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August 1, 1979Circulation279 citationsOpen Access

Two periods of early ventricular arrhythmia in the canine acute myocardial infarction model.

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EKElieser KaplinskySOSatoshi OgawaCBC. William Balke

Key Points

  • This research aims to explore the occurrence and timing of early ventricular arrhythmias following coronary artery ligation in a canine model.
  • 41 open-chest mongrel dogs were anesthetized using pentobarbital sodium for the experiment.

Structured PICO

P
Population
41 open-chest mongrel dogs anesthetized with pentobarbital sodium (Nembutal)
I
Intervention
Ligation of the left anterior descending coronary artery
O
Outcome
Time course of ventricular arrhythmias in the early period (0-30 minutes) after ligationsurrogate

In a canine acute myocardial infarction model, early ventricular arrhythmias occur in two distinct temporal phases (immediate and delayed) that may involve different reentrant mechanisms.

Abstract

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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Cite This Study

Kaplinsky et al. (1979) studied this question.

synapsesocial.com/papers/6a1fdcf8f355831892049801https://doi.org/10.1161/01.cir.60.2.397
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