Excitation of ischemic myocardium: altered properties of conduction, refractoriness, and excitability

Abstract

Reentrant ventricular arrhythmias arise in variable epicardium overlying the “transmural” infarction zone in the dog 3 to 9 days after left anterior descending coronary artery ligation. Effects of pacing (90 to 360 beats/minute) from the epicardium in the normal zone and ischemic zone were studied in 18 dogs using standard ECG leads and epicardial recordings. Pacing in the normal zone at any stimulus strength showed no changes in QRS morphology at these heart rates. During pacing at ischemic zone sites, QRS morphology changed with heart rate in association with conduction delays in the ischemic zone. This effect could be reversed by increasing the stimulus strength. Refractoriness in the ischemic zone was tested by programmed pacing. Abnormally short (≤ 130 msec.) and long (≥ 330 msec.) refractoriness coexisted within the ischemic zone. This marked dispersion of refractoriness was related to the occurrence of reentrant ventricular arrhythmia. In 10 dogs a 3 × 4 cm. section of ventricular epicardium was removed which included normal and ischemic zones. Action potentials were recorded during superfusion with Tyrode's solution at 37°C. Rate-dependent reentrant ventricular arrhythmias were initiated in 90% of the tissue studied. At a constant stimulus strength, action potentials recorded close to the stimulation site showed progressively shorter (< 100 msec.), diminutive responses as the heart rate was increased. Intermittent failure of excitation was noted at higher rates. Rate-sensitive changes in conduction, refractoriness, and excitation are determinants of reentrant ventricular arrhythmia originating in the ischemic zone epicardium.