Several investigators around the turn of the 19th century confirmed the association between coronary artery occlusion, coronary artery reperfusion and ventricular fibrillation (VF) experimentally.^w1 MacWilliam was probably the first to recognise the clinical importance of these findings in humans, suggesting in 1889 that syncope could result from coronary occlusion, VF with loss of cardiac output.^w1 MacWilliam also described termination of VF in man that was achieved by repetitive electric shocks applied through a large pair of electrodes placed over the cardiac apex and the sixth or seventh dorsal vertebra.^w2

Mines and Garrey subsequently described the role of re-entry as a mechanism for fibrillation in the early part of the 20th century.^w1 Mines suggested that an area of conduction block must be present to facilitate re-entry.^w1 This observation is explained in fig 1. Prolonged myocardial repolarisation will provide an area of functional conduction block (as occurs in ischaemic ventricular tissue) and thus a substrate for re-entry.

Garrey also noted that a “critical mass” of cardiac tissue was required to maintain fibrillation.^w2 These seminal observations have provided a foundation for our understanding of ventricular fibrillation.

It is generally agreed that spontaneous re-entrant arrhythmias can be initiated by the interaction between a propagating wavefront and …