The aim of the present study was to investigate the effect of lidocaine
(L) on ventricular tachyarrhythmias with special reference to
ventricular fibrillation (VF). Myocardial infarction (MI) was created in
39 dogs by doubly ligating the left anterior descending (LAD) coronary
artery. Ah animals surviving the infarction (n = 33) were subjected to
programmed ventricular stimulation 7.6 +/- 3.2 days later. Local
electrical activity was recorded from the subepicardium of the left
ventricular wall by means of a specially designed composite electrode. L
(2 and 4 mg/kg i.v.) facilitated the induction of sustained monomorphic
ventricular tachycardia (sVT) in 8 dogs with nonsustained polymorphic
ventricular tachycardia (nsVT) in the control. In 13 dogs developing sVT
during control stimulation, L slowed the rate of tachycardia in 8
animals (first-dose effect), while it abolished arrhythmia induction in
5 animals (second-dose effect). It was interesting that L (2 mg/kg)
abolished reproduction of control VF in 12 animals by converting it into
sVT. L significantly depressed conduction and prolonged ventricular
refractoriness in the infarction zone. The results suggest that L
facilitates induction of sVT in conscious dogs with recent MI, thereby
decreasing susceptibility of infarcted myocardium to aggressive
polymorphic nsVT or VF. The capability of L to exacerbate slow
conduction in the infarction zone seems not to favor the development of
VF during this stage of MI
