.05). Cibenzoline significantly increased ERP-A (186 +/- 25 to 21 2 +/- 26 ms, p < 0.05) in group A, but not in group B. There were sign ificant decreases in the RAFZ [25 +/- 19 to 9 +/- 15 ms (p < 0.05) and FAAZ 22 +/- 29 to 11 +/- 21 ms, (p < 0.05)] in group A, but not in gr oup B. The results suggest that cibenzoline can suppress paroxysmal at rial fibrillation by prolongation of ERP-A and may also have preferent ial effects on the substrate of atrial fibrillation and RAF.