In the normal heart, the impulse generated in the sinus node stops after sequential activation of atria and ventricles because it is surrounded by refractory tissue that it has just excited. A new impulse must arise in the sinus node before the chambers of the heart are subsequently activated, and there is a fairly long interval between the end of the refractory period after one activation and the beginning of the next one. When an impulse propagates through tissue in which differences in refractory periods exist, propagation may fail in regions with the longest refractory periods. These regions will be available for reexcitation, provided that the impulse propagating through areas where excitability has more fully recovered can return to the site of block. Because normally there is a long diastolic interval where excitability is normal, such a situation is most likely to occur during propagation of premature impulses, because refractory periods shorten at short cycle lengths, and therefore, the pathway over which the impulse must propagate to return to the site of unidirectional block is shortened as well. Briefly, reentry may occur when there is a region of unidirectional block, when refractory periods are short, and when conduction is slow. To prove that an arrhythmia is due to reentry, one must demonstrate the presence of a zone of unidirectional block, map the activation sequence during the arrhythmia so that one can follow this sequence along a circular pathway until the wave front reenters the site of origin, and terminate the arrhythmia by cutting through the reentrant circuit.


In 1887 McWilliam suggested for the first time that disturbances in conduction could be a mechanism for tachyarrhythmias. In 1913 and 1914 Mines and Garrey conducted experiments that firmly established reentrant excitation as an arrhythmogenic mechanism, which was confirmed by Lewis in 1920. It was not until the 1960’s, when extensive mapping could be performed both in patients and during animal experiments, that reentry was widely demonstrated in a variety of arrhythmias.

Anatomical and functional reentry

In anatomical reentry, well defined anatomical structures are part of the reentrant circuit. Examples are the accessory atrioventricular connection in the Wolff-Parkinson-White syndrome, left and right bundle branches in bundle branch reentry, and surviving bundles of myocardium embedded in the scar of a healed myocardial infarction.

In functional reentry, the reentrant impulse propagates around an area with a functional (i.e. unassociated with an anatomical barrier) conduction block. In the leading circle concept, during wave rotation, the wavefront impinges on its refractory tail. The leading circle is the smallest possible pathway in which the impulse can continue to circulate, and in which the stimulating efficacy of the wavefront is just enough to excite the tissue ahead which is still in its relative refractory phase. Centripetal wavelets from the leading circle keep the core permanently refractory. Because the wavefront propagates through partially refractory tissue, the conduction velocity is reduced. Whereas in the leading circle model of functional reentry excitability is the crucial factor that determines the reentrant circuit, where the core is kept permanently refractory by centripetal wavelets, it has become apparent that the curvature of the circulating wavefront is another important factor in maintaining functional reentry. A curving wavefront may cease to propagate altogether when a critical curvature is reached, despite the presence of excitable tissue. The difference between such spiral waves, or rotors, and leading circle reentry is that in the latter the core is permanently refractory, whereas in the former the core is excitable but not excited. Examples of functional reentry are atrial and ventricular fibrillation and atrioventricular nodal reentry.

Michiel J Janse MD, Amsterdam The Netherlands