ATTENUATION OF THE ISCHEMIA-INDUCED FALL OF ELECTRICAL VENTRICULAR-FIBRILLATION THRESHOLD BY A CALCIUM-ANTAGONIST, DILTIAZEM

Calcium antagonists have been reported to decrease the incidence of su dden death in postinfarction management and vulnerability to fibrillat ion secondary to experimental coronary occlusion. In order to confirm such beneficial results regarding ischaemic ventricular fibrillation, the threshold intensity for fibrillation electrically induced with imp ulses of 100 ms and 180 beats . min-1 was measured during the course o f ischaemias obtained by total occlusion of the left anterior descendi ng coronary artery near its origin in open-chest pigs. The variations of electrical fibrillation threshold with ischaemia duration (30, 60, 120, 180, 240, 360 s) were compared under control conditions and after iv. diltiazem (0.50 mg . kg-1 plus 0.02 mg . kg-1 . min-1 over 25 min ). Electrical fibrillation threshold was not influenced by diltiazem b efore, but raised during ischaemia, particularly from the 60th s (1.7 to 4.0 mA), with delay in the triggering of fibrillation which occurs when the fibrillation threshold falls down to the pacing threshold (0. 2 to 0.3 mA). In 6 pigs out of 8, fibrillation was even avoided in the longest of the ischaemic periods considered (360 s), for fibrillation threshold ceased falling before reaching the critical level. These ex perimental results obtained with diltiazem are consistent with the cli nical effectiveness of calcium antagonists recently observed in the pr evention of postinfarction sudden death, provided that myocardial cont ractility is not too much adversely affected. But, left ventricular dP /dt(max) was not reduced by more than 6.8% in the present experiments.