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See article by Chen et al. [14] (pages 220–232) in this issue. Ventricular and atrial fibrillation have fascinated clinical cardiologists and cardiac scientists since the beginning of the last century [1,2]. They are important determinants of cardiac mortality and morbidity, and their biophysical mechanisms share close similarities with spatio-temporal instabilities occurring in other excitable media, such as chemical and biological non-cardiac excitation–diffusion systems [3,4].Normal cardiac electrical excitation requires propagation from a pacemaker site and extinguishes after recovery to the resting state to be reexcited only by a new pacemaker pulse. However, even the normal myocardium fibrillates relatively easily if electrically stimulated by an appropriate protocol. In diseased states, tachycardia and fibrillation may arise from a local site hosting a pathological substrate (e.g. regional ischemia) and/or be perpetuated by a more general change in the electrophysiological properties of the tissue (e.g. general shortening of the refractory period). The observation in the experimental laboratory of the sudden transition of a regularly beating heart to fibrillatory activity of cardiac muscle had already stimulated important experiments early last century. Another series of key experiments by Dr. Gordon Moe and his collaborators started in 1959 [5]. By selecting the appropriate tools, these investigators could distinguish between two types of experimentally induced atrial fibrillation (AF). In a first case, local application of aconitine [6] would produce a type of AF that terminated upon mechanical isolation of the source (aconitine deposit) that initiated rapid focal excitation. In the second case, AF was induced by vagal stimulation and created AF, which was self-sustained. In this case, re-entry, requiring a critical mass of tissue for the circulating excitations to persist, was most likely responsible for maintenance of the arrhythmia. In 1964, based on a simulation study, Moe and Abildskov formulated the classical ‘multiple-wavelet’ hypothesis to … * Tel.: +41-31-631-8740; fax: +41-31-631-8785 kleber{at}pyl.unibe.ch

The fibrillating atrial myocardium. What can the detection of wave breaks tell us?