A computer model study of the ventricular fibrillation vulnerable window: sensitivity to regional conduction depressions.
The cardiac vulnerable window is typically defined to be that portion of the cardiac cycle during which ectopic stimuli can induce ventricular fibrillation (VF). We have used cardiac electrophysiological computer modeling to investigate how the size and shape of the cardiac vulnerable window is affected by regional conduction velocity depressions (RCVDs), as might be found in ischemia. Computer simulations were performed on a three-dimensional finite-state, discrete-element model of the ventricles of a dog heart, with simulated RCVDs of 0% (normal) to 100% (infarcted) isolated to the apical region of this heart. Using a programmed electrical stimulation protocol, vulnerability was quantified as the number of ectopic stimuli necessary to induce VF. We observed a nonlinear and nonmonotonic relation between increases in RCVD and the vulnerability of the heart to ectopic stimuli. The size and shape of the vulnerable window remained stable through RCVDs of 30%, expanded rapidly thereafter through RCVDs of 90%, and then contracted significantly at the RCVD of 100%. These increases in vulnerability were manifest as both a lowering of the overall stimulus thresholds necessary for fibrillation (window "deepening"), and an increase in the fraction of the cardiac cycle susceptible to these ectopic stimuli (window "widening"). In all cases of induced VF, the mechanism of induction was through reentry facilitated by temporary functional block. Moreover, the ability to form such a block--and thus the likelihood of subsequent VF--was enhanced as the RCVD increased. Taken together, these results demonstrate the complex relation between vulnerability and RCVD and, at the very least, suggest that the entire shape of the vulnerable window, rather than just its minimum threshold, is important when determining a heart's electrical stability. These conclusions are supported by results obtained from an experimental study--which utilized a similar programmed stimulation protocol--of normal and ischemic canine hearts.
Fishler
M G
MG
Johns Hopkins University School of Medicine, Department of Biomedical Engineering, Baltimore, MD 21205.
Thakor
N V
NV
D000818:Animals; D002304:Cardiac Pacing, Artificial; D003198:Computer Simulation; D004285:Dogs; D004553:Electric Conductivity; D004558:Electric Stimulation; D004562:Electrocardiography; D004594:Electrophysiology; D006329:Heart Conduction System / Q000503:physiopathology*; D008955:Models, Cardiovascular; D014693:Ventricular Fibrillation / Q000503:physiopathology*