PREFERENTIAL ACTION OF MEXILETINE ON CENTRAL COMMON PATHWAY OF REENTRANT VENTRICULAR-TACHYCARDIA

Citation
Y. Aizawa et al., PREFERENTIAL ACTION OF MEXILETINE ON CENTRAL COMMON PATHWAY OF REENTRANT VENTRICULAR-TACHYCARDIA, Journal of the American College of Cardiology, 28(7), 1996, pp. 1759-1764
Citations number
25
Categorie Soggetti
Cardiac & Cardiovascular System
ISSN journal
07351097
Volume
28
Issue
7
Year of publication
1996
Pages
1759 - 1764
Database
ISI
SICI code
0735-1097(1996)28:7<1759:PAOMOC>2.0.ZU;2-D
Abstract
Objectives. The action of mexiletine on diseased myocardium was assess ed in reentrant ventricular tachycardia (VT). Background. Whether clas s Ib antiarrhythmic agents exert a preferential action on the central common pathway of reentrant ventricular tachycardia has not yet been s tudied in humans. Methods. In 10 consecutive patients (7 with a previo us myocardial infarction, 3 with nonischemic disease), VT was induced and entrained with rapid pacing. The orthodromic conduction time was m easured from stimulus to the entrained electrogram at the exit from th e presumed central common pathway (i.e., the earliest site of activati on). Mexiletine at 125 to 250 mg was administered intravenously, and w hen VI with the same configuration was induced, the study was repeated . The action of mexiletine on the central common pathway was assessed from the changes in VT cycle length and orthodromic conduction time. T he effects on QRS complex duration, local conduction time between the exit and the pacing site and duration of the local electrogram were co mpared between normal and diseased myocardium. Results. Mexiletine pro longed the VT cycle length in all patients, from (mean +/- SD) 316 +/- 30 to 360 +/- 64 ms (mean change 20 +/- 7%, p < 0.001); during entrai nment of VT, the orthodromic conduction time was prolonged, from 306 /- 58 to 367 +/- 89 ms (mean change 18 +/- 9%, p < 0.001). These chang es were highly correlated (r = 0.95, p < 0.001). QRS duration changed little (4 +/- 3%), and local conduction time showed no change. The dur ation of the fragmented electrogram width was prolonged by mexiletine: from 146 +/- 50 to 176 +/- 56 ms (mean change 23 +/- 8%, during VT, p < 0.001). Only a slight change occurred in the effective refractory p eriod, both at the pacing site and at the exit. Conclusions. Mexiletin e caused little change in conduction time in normal myocardium but pro longed VT cycle length, orthodromic conduction time and duration of th e local electrogram at the earliest site of activation of VT. From the se findings, a preferential action of mexiletine on diseased myocardiu m was suggested but seemed to occur only at higher frequencies during tachycardia. (C) 1996 by the American College of Cardiology