PROFIBRILLATORY EFFECTS OF LIDOCAINE IN THE ACUTELY ISCHEMIC PORCINE HEART

Because recent clinical studies have failed to show evidence of the be nefit of lidocaine in the arrhythmias occurring in the early stage of myocardial infarction and have even shown an increased mortality in pa tients thus treated, we investigated the value of lidocaine as a prote ctive agent against ventricular fibrillation related to myocardial isc hemia in the in situ heart of anesthetized open-chest pigs subjected t o transient total occlusion of the proximal left anterior descending c oronary artery (LAD) under ventricular pacing at a constant high rate. Vulnerability to the fibrillatory process induced by coronary occlusi on was assessed both by time to onset of ventricular fibrillation (TF) and by electrical ventricular fibrillation threshold (EFT) determined after coronary occlusions of increasing duration (30, 60, 120, 180 s) . Monophasic action potential (MAP) was recorded concurrently in the n onischemic and ischemic areas. Lidocaine, even in relatively high dose s (2-4 mg . kg(-1)), did not prolong TF, nor did it increase EFT. On t he contrary, TF was significantly shortened and EFT was significantly decreased (15-30%) at the maximal concentrations of lidocaine, with re turn to control values in 40-60 min. Therefore, lidocaine tends to inc rease the risk of ischemic ventricular fibrillation (VF): It fails to control the extreme enhancement of excitability and worsens conduction disorders, even though it decreases normal conduction only slightly. Use of lidocaine against rhythm disorders in acute myocardial infarcti on (AMI), is at least debatable and probably contraindicated.