Effects of gallopamil and nifedipine on ventricular arrhythmias, ventricular fibrillation, epicardial conduction delays and changes in the ventricular fibrillation threshold with time during myocardial ischaemia and reperfusion

Malignant ventricular arrhythmias, especially ventricular fibrillation, which often occur within minutes after occlusion of a coronary vessel, are the commonest cause of sudden cardiac death (1–3). The ventricular arrhythmias which occur in animals after coronary occlusion performed once for 20–30 minutes close to the origin of the vessel show a phasic frequency distribution (4, 5). There is a build-up of the arrhythmias between the 2nd and 10th minute (phase Ia) and between the 15th and 20th minute (phase Ib). They are distinctly less severe in the interval between the two phases.