EFFECTS OF A CLASS-III ANTIARRHYTHMIC DRUG AND BIPHASIC SHOCKS ON THEPOSTDEFIBRILLATION REFRACTORY PERIOD OF RELATIVELY REFRACTORY MYOCARDIUM

Citation
Y. Murakawa et al., EFFECTS OF A CLASS-III ANTIARRHYTHMIC DRUG AND BIPHASIC SHOCKS ON THEPOSTDEFIBRILLATION REFRACTORY PERIOD OF RELATIVELY REFRACTORY MYOCARDIUM, Journal of cardiovascular electrophysiology, 7(7), 1996, pp. 603-611
Citations number
38
Categorie Soggetti
Cardiac & Cardiovascular System
ISSN journal
10453873
Volume
7
Issue
7
Year of publication
1996
Pages
603 - 611
Database
ISI
SICI code
1045-3873(1996)7:7<603:EOACAD>2.0.ZU;2-E
Abstract
Introduction: This study was designed to test whether the refractory s tate of nondepolarized myocardium is a major determinant of electrical defibrillation.Methods and Results: Postshock recovery interval (PSRI ) was estimated by measuring the residual refractory period after an a ppropriately timed field stimulus (1 to 16 V). The PSRI and transcardi ac defibrillation threshold (DFT) were compared before and during the administration of E-4031, a new Class III antiarrhythmic drug (group 1 , n = 10), or between monophasic and biphasic shocks (group 2, n = 14) in anesthetized open chest dogs. Group 1: E-4031 reduced the DFT from 2.6 +/- 0.6 J to 1.8 +/- 0.6 J (P < 0.01). The PSRI increased with th e increase of the applied voltage and was almost always greater during E-4031 infusion than at baseline. There was an inverse correlation be tween the changes of DFT and PSRI measured with a 14-V stimulus (r = - 0.80, P < 0.01) and a 16-V stimulus (r = -0.80, P < 0.01), Group 2: Me an DFTs were not statistically different between the two waveforms (3. 3 +/- 1.0 J vs 2.9 +/- 1.4 J). However, there also was an inverse corr elation between the differences in individual PSRIs and DFTs of the tw o waveforms (10-V stimulus: r = -0.62, P < 0.05; 16-V stimulus: r = -0 .75, P < 0.01). Conclusions: Modulation of defibrillation efficiency b y E-4031 infusion or by changes of the shock waveform was related to t he effect of these interventions on PSRI. These results suggest an ind ependent role for the refractoriness of nondepolarized myocardium in t he mechanism of defibrillation.