"THEORY & COMP IN MOL BIO PHY", AUG 9-20, 2006, LA JOLLA, CA

点击翻译按钮获取中文摘要

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. In normal cardiac conduction, a roughly rectilinear wave of electrical activation causes the wave of muscular contraction that is the heartbeat. In ventricular fibrillation (VF), the leading cause of sudden cardiac death, the wave of electrical activation breaks up into a multi-wave chaotic state. Our research has focused on the question: why does the wave break up? The traditional view was that the wave was broken up by anatomic heterogeneity: such factors as fibrosis, infarct, and loss of cell-to-cell electrical coupling were thought to play the decisive role. However, nonlinear dynamicists have proposed another mechanism: rectilinear waves, governed by reaction-diffusion partial differential equations, can become unstable and break up, even in perfectly homogeneous tissue, due to electrical instabilities. Our work in cardiac tissue preparations has shown that interventions that address these electrical instabilities can prevent fibrillation. (Garfinkel, Kim et al. 2000) The objective of this research is to answer the questions: how important are these two types of factors (anatomical heterogeneity and purely dynamical instability) in generating and sustaining fibrillation? How do they interact?