Circulation, Vol 52, 760-765, Copyright © 1975 by American Heart Association
R Levites, VS Banka and RH Helfant
In order to determine the electrophysiological changes that occur during
coronary occlusion and following reperfusion, 19 mongrel dogs were studied.
Refractory periods were determined by the extrastimulus method in
nonischemic and ischemic zones prior to and after variable periods of left
anterior descending artery occlusion and reperfusion. After 15-30 minutes
of occlusion, refractory periods in the nonischemic zones remained
unchanged while in the ischemic zone they shortened by 17%, resulting in a
dispersion of refractoriness. Within three minutes of reperfusion,
arrhythmias appeared together with a marked directional change of
refractory periods to a prolongation by 34% (P less than 0.001) in the
ischemic zone and by 3% (P less than 0.02) in the nonischemic zone.
Refractory periods returned to baseline values after 60 minutes of
reperfusion. After 60-90 minutes of occlusion, refractory periods in the
nonischemic zones were unchanged whereas in the ischemic zone they
demonstrated a decrease by 28% (P less than 0.01), again resulting in a
dispersion of refractoriness. Within five minutes of reperfusion,
refractory periods in the ischemic zone prolonged by 44% (P less than
0.001). Similar but smaller directional changes were also seen in
nonischemic zones. Concomitant with the observed prolongation in refractory
periods frequent ventricular ectopic activity was again documented. In
addition, refractory periods did not return to control values after periods
of observation up to 120 minutes in this group. In seven dogs, complete
heart block was induced to ascertain the rate of idioventricular pacemaker
and the effect of ventricular overdrive on the escape interval. Control
ventricular rates (53.3 +/- 5.7 beats/min) remained unchanged (52.3 +/-
5.6) following coronary occlusion, but decreased to 48.0 +/- 4.4 (P less
than 0.05) during reperfusion. Mean control escape intervals (1.8 +/- 0.2
sec) did not change after occlusion (1.7 +/- 0.2 sec) but prolonged to 2.1
+/- 0.2 sec (P less than 0.05) following reperfusion. In conclusion: 1)
sudden prolongation in refractory periods following reperfusion leads to an
overshoot resulting in a dispersion of refractoriness temporally related to
the onset of ventricular arrhythmias and 2) re-entry, and not enhanced
automaticity, appears to be the mechanism for postperfusion arrhythmias.
ARTICLES
Electrophysiologic effects of coronary occlusion and reperfusion. Observations of dispersion of refractoriness and ventricular automaticity
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