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Krannert Institute of Cardiology and Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana 46202
Coronary occlusion and reperfusion
produce tachyarrhythmias. We tested the hypothesis that variations in
transmural activation after global ischemia and reperfusion
were responsible for arrhythmias. We arterially perfused 36 isolated
transmural wedges from canine left ventricular free walls. After 
100
min of stabilization, the artery was occluded for 25 min, followed by
reperfusion at various flow rates. We recorded 256 channels of
fluorescent action potentials on transmural surfaces from preocclusion
to >15 min after reperfusion. During endocardial pacing at 300 ms,
ischemia of 570 ± 165 s (n = 34)
produced 1:1 endocardial conduction and then 2:1 and 4:1 block as the
wave fronts conducted toward epicardium. Transmural reentry
appeared after 535 ± 146 s of ischemia
(n = 31). Further ischemia caused epicardial
inactivation and eliminated reentry (n = 24).
During reperfusion, tissues progressed through sequences of epicardial
inactivation and reappearance of activation with 1:1, 2:1, and 4:1
conduction; both sustained and nonsustained reentry occurred. We
conclude that heterogeneous activation responses to endocardial pacing
during acute ischemia provide the substrate for initiating
reentry, suppressed reentry during further ischemia, and caused
reentry during reperfusion.
heart; optical mapping; arterial occlusion; tachyarrhythmias; fibrillation
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