Influences Of Ischemia On Ventricular Fibrillation Threshold And Vulnerable Period In A 3D Computer Model Of A Heart

A computer model has been developed to simulate the threedimensional nature of electrical propagation through the ventricles of a heart. With it, we have investigated how the vulnerability of the heart to ventricular fibrillation (VF) is influenced by increasing degrees of localized ischemia. Vulnerability was quantified by determining the minimum number of premature stimuli required to induce VF (ie: tk VF threshold). The premature stimuli were timed such that stimuli depolarized an ectopic site after a constant delay relative to the end of the site’s absolute refractory period. For the normal heart (ie: 0% ischemia), a well-defined 16 msec “window of vulnerability’’ to VF induction was found to exist exclusively during the ectopic site’s relative refractory period. This window remained constant in shape and size up through ischemic levels of 30%. However, as the degree of ischemia increased through W%, the Vulnerable period increased in both breadth and depth, such that VF became inducible at progressively longer and shorter delays, and the VF thresholds for all delays within the window fell. These trends reversed directions for the infarcted heart (ie: 100% ischemia), although they did not quite etu urn to the levels found in the normal case. Thus, ischemia influenced this model’s vulnerability to VF through two mechanisms : it globally decreased the threshold at which VF occurred, and it increased the span of time within the cardiac cycle during which the heart was susceptible to premature stimuli.