Abstract
In 1962 Moe[1] proposed the so-called multiple wavelet hypothesis to explain the mechanisms of self perpetuating atrial fibrillation. According to this hypothesis fibrillation is maintained by the presence of a number of independent wavelets that travel randomly through the myocardium around multiple barriers of refractory tissue. The key element of this hypothesis is that the “wavefront becomes fractionated as it divides about islets or strands of refractory tissue, and each of the daughter wavelets may now be considered as independent offspring. Such a wavelet may accelerate or decelerate as it encounters tissue in a more or less advanced state of recovery. It may divide again or combine with a neighbor; it may be expected to fluctuate in size and change in direction. Its course, though determined by the excitability or refractoriness of surrounding tissue, would appear to be as random as Brownian motion”[2].
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© 1992 Springer Science+Business Media Dordrecht
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Allessie, M.A., Kirchhof, C. (1992). Termination of Atrial Fibrillation by Class IC Antiarrhythmic Drugs, a Paradox?. In: Kingma, J.H., van Hemel, N.M., Lie, K.I. (eds) Atrial Fibrillation, a Treatable Disease?. Developments in Cardiovascular Medicine, vol 139. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-1816-3_4
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DOI: https://doi.org/10.1007/978-94-011-1816-3_4
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