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