Author + information
- Received February 15, 1996
- Revision received July 11, 1996
- Accepted August 13, 1996
- Published online December 1, 1996.
- Yoshifusa Aizawa, MD⁎,
- Akira Abe, MD,
- Kohji Ohira, MD,
- Hiroshi Furushima, MD,
- Masaomi Chinushi, MD and
- Satoshi Fujita, MD
- ↵⁎Address for correspondence: Dr. Yoshifusa Aizawa, The First Department of Internal Medicine, Asahimachi-dori, Niigata, 951 Japan.
Objectives The action of mexiletine on diseased myocardium was assessed in reentrant ventricular tachycardia (VT).
Background Whether class Ib antiarrhythmic agents exert a preferential action on the central common pathway of reentrant ventricular tachycardia has not yet been studied in humans.
Methods In 10 consecutive patients (7 with a previous myocardial infarction, 3 with nonischemic disease), VT was induced and entrained with rapid pacing. The orthodromic conduction time was measured from stimulus to the entrained electrogram at the exit from the presumed central common pathway (i.e., the earliest site of activation). Mexiletine at 125 to 250 mg was administered intravenously, and when VT 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. The effects on QRS complex duration, local conduction time between the exit and the pacing site and duration of the local electrogram were compared between normal and diseased myocardium.
Results Mexiletine prolonged the VT cycle length in all patients, from (mean ± SD) 316 ± 30 to 360 ± 64 ms (mean change 20 ± 7%, p < 0.001); during entrainment of VT, the orthodromic conduction time was prolonged, from 306 ± 58 to 367 ± 89 ms (mean change 18 ± 9%, p < 0.001). These changes were highly correlated (r = 0.95, p < 0.001). QRS duration changed little (4 ± 3%), and local conduction time showed no change. The duration 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 period, both at the pacing site and at the exit.
Conclusions Mexiletine caused little change in conduction time in normal myocardium but prolonged VT cycle length, ortho-dromic conduction time and duration of the local electrogram at the earliest site of activation of VT. From these findings, a preferential action of mexiletine on diseased myocardium was suggested but seemed to occur only at higher frequencies during tachycardia.
This work was supported by a grant for “Sudden Death in Adults” and a grant for “Application and Evaluation of Nonpharmacological Therapy in Arrhythmias,” both from the Health and Welfare Ministry, Tokyo and Nakatani Electronic Measuring Technology, Tokyo, Japan.
- Received February 15, 1996.
- Revision received July 11, 1996.
- Accepted August 13, 1996.
- American College of Cardiology