Ischemic preconditioning significantly delayed the rapid impairment of myocardial impedance and the associated phase 1b ventricular arrhythmias during coronary occlusion in pigs (P<.05).
Does ischemic preconditioning delay changes in myocardial impedance and arrhythmias during coronary artery occlusion in pigs?
Ischemic preconditioning delays the rapid impairment of myocardial impedance and associated phase 1b arrhythmias during coronary occlusion in a porcine model.
p-value: p=<.05
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 omega x cm and phase angle degrees), 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 omega x cm), increased rapidly to 488+/-100 omega x cm at 60 minutes, and reached a plateau value (718+/-266 omega x cm, ANOVA; P<.01) at 150+/-69 minutes. By contrast, phase-angle changes began after 17 minutes of ischemia (-3.0+/-1.6 degrees to -4.2+/-1.2 degrees at 29+/-8 minutes) and evolved faster thereafter (-12.5+/-5.3 degrees 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.
Cinca et al. (Tue,) conducted a other in Myocardial ischemia (n=24). Ischemic preconditioning vs. No preconditioning was evaluated on Myocardial impedance (resistivity and phase angle), epicardial ST segment, and ventricular arrhythmias (p=<.05). Ischemic preconditioning significantly delayed the rapid impairment of myocardial impedance and the associated phase 1b ventricular arrhythmias during coronary occlusion in pigs (P<.05).