Baher Ali, Qu Zhilin, Hayatdavoudi Ashkan, Lamp Scott T, Yang Ming-Jim, Xie Fagen, Turner Stephen, Garfinkel Alan, Weiss James N
David Geffen School of Medicine at UCLA, Division of Cardiology, 47-123 CHS, 10833 LeConte Ave., Los Angeles, CA 90095-1679, USA.
Am J Physiol Heart Circ Physiol. 2007 Jan;292(1):H180-9. doi: 10.1152/ajpheart.00944.2005. Epub 2006 Aug 4.
Short-term cardiac memory refers to the effects of pacing history on action potential duration (APD). Although the ionic mechanisms for short-term memory occurring over many heartbeats (also called APD accommodation) are poorly understood, they may have important effects on reentry and fibrillation. To explore this issue, we incorporated a generic memory current into the Phase I Luo and Rudy action potential model, which lacks short-term memory. The properties of this current were matched to simulate quantitatively human ventricular monophasic action potential accommodation. We show that, theoretically, short-term memory can resolve the paradox of how mother rotor fibrillation is initiated in heterogeneous tissue by physiological pacing. In simulated heterogeneous two-dimensional tissue and three-dimensional ventricles containing an inward rectifier K(+) current gradient, short-term memory could spontaneously convert multiple wavelet fibrillation to mother rotor fibrillation or to a mixture of both fibrillation types. This was due to progressive acceleration and stabilization of rotors as accumulation of memory shortened APD and flattened APD restitution slope nonuniformly throughout the tissue.