BACKGROUND: Previous studies have shown that acute myocardial ischemia in the dog results in much greater activation delays in epicardial than endocardial tissue. These results have been interpreted to indicate enhanced sensitivity of epicardial conduction properties to acute ischemia. This study was designed to test the hypothesis that the ischemic epicardial activation delay during supraventricular rhythms is due to slow conduction across the ischemic myocardial wall prior to epicardial activation and not to enhanced epicardial conduction slowing per se. METHODS AND RESULTS: Changes in epicardial and endocardial activation were measured with transmural decapolar needle electrodes during successive 5-minute left anterior descending coronary artery (LAD) occlusions separated by 30-minute reperfusion periods. Occlusions were performed during left atrial pacing, right ventricular pacing with a stimulating electrode located along the longitudinal axis of epicardial fiber orientation in the ischemic zone, or left ventricular pacing in nonischemic tissue located on a line transverse to fiber orientation in the ischemic zone. During both atrial and left ventricular pacing, activation in the ischemic zone began in the endocardium. Epicardial activation resulted from transmural conduction and was markedly delayed compared with endocardial activation during acute myocardial ischemia. During right ventricular stimulation, the ischemic zone epicardium was activated via longitudinal epicardial conduction, and its activation was only slightly delayed by acute ischemia. Epicardial activation mapping was used to assess ischemia-induced changes in longitudinal epicardial conduction velocity and to compare them with changes in transmural velocity during atrial or left ventricular pacing. Longitudinal conduction in the ischemic epicardium was slowed by 13 +/- 4% (mean +/- SE) relative to preischemic control values in contrast to transmural conduction, which was slowed 50 +/- 4% by LAD occlusion during atrial pacing and 49 +/- 5% during left ventricular pacing (both P < .001 versus longitudinal epicardial conduction). Transmural activation studies showed that the midmyocardium is the site of most of the ischemic activation delay during transmural propagation. CONCLUSIONS: Epicardial activation is more delayed than endocardial by acute ischemia during supraventricular rhythms in dogs because of slowed conduction across the myocardial wall, not because of enhanced sensitivity of epicardial conduction to depression by acute ischemia.
BACKGROUND: Previous studies have shown that acute myocardial ischemia in the dog results in much greater activation delays in epicardial than endocardial tissue. These results have been interpreted to indicate enhanced sensitivity of epicardial conduction properties to acute ischemia. This study was designed to test the hypothesis that the ischemic epicardial activation delay during supraventricular rhythms is due to slow conduction across the ischemic myocardial wall prior to epicardial activation and not to enhanced epicardial conduction slowing per se. METHODS AND RESULTS: Changes in epicardial and endocardial activation were measured with transmural decapolar needle electrodes during successive 5-minute left anterior descending coronary artery (LAD) occlusions separated by 30-minute reperfusion periods. Occlusions were performed during left atrial pacing, right ventricular pacing with a stimulating electrode located along the longitudinal axis of epicardial fiber orientation in the ischemic zone, or left ventricular pacing in nonischemic tissue located on a line transverse to fiber orientation in the ischemic zone. During both atrial and left ventricular pacing, activation in the ischemic zone began in the endocardium. Epicardial activation resulted from transmural conduction and was markedly delayed compared with endocardial activation during acute myocardial ischemia. During right ventricular stimulation, the ischemic zone epicardium was activated via longitudinal epicardial conduction, and its activation was only slightly delayed by acute ischemia. Epicardial activation mapping was used to assess ischemia-induced changes in longitudinal epicardial conduction velocity and to compare them with changes in transmural velocity during atrial or left ventricular pacing. Longitudinal conduction in the ischemic epicardium was slowed by 13 +/- 4% (mean +/- SE) relative to preischemic control values in contrast to transmural conduction, which was slowed 50 +/- 4% by LAD occlusion during atrial pacing and 49 +/- 5% during left ventricular pacing (both P < .001 versus longitudinal epicardial conduction). Transmural activation studies showed that the midmyocardium is the site of most of the ischemic activation delay during transmural propagation. CONCLUSIONS: Epicardial activation is more delayed than endocardial by acute ischemia during supraventricular rhythms in dogs because of slowed conduction across the myocardial wall, not because of enhanced sensitivity of epicardial conduction to depression by acute ischemia.