DISCREPANT EFFECTS OF MEXILETINE ON CYCLE LENGTH OF VENTRICULAR-TACHYCARDIA AND ON THE EFFECTIVE REFRACTORY PERIOD IN THE AREA OF SLOW CONDUCTION

Objective-Monomorphic sustained ventricular tachycardia (VT) can often be entrained and interrupted at a critical paced cycle length. The ai m was to evaluate a possible determinant of this phenomenon by observi ng the action of mexiletine on the critical paced cycle length and oth er variables. Methods-Nine consecutive patients with symptomatic VT we re studied. After induction of VT, the area of slow conduction was map ped as the earliest site of the activation or the site with mid-diasto lic potential during the tachycardia. Rapid pacing was performed at a site distant from the tachycardia circuit to entrain the tachycardia, starting at a cycle length 10-20 ms shorter than the VT cycle length, and repeated after a decrement of the cycle length in steps of 10 ms t o obtain the longest paced cycle length that interrupted the tachycard ia: the block cycle length. The effective refractory period (ERP) was measured at the pacing site at which the myocardium was presumed to be normal and also in the area of slow conduction. The effects of mexile tine on the cycle length of VT, the block cycle length, and the ERP at two sites were obtained before and after mexiletine administration. T he relation between the cycle length of VT and block cycle length and their changes were also analysed. Results-11 VTs with the same morphol ogy were induced before and after mexiletine administration. The VT cy cle length was prolonged by mexiletine from 309 (SD 53) to 361 (47) ms , and it was interrupted at block cycle lengths of 247 (37) and 307 (4 1) ms, respectively, the changes being 18 (12)% and 23 (8)% (both P < 0.001). All VTs were entrained, and during pacing at the block cycle l ength there was abrupt loss of fusion and change in the presystolic el ectrogram, always associated with interruption of VT on cessation of r apid pacing. A good correlation was observed between the VT cycle leng th and the block cycle length (r = 0.77 to 0.80). The ERP at the pacin g site (normal myocardium) and in the area of slow conduction showed n o significant change: 241 (21) v 240 (22) ms and 262 (9) v 252 (9) ms, respectively. The block cycle length was longer than the ERP after me xiletine administration: 362 (55) v 252 (9) ms (P < 0.02). Conclusions -Mexiletine prolonged the cycle length of VT and the VT-interrupting c ritical cycle length but not the ERP. The prolongation of the VT cycle length and the block cycle length by mexiletine seemed to be unrelate d to the action potential duration, but related to depressed intercell ular conduction.