Epicardial, endocardial and transmural mapping in assessing electrophysiological effects of 14-C lidocaine and 14-C propafenone on activation times in experimental chronic myocardial infarction. Correlations with myocardial drugs concentrations.

The electrophysiological effects of lidocaine (L) and propafenone (P) in chronic myocardial infarction in relation to tissue drug concentrations (TDC) are unknown. Thus of 16 dogs with one week old myocardial infarction, 8 received propafenone 2 mg/kg and 8 lidocaine 5 mg/kg followed by 0.2 mg/kg/min of either drug for 60 min. Epicardial (EPI) mapping (greater than 30 points) was performed with a bipolar electrode. Endocardial (ENDO) and transmural (TRANS) mapping (greater than 20 points) were performed with 4 pairs of needle mounted bipolar electrodes. The % change in activation times (% delta AT) in EPI, ENDO and TRANS was evaluated in normal (N) and infarcted (I) zones at control and 60 min after drugs. Ventricular arrhythmias (VA) were studied with programmed extra stimulation. Results (P less than 0.01 to L, P less than 0.01 to N zone, # P less than 0.05 to ENDO): (Table: see text) At 60' ventricular tachycardia and ventricular fibrillation were both still inducible in 50% in the lidocaine group (37% in control), while only in 16% in the propafenone group (62% in control). Despite lower drug concentrations in the infarct, the effects on AT are comparable to normal zones for both drugs. In conclusion lidocaine reduces and propafenone increases AT, affecting in opposite directions the inducibility of reentrant ventricular arrhythmias.