(Circulation. 1997;96:3079-3086.)
© 1997 American Heart Association, Inc.
Articles |
Changes in Myocardial Electrical Impedance Induced by Coronary Artery Occlusion in Pigs With and Without Preconditioning
Correlation With Local ST-Segment Potential and Ventricular Arrhythmias
From the Laboratorio de Cardiología Experimental, Servicio de Cardiología, Hospital General Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Spain.
Correspondence to Juan Cinca, MD, Servicio de Cardiología, Hospital General Universitari Vall d'Hebron, Passeig Vall d'Hebron 119-129, 08035 Barcelona, Spain. E-mail jcinca{at}ar.vhebron.es
Background Myocardial ischemia increases tissue electrical resistivity leading to cell-to-cell uncoupling, and this effect is delayed by ischemic preconditioning in isolated myocardium. Alterations in myocardial resistivity elicited by ischemia in vivo may influence arrhythmogenesis and local ST-segment changes, but this is not well known.
Methods and Results Myocardial impedance (resistivity
[
· cm] and phase angle [°]), epicardial ST segment,
and ventricular arrhythmias were analyzed
during 4 hours of coronary artery occlusion in 11
anesthetized open-chest pigs; these were compared with 13 other
pigs submitted to a similar coronary occlusion preceded by
ischemic preconditioning. Myocardial resistivity rose slowly
during the first 34±7 minutes of occlusion (237±41 to 359±59
· cm), increased rapidly to 488±100 · cm at 60
minutes, and reached a plateau value (718±266 · cm, ANOVA;
P<.01) at 150±69 minutes. By contrast, phase-angle changes
began after 17 minutes of ischemia (-3.0±1.6° to
-4.2±1.2° at 29±8 minutes) and evolved faster thereafter
(-12.5±5.3° at 144±56 minutes). Marked changes in myocardial
impedance were observed during the reversion of ST-segment elevation
that occurred 1 to 4 hours after occlusion, but impedance changes were
less apparent during the early ST-segment recovery seen at 15 to 35
minutes of ischemia. The second arrhythmia peak (30±5
minutes) coincided with the fast change in tissue impedance, and both
were delayed (P<.05) by ischemic
preconditioning.
Conclusions A rapid impairment of myocardial impedance occurs after 30 minutes of coronary occlusion, and its onset is better defined by shift in phase angle than by rise in tissue resistivity. Phase 1b arrhythmias are associated with marked impedance changes, and both are delayed by preconditioning. Reversion of ST-segment elevation is partially associated with impairment of myocardial impedance, but other factors play a role as well.
Key Words: ischemia • infarction • arrhythmia • electrophysiology
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