Electrophysiological and antiarrhythmic effects of lidocaine in canine acute myocardial ischemia

Abstract

The electrophysiologic effects of temporary (15 minute) ligations of the left anterior descending coronary artery were examined in 16 dogs. Monophasic action potential duration (APD) and effective refractory period (ERP) were determined in the ischemic and normal zones. Intervals (Q-EG) were measured from the onset of the QRS in a standard ECG lead to the major deflection of electrograms recorded in these zones. Control ligations were compared to those in which a 2 mg./Kg. intravenous bolus of lidocaine was administered immediately after ligation followed by a constant rate intravenous infusion of 70 μg/Kg./minute. Lidocaine reduced the number of ventricular beats per minute (17 to 8) (p < .01) and at the same time it prolonged ERP only in the ischemic zone (14 msec.; p < .01), shortened APD only in the normal zone (8 msec.; p < .05), reduced APD ERP in the ischemic zone (1.12 to 1.01; p < .01), and to a lesser extent in the normal zone (1.17 to 1.12; p < .05), and it prolonged conduction only in the ischemic zone (10 msec. at peak effect; p < .01). During the control ligation, APD in the ischemic zone was 8 msec. shorter than in the normal zone (p < .05), while with lidocaine the difference was reduced to 3 msec. (N.S.). The effects of lidocaine reducing the disparity in APD between ischemic and normal zones in prolonging conduction and refractoriness in the ischemic zone and in reducing APD ERP may explain the demonstrated antiarrhythmic properties in acute myocardial ischemia.