ELECTROPHYSIOLOGICAL MECHANISMS OF VENTRI CULAR ARRHYTHMIAS OF MYOCARDIAL-INFARCTION

In experimental models of coronary occlusion, the physiopathology of v entricular arrhythmias varies with its timing, there being three main phases : early, late and chronic. The early phase covers the first 30 minutes and is dominated by tachycardias and fibrillations resulting f rom multiple micro-reentry circuits which are the consequence of major changes in conduction and excitability created by acute ischaemia. Th ese arrhythmias may be triggered by extrasystoles which have a differe nt mechanism related to the injury current generated in the border zon e between ischaemic and healthy cells. The late phase lasts about 72 h ours : it is characterised by polymorphic ventricular extrasystoles an d bursts of relatively slow ventricular tachycardia. Much more rapid t achycardia can be induced by stimulation. The origin of these arrhythm ias is usually in the surviving Purkinje fibres of the subendocardium. The mechanisms are variable : abnormal automaticity, reentry or activ ity triggered by delayed after depolarisations. During the chronic pha se, reentrant tachycardia is possible but only when induced by stimula tion. Delayed conduction is the consequence of non-uniform anisotropis m related to the disorientation of the myocardial fibres caused by fib rosis. In the clinical situation, most research has been centered on s ustained monomorphic ventricular tachycardias of the chronic phase. Th eir mechanism is almost exclusively reentry (the circuits usually bein g located in the subendocardium) as suggested by the triggering and in terruption of clinical tachycardias by stimulation, the recording of f ragmented activation or prepotentials at the site of emergence of the tachycardia and the phenomena of pacing.