Remnant myocytes in the mid-wall and epicardium of infarct scars support normal electrical activation during RA pacing, but delayed conduction emerges upon direct epicardial stimulation.
INTRODUCTION: This study examines the consequences of a large transmural apical infarct on the epicardial electrical activity in isolated rabbit hearts. METHODS AND RESULTS: Hearts were isolated 8 weeks after coronary artery ligation. Membrane voltage from the epicardial surface of the left ventricle (LV) including the infarct was monitored using the voltage sensitive dye RH237. Optical action potentials were detected from the epicardial surface of the infarct; the signal amplitude was approximately 20% of those in the noninfarcted zone (NZ). Epicardial activation mapping of the LV free wall showed that during right atrial (RA) pacing, the activation sequence was not significantly different between infarcted and sham-operated groups. However, direct stimulation of the epicardium in the NZ revealed an area of slow conduction velocity (CV approximately 5 cm/s(-1), approximately 10% of normal values) at the margin of the infarct zone (IZ). Within the IZ, CV was approximately 50% of normal. A prominent endocardial rim of myocardium in the infarct was not the source of epicardial optical signals because chemical ablation of the endocardium did not affect the epicardial activation pattern. CONCLUSION: Therefore, remnant groups of myocytes in the mid-wall and epicardium of the infarct scar support normal electrical activation during RA pacing. Areas of delayed conduction emerge only on epicardial stimulation.
Walker et al. (Wed,) studied this question.
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