© 2000 by European Society of Cardiology
Copyright © 2000, European Society of Cardiology
The fibrillating atrial myocardium. What can the detection of wave breaks tell us?
Department of Physiology, University of Bern, Bühlplatz 5, CH-3012 Bern, Switzerland
* Tel.: +41-31-631-8740; fax: +41-31-631-8785 kleber@pyl.unibe.ch
Received 30 August 2000; accepted 30 August 2000
| The first 150 words of the full text of this article appear below. |
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