Circulation, Vol 60, 397-403, Copyright © 1979 by American Heart Association
E Kaplinsky, S Ogawa, CW Balke and LS Dreifus
The time course of ventricular arrhythmias in the early period (0--30
minutes) after ligation of the left anterior descending coronary artery was
studied in 41 open-chest mongrel dogs anesthetized with pentobarbital
sodium (Nembutal). ECGs and seven single and composite electrograms from
various regions in and around the ischemic zone were recorded throughout
the experiments. Two periods of ventricular arrhythmias were clearly seen.
The first occurred 2--10 minutes after coronary ligation, peaking at 5--6
minutes, and was designated as immediate ventricular arrhythmias (IVAs).
There was a distinct correlation between incidence, severity, onset and
termination of IVA and the degree of local delay and fragmentation of the
normal sinus activation spread in the ischemic subepicardial zone. The
second wave of ventricular arrhythmias occurred 12--30 minutes after
ligation independently of the previous increased delay and fragmentation of
activation in the ischemic subepicardium. Delayed ventricular arrhythmias
(DVAs) were as severe as IVAs--there were nine instances of ventricular
fibrillation during DVA and seven during IVA. While the mechanism of IVA is
most probably related to reentry accompanied by delay and fragmentation of
ischemic subepicardial activation, the mechanism of DVA remains unclear.
Our evidence suggests that DVAs are also reentrant, with the reentry
pathways located in deep myocardial structures or involving microscopic
pathways at the Purkinje muscle junction.
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Two periods of early ventricular arrhythmia in the canine acute myocardial infarction model
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