The normal site of initiation of the cardiac impulse is the sinus node, where a spontaneous decline in the transmembrane potential during diastole, referred to as the pacemaker potential or diastolic depolarization, results in an action potential that is propagated to the rest of the heart. When impulse initiation occurs in a group of cells in another location, the term ectopic focus is used. There are two major causes for ectopic impulse generation that may result in cardiac arrhythmias: automaticity and triggered activity. Automaticity is the result of spontaneous diastolic depolarization, triggered activity is caused by so-called afterdepolarizations. Normal automaticity outside the sinus node is found in subsidiary, or latent, pacemakers in the atrioventricular node and in the specialized ventricular conduction system. These latent pacemakers will activate the heart when the normal pacemaker, the sinus node, is dysfunctional or when there is conduction block between sinus node and the rest of the heart. As such they are life -saving. Abnormal automaticity may occur anywhere when a group of cells is partially depolarized. Arrhythmias caused by abnormal automaticity are certain atrial tachycardias and accelerated idioventricular rhythms during the subacute phase of myocardial infarction, arising in cells of the specialized conduction system (Purkinje cells) overlying the infarct.
Triggered activity is dependent on afterdepolarizations, oscillations in membrane potential that follow an action potential. Early afterdepolarizations occur during the repolarization phase of the action potential, delayed afterdepolarizations occur when repolarization is complete. When the amplitude of an afterdepolarization is large enough it can initiate an action potential, or a series of action potentials which are called triggered. Delayed afterdepolarizations occur during intracellular calcium overload, such as during digitalis intoxication, heart failure, or enhanced adrenergic activity. They occur particularly at rapid heart rates. Early afterdepolarizations occur at slow heart rates and conditions in which action potential duration is prolonged, such as during various forms of the long QT syndrome or during exposure to certain antiarrhythmic drugs that prolong the action potential (class III drugs, such as quinidine, flecainide, sotalol). The resulting arrhythmia is called Torsade de pointes, with characteristic twisting of the QRS complex in the electrocardiogram around the base line.
For many decades there has been debate about the question whether arrhythmias were due to ectopic foci or reentry. David Scherf was, since 1929, the great pioneer of attributing arrhythmias to abnormal foci, so much so that when in 1932 Holzmann and Scherf were the first to state that the abnormal electrocardiogram in the Wolff-Parkinson-White syndrome was due to an abnormal accessory pathway between atria and ventricles, he convinced his co-author that the arrhythmias in this syndrome would be due to an abnormal focus in this pathway. Later research proved that reentry was the cause, as had been predicted by G.R.Mines in 1914. Nowadays it is generally accepted that both mechanisms may play a role in a particular arrhythmia, where a premature impulse in an ectopic focus may trigger a sustained reentrant arrhythmia.
Often, arrhythmias caused by an ectopic focus are innocuous, such as in single atrial or ventricular premature beats (extra systoles) and no therapy is necessary. If they give rise to sustained arrhythmias, mapping of the spread of activation during the arrhythmias may detect the abnormal focus and radiofrequency ablation may be the proper cure.
Michiel J Janse MD, Amsterdam The Netherlands