Characteristics of conduction of premature impulses during acute myocardial ischemia and reperfusion: a comparison of epicardial and endocardial activation.

Abstract

The epicardial and endocardial conduction of premature impulses were studied during acute myocardial ischemia and reperfusion in dogs. The left anterior descending artery was ligated below the 2nd diagonal branch and 30 min later, below the 1st diagonal branch; the 2nd ligation was released 30 min later. Five transmural electrode needles were introduced into the anterior wall of the left ventricle, each with an epicardial, endocardial and a midwall bipole. During fixed atrial pacing, premature stimuli were delivered at the midwall at each needle site in series. Conduction times were defined as the interval between the premature pacing artifact and the 1st high-frequency deflection in the epicardial and in the endocardial electrograms. Myocardial conduction was assessed in myocardial segments representing normal, ischemic and reperfused myocardium and their borders. In the normal myocardium, epicardial conduction was slower than endocardial conduction. Ischemia slowed conduction transmurally; the epicardial conduction was consistently slower than endocardial conduction. Ischemia-induced changes in conduction differed considerably, depending on the proximity of the ischemic segment to normal or ischemic or reperfused myocardium. Reperfusion returned these changes toward normal; the rate of recovery was slower than the rate of depression of conduction seen with the onset of ischemia. Borders between ischemic segments of different duration showed significant disparity between epicardial and endocardial conduction. There apparently is significant disparity between epicardial and endocardial conduction of premature impulses in the normal myocardium, but more importantly, during ischemia. These observations are relevant in view of the recent interest in mapping of ventricular arrhythmias for surgical ablation of reentrant circuits.