Electrophysiology of arrhythmias

In this review, a brief overview of the different arrhythmogenic mechanisms is given, emphasizing that the mechanisms for initiation and maintenance of tachyarrhythmias are often not the same. Normal automaticity in Purkinje fibers, surrounded by partially depolarized tissue providing entrance block, is most likely responsible for ventricular premature beats and enhanced automaticity can lead to (rare) cathecholamine dependent ventricular tachycardias. Abnormal automaticity in partially depolarized cells may underlie ectopic atrial tachycardias and accelerated idioventricular rhythms in the subacute phase of myocardial infarction. Triggered activity based on early afterdepolarizations may trigger torsade de pointes in both the congenital and acquired long QT syndrome. The various mutations, affecting both potassium and sodium channels, will be discussed. Cellular calcium overload, which may occur in digitalis intoxication, hypertrophy and heart failure, is the cause for delayed afterdepolarizations and triggered activity. Reentry, anatomical and functional, ordered or reentry, is by far the most common cause of both atrial and ventricular tachycardias and fibrillation. Special attention will be given to the phenomenon of "electrical remodeling" in which prolonged episodes of rapid electrical activity leads to changes in ion channel function, which in their turn cause long lasting electrophysiological alterations.