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Francis X. Witkowski

Researcher at University of Alberta

Publications -  26
Citations -  1199

Francis X. Witkowski is an academic researcher from University of Alberta. The author has contributed to research in topics: Ventricular fibrillation & Defibrillation. The author has an hindex of 12, co-authored 26 publications receiving 1170 citations. Previous affiliations of Francis X. Witkowski include Dalhousie University.

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Journal ArticleDOI

Spatiotemporal evolution of ventricular fibrillation

TL;DR: High spatial and temporal resolution mapping of optical transmembrane potentials can easily detect transiently erupting rotors during the early phase of ventricular fibrillation, characterized by a relatively high spatiotemporal cross-correlation.
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Intramural reentry as a mechanism of ventricular tachycardia during evolving canine myocardial infarction.

TL;DR: Detailed anatomical analysis of the resultant infarcts demonstrated the thin surviving epicardial tissue rim to be the site of conduction delay necessary for reentry, whereas ‘preferred pathways’ of exit into the subendocardial plane occurred at the infarCT borders and were of variable configuration.
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Mechanism of cardiac defibrillation in open-chest dogs with unipolar DC-coupled simultaneous activation and shock potential recordings.

TL;DR: The hypothesis that a critical mass of myocardium must be affected for successful defibrillation is supported and that unsuccessful defibrillillation is always accompanied by residual fibrillating activity in at least one site.
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Evidence for determinism in ventricular fibrillation.

TL;DR: Using a recently formulated technique for in vivo cardiac transmembrane current estimation and a newly formulated measure of nonlinear determinism, ventricular fibrillation in vivo exhibits deterministic dynamics similar to those previously used in chaos control.
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In vivo estimation of cardiac transmembrane current.

TL;DR: A remarkably simple in vivo technique that incorporates an electrode array with cellular dimensions to continuously estimate the extracellular counterparts of cardiac Ims, culminating in either severely depressed Na(+)- mediated or Ca(2+)-mediated activations.