Abstract

The aim was (1) to test the hypothesis that the prevention of haemodynamic deterioration decreases arrhythmia formation in the infarcting heart and augments the antiarrhythmic effects of beta blockade; and (2) to assess the ventricular fibrillation threshold as an index of innate arrhythmogenic propensity. Changes in ventricular fibrillation threshold as an index of innate arrhythmogenic propensity. Changes in ventricular fibrillation threshold were determined for 50 min after anterior descending coronary artery occlusion in open chest pigs (group 1, n = 5). In group 2 (n = 9), ventricular fibrillation threshold was studied in the same way but cardiac output was maintained at 100 ml.min-1.kg-1 body weight and mean aortic pressure at 60(SEM 3) mm Hg by means of right heart and arterio-arterial bypass. In both groups intravenous propranolol 1.2 mg.kg-1 was injected 35-40 min after coronary artery occlusion. In group 3 (n = 6) spontaneous arrhythmias following coronary artery occlusion were recorded to test how well the ventricular fibrillation threshold reflected the incidence and time course of these arrhythmias. In group 1, there was a deep trough in ventricular fibrillation threshold--from 11.3(0.3) mA to 6.0(0.3) mA--within 10 min of coronary artery occlusion (47% decrease, p < 0.001). There was a shallower trough between 10 and 30 min. In group 2, preocclusion ventricular fibrillation threshold increased from 13.9(1.2) mA to 32.1(5.6) mA (p < 0.05) because of stabilised haemodynamics. After coronary occlusion, fibrillation threshold remained high throughout, being 22.7(1.3) mA and 20.4(1.1) mA at the times of the expected troughs (p < 0.005 v group 1 for both values). Propranolol increased ventricular fibrillation threshold by 24(7)% in group 1 (p < 0.05) and by 53(8)% in group 2 (p < 0.0005). In group 3 spontaneous arrhythmias followed a biphasic pattern, similar to group 1. There was a positive correlation between ventricular fibrillation threshold and arrhythmia score (r = 0.84). (1) Haemodynamic stabilisation increased ventricular fibrillation threshold during ischaemia and enhanced the antiarrhythmic effects of beta blockade. (2) The ventricular fibrillation threshold accurately reflects the incidence and time course of spontaneous arrhythmias in this model.

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