CHANGES IN MYOCARDIAL ELECTRICAL-IMPEDANCE INDUCED BY CORONARY-ARTERYOCCLUSION IN PIGS WITH AND WITHOUT PRECONDITIONING - CORRELATION WITHLOCAL ST-SEGMENT POTENTIAL AND VENTRICULAR ARRHYTHMIAS

Citation
J. Cinca et al., CHANGES IN MYOCARDIAL ELECTRICAL-IMPEDANCE INDUCED BY CORONARY-ARTERYOCCLUSION IN PIGS WITH AND WITHOUT PRECONDITIONING - CORRELATION WITHLOCAL ST-SEGMENT POTENTIAL AND VENTRICULAR ARRHYTHMIAS, Circulation, 96(9), 1997, pp. 3079-3086
Citations number
39
Categorie Soggetti
Peripheal Vascular Diseas",Hematology
Journal title
ISSN journal
00097322
Volume
96
Issue
9
Year of publication
1997
Pages
3079 - 3086
Database
ISI
SICI code
0009-7322(1997)96:9<3079:CIMEIB>2.0.ZU;2-6
Abstract
Background Myocardial ischemia increases tissue electrical resistivity leading to cell-to-cell uncoupling, and this effect is delayed by isc hemic preconditioning in isolated myocardium. Alterations in myocardia l resistivity elicited by ischemia in vivo may influence arrhythmogene sis and local ST-segment changes, but this is not well known. Methods and Results Myocardial impedance (resistivity [Ohm . cm] and phase ang le [degrees]), epicardial ST segment, and ventricular arrhythmias were analyzed during 4 hours of coronary artery occlusion in 11 anesthetiz ed open-chest pigs; these were compared with 13 other pigs submitted t o a similar coronary occlusion preceded by ischemic preconditioning. M yocardial resistivity rose slowly during the first 34+/-7 minutes of o cclusion (237+/-41 to 359+/-59 Ohm . cm), increased rapidly to 488+/-1 00 Ohm . cm at 60 minutes, and reached a plateau value (718+/-266 Ohm . cm, ANOVA; P<.01) at 150+/-69 minutes. By contrast, phase-angle chan ges 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 impedanc e were observed during the reversion of ST-segment elevation that occu rred 1 to 4 hours after occlusion, but impedance changes were less app arent 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 onse t is better defined by shift in phase angle than by rise in tissue res istivity. Phase 1b arrhythmias are associated with marked impedance ch anges, and both are delayed by preconditioning. Reversion of ST-segmen t elevation is partially associated with impairment of myocardial impe dance, but other factors play a role as well.