Arrhythmogenic changes in action potential configuration in the ventricle induced by DC shocks

Citation
I. Kodama et al., Arrhythmogenic changes in action potential configuration in the ventricle induced by DC shocks, J ELCARDIOL, 32, 1999, pp. 92-99
Citations number
30
Categorie Soggetti
Cardiovascular & Respiratory Systems
Journal title
JOURNAL OF ELECTROCARDIOLOGY
ISSN journal
00220736 → ACNP
Volume
32
Year of publication
1999
Supplement
S
Pages
92 - 99
Database
ISI
SICI code
0022-0736(1999)32:<92:ACIAPC>2.0.ZU;2-X
Abstract
Failure of defibrillation by direct current (DC) shocks is the result in pa rt of new ventricular tachyarrhythmias induced by the shocks. We investigat ed the arrhythmogenic substrate produced by the shocks. Fluorescent action potential (AP) signals were recorded from rabbit hearts perfused in vitro w ith the use of our original optical recording system. Localized application of 10-ms shocks (S2) during the plateau phase of APs by basic stimuli (S1) caused field intensity (FI)-dependent changes in APs: (a) S2 > 7 V/cm caus ed additional depolarization, giving rise to a prolongation of AP duration (APD); (b) With S2 > 20 V/cm, terminal repolarization was inhibited, and su bsequent postshock S1 APs for 1 to 5 min were characterized by decreases in the maximum diastolic potential and amplitude of APs; and (c) S2 > 30 V/cm often resulted in a prolonged refractoriness, oscillation of membrane pote ntial leading to ventricular tachycardia or fibrillation (VT/VF). The right ventricle was more susceptible than other regions for the aftereffects of high-intensity shocks. Using an 8-channel recording system, we compared the effect of IO-ms monophasic (M) and 5/5-ms biphasic (B) shocks applied to t he whole ventricles with FI of 1 to 20 V/cm at the signal recording sites. B shocks were less potent than M shocks in the FI-dependent action potentia l duration (APD) prolongation, and in the shock-induced enhancement of APD dispersion. Incidence and duration of VT/VF induced by M shocks were signif icantly greater than those by B shocks. These findings suggest that DC shoc ks will cause two types of arrhythmogenic substrate: one induced at sites o f high FI, and the other at sites with moderate FI. The former would produc e local block or focal repetitive excitation due to prolonged depolarizatio n and oscillation of membrane potential, and the latter circuitous movement of wavefronts through an enhancement of spatial inhomogeneity of repolariz ation.