THERAPY AND PREVENTION ARRHlYTHMIA Effects of lidocaine and procainamide

The effect of lidocaine (n = 6) and procainamide (n = 12) on electrogram characteristics from electrically normal right ventricular and electrically abnormal left ventricular endocardial sites was determined in 18 patients with prior myocardial infarction. Bipolar electrograms were recorded during sinus rhythm with No. 6F catheters positioned at a left ventricular abnormal site (electrograms fulfilling two of the following criteria: amplitude <3 mV, duration >70 msec, or an amplitude to duration ratio < .046) and normal sites at the right ventricular apex (RVA) and right ventricular outflow tract (RVOT). All electrograms were recorded from the same location before and after intravenous lodicaine or procainamide administered to obtain mean serum concentrations of 4.2 ± 0.6 and 9.42 ± 2 Fg/ml respectively. Lidocaine and procainamide had no significant effect on sinus cycle length or electrogram amplitude. After lidocaine, no significant change in QRS width (112 ± 23 vs 114 + 24 msec), left ventricular electrogram duration (76 ± 21 vs 78 15 msec), or right ventricular electrogram duration (RVA 33 + 9 vs 33 + 10 msec, RVOT 31 9 vs 33 + 11 msec) was noted during sinus rhythm. At a paced cycle length of 600 msec, there was also no change in the paced QRS duration (197 vs 198 msec), the RVA electrogram duration (30 vs 32 msec), the RVOT electrogram duration (49 vs 52 msec), or the left ventricular electrogram duration (102 vs 108 msec). In contrast, after procainamide, QRS width prolonged from 110 + 31 to 127 + 33 msec (p < .001), and electrogram duration increased significantly (p < .001) at the left ventricular site (84 ± 17 to 101 ± 23 msec), the RVA (32 ± 11 to 38 ± 13 msec), and the RVOT (37 + 12 to 44 ± 15 msec). Similarly, at a pacing cycle length of 600 msec, QRS duration increased from 194 to 226 msec (p < .001), RVA electrogram duration increased from 32 to 36 msec (p < .05), RVOT electrogram duration increased from 34 to 39 msec, and left ventricular electrogram duration increased from 86 to 108 msec. The observations that lidocaine had no effect on local electrogram duration and procainamide prolonged indexes of conduction in both normal and chronically infarcted myocardium to the same degree are consistent with, but do not establish with certainty, the hypothesis that the ionic basis for impulse propagation is similar in normal and infarcted tissue. Circulation 77, No. 5, 1030-1037, 1988. THE EFFECTS of antiarrhythmic therapy on intraventricular electrograms in electrically normal and From the Clinical Electrophysiology Laboratory, Hospital of the University of Pennsylvania, Cardiovascular Section, Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia. Supported in part by grants from the American Heart Association, Southeastern Pennsylvania Chapter, Philadelphia, and National Heart, Lung, and Blood Institute, Bethesda (HL 28093, HL07346). Address for correspondence: Mark E. Josephson, M.D., Chief, Cardiovascular Section, Room 994 Founders Pavillion, Hospital of the University of Pennsylvania, 3400 Spruce St., Philadelphia, PA 19104. Received March 24, 1987; revision accepted Jan. 21, 1988. Dr. Schmitt was supported by the German Research Foundation (Deutsche Forschungsgemeinschaft). Dr. Josephson is the Robinette Foundation Professor of Medicine (Cardiovascular Diseases). *Present address: University Hospitals, 1500 E. Medical Center Dr., Ann Arbor, MI 48109-0022. 1030 electrically abnormal endocardial regions have not been previously described. Although the effect of lidocaine' and procainamide2`4 on indexes of conduction and refractoriness in the atrium, the atrioventricular node, the His-Purkinje system, and ventricular muscle have been documented, it is not known whether lidocaine and procainamide exert different effects on normal and abnormal endocardial electrograms. In addition, along with other studies it may help provide a clue to the mechanism for the efficacy of antiarrhythmic agents in the management of ventricular tachyarrhythmias associated with chronic coronary artery disease and may help to further define the electrophysiologic characteristics of myocardial cells that survive in infarcted areas. Thus, the purpose of our study was CIRCULATION by gest on A ril 4, 2017 http://ciajournals.org/ D ow nladed from THERAPY AND PREVENTION-ARRHYTHMIA to determine the effect of lidocaine and procainamide on electrogram characteristics at normal and chronically infarcted sites.