[Cellular electrophysiology of abnormal automaticity foci]

Foci of abnormal automaticity are the result of either 1) an abnormal pacemaker discharging spontaneously in the absence of an initiating stimulation usually arising in the midst of depolarised myocardial fibres but also from zones of physiological subsidiary automaticity normally inhibited during sinus rhythm, or 2) automatic activity triggered by an initiating stimulus related to oscillating after-depolarisation or early after-depolarisation. Oscillating after-depolarisation, the clinical expression of which was thought initially to be limited to digitalis toxicity, can arise in any experimental situation associated with calcium overload of the cell. Early after-depolarisation which often occurs during the terminal phase of the action potential of the Purkinje fibres, arises under different experimental conditions to those giving rise to oscillating after-depolarisation. Cellular electrophysiological techniques demonstrate the mechanism responsible for abnormal automaticity and the sites of action of antiarrhythmic drugs. Close collaboration between cellular electrophysiologists and clinicians is necessary to establish the responsibility of mechanisms demonstrated in vitro in the genesis of clinical arrhythmias.