Copyright © 1993 by the European Society of Cardiology.
© 1993 The Europen Society of Cardiology
Increased dispersion of ventricular repolarization and ventricular tachyarrhythmias in the globally ischaemic rabbit heart
From the Cardiovascular Medicine Division, Falk Cardiovascular Research Center, Stanford University School of Medicine Stanford, CA 94305, U.S.A.
accepted 15 June 1993.
Correspondence. Robert W. Kurz, MD. First Medical Department, Donauspital Langobardenstr. 122, A-1220, Vienna, Austria
Abstract
Contemporary concepts of ischaemic ventricular tachyarrhythmias (VTA) are based on increased electrophysiological heterogeneity of the myocardium. We developed a multi-site monophasic action potential recording system for an isolated rabbit heart to study the effects of global ischaemia on the electrophysiological properties at different ventricular sites simultaneously. The hearts were paced from the right ventricle (RV) andconduction time (CT), action potential duration (APD) and total repolarization time (TRT= [CT + APD]) were measured during normal perfusion and ischaemia. The dispersion of these parameters was calculated as the maximal difference between simultaneous recordings. Inducibility of VTA by programmed extrastimulation (ES) was investigated under normal and ischaemic conditions.
During global ischaemia, CT increased progressivey showing a faster and greater increase at the left ventricle (LV) than at the RV. After 10 min the prolongation of CT reached a plateau at the LV while it continued to rise in the RV. The dispersion of CT increased from 14 ± 2.7 ms during normal perfusion to a maximum of 79.8 ± 17.2 ms after 14 min of ischaemnia (P<00001). APD was uniform at the three sites (190.9±02, 185.0 and 179.3±9.8 ms, ns) during normal perfusion but changed non-uniformly during ischaemia. There was a transient lengthening of APD until 1 and 3 min of ischaemia at the LV sites followed by a rapid shortening of APD. At the RV site, APD continued to increase until 5 min of ischaemia and then shortened gradually. Consequently, dispersion of APD showed a rapid initial rise from 177.8 ± 2.7 ms to 77.8 ± 10 ms (P<0.0001) followed by a slower final increase. TRT was uniform during normal perfusion (210.4 ± 10.3, 213.1±7.8, 212.1±10.3 ms, ns) but became non-uniform during global ischaemia. The dispersion of TRT increased from 15.4±4.2 ms to 92.6 ± 23.2 ms (P<0.0001) during 14 min of global ischaemia. Both CT and APD contributed independently to TRT and could either augment or partially compensate for the ischaemic alterations of the other parameter.
ES induced VTA only during ischaemia (3.7±1.1 VTA per heart, P<0.0001) at coupling intervals between 220 and 380 ms. The dispersion of TRT of the last regular beat preceding VTA was 67.7±17.4 ms (P<0.001). ES which triggered VTA showed a more than two-fold increase of CT dispersion compared to the last steady state beat (122.7±29.4%, P = 0.0001).
The present results show that global ischaemia results in considerable electrophysiologic heterogeneity in the intact heart. These changes may be regarded as a suitable basis of VTA, induced by ES.
Key Words: Ischaemia • monophasic • action-potential • conduction • repolarization • dispersion • extrastimulation • ventricular • arrhythmia
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