Differential effects of procainamide, lidocaine and acetylstrophanthidin on body surface potentials and epicardial conduction in dogs with chronic myocardial infarction

Abstract

Twenty-eight anesthetized mongrel dogs were studied 2 to 74 months after experimental myocardial infarction in order to examine the effects of procainamide, lidocaine and acetylstrophanthidin on conduction within the infarcted region and the way such effects relate to changes in body surface potentials and antiarrhythmic efficacy. In each animal, 100 to 200 QRS complexes in the X, Y, Z leads were signal averaged, vector summed and high pass filtered at 50 Hz. Susceptibility to ventricular arrhythmia was evaluated using routine programmed ventricular extrastimulation in the anesthetized open chest animal. Epicardial electrograms were sequentially recorded at 45 standard sites within the infarcted region and referenced to the beginning of the QRS complex. Of the three agents, only procainamide exhibited antiarrhythmic action whereas lidocaine and acetylstrophanthidin produced inconsistent effects. Procainamide prolonged the time at which activity in the epicardial electrographic recordings ended relative to the beginning of the body surface QRS complex. This effect was significantly greater in electrograms that ended late in the QRS complex in the control state than for those that ended earlier. Such preferential effect on more abnormal sites was reflected on the body surface as a greater effect of procainamide in prolonging the lower energy terminal portion of the signal-averaged QRS complex than the earlier high energy portion. In contrast, lidocaine significantly prolonged the time at which electrograms ended only for those relatively normal electrograms that ended early in the QRS complex in the control state. In the signal-averaged body surface QRS complex, lidocaine produced a small but significant prolongation of the early high energy portion of the QRS complex but no change in the late portion. Acetylstrophanthidin produced a significant prolongation in early-ending electrograms and, surprisingly, significantly shortened the end time of electrograms that ended late in the QRS complex in the control state. Such effects were not reflected, however, on the body surface because acetylstrophanthidin had no significant effect on either the early or the late portion of the QRS complex. It is concluded that procainamide's differential effect between early- and late-ending electrograms is detected on the body surface by a greater prolongation in the terminal portion of the QRS complex. The signal-averaged body surface QRS complex is less sensitive in detecting the more subtle effects on conduction caused by lidocaine and acetylstrophanthidin.(ABSTRACT TRUNCATED AT 400 WORDS)

The clinical utility of procainamide‐induced late potentials on the signal averaged ECG

“…In the present study, Procainamide prolonged fQRSd and LAS40 and attenuated RMS40, consistent with previous work in humans 22 and dogs 23 post myocardial infarction. This may have occurred secondary to the depolarization or repolarization mechanisms described above.…”

The effects of oral pretreatment with zofenopril, an angiotensin-converting enzyme inhibitor, on early reperfusion and subsequent electrophysiologic stability in the pig

“…Signal averaging of the ECG showed that in all untreated animals late potentials had developed, whereas in the zofenopril-treated animals no late potentials were present and signalaveraging parameters were (partly) recovered. The combination of a longer QRS duration, a decreased V-30, and a longer D-30, i.e., the presence of late potentials, has been shown to be the body surface representation of delayed conduction in partially surviving fibers in the infarct [24]. Therefore, zofenopril induces a modulation of infarct properties related to tachyarrhythmias.…”

Promotion of Ventricular Tachycardia Induction by Procainamide in Dogs with Inducible Ventricular Fibrillation Late After Myocardial Infarction

“…The study end points were either induction of a ventricular arrhythmia lasting at least 10 PACE, Vol. 13 July 1990…”