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A review of early intervention studies with beta blockers in patients with myocardial infarction.

Transmembrane potentials and local extracellular electrograms were recorded from isolated Langendorff perfused canine and porcine hearts. Experiments were also performed on hearts in open-chested anaesthetized animals. Following occlusion of a major coronary artery, resting membrane potential decreased, resulting in depression of the TQ segment. Action potential amplitude and upstroke velocity decreased, leading to ST elevation and delayed activation. At resting membrane potentials around -60 mV, ischaemic cells became inexcitable. Arguments are presented that action potentials during the first 10 min of ischaemia, when malignant ventricular arrhythmias frequently occur, are not 'slow responses' but are instead 'depressed fast responses' where inward current is carried by Na+ ions through partially inactivated fast channels. Mapping experiments, in which 60 to 98 electrograms were simultaneously recorded during spontaneous ventricular arrhythmias demonstrated that ventricular tachycardia is due to macro-re-entry with the re-entrant pathway having a wavelength of the order of 6 cm. No evidence was found for macro-re-entry being the cause of ventricular premature depolarizations. A hypothesis is put forward, whereby the experimental findings of a 'focal' origin are explained on the basis of electrotonic transmission through a small inexcitable zone close to the ischaemic border