Simulated interactions between a Class III antiarrhythmic drug and a figure 8 reentry.
Ventricular Fibrillation is responsible for a majority of sudden cardiac death, but little is known about how ventricular tachycardia (VT) degenerates into ventricular fibrillation. Several clinical studies focused only on preventing VT with a class III antiarrhythmic drug resulted in many deaths. Our simulations investigate the interactions between an antiarrhythmic drug likely to suppress a VT and a Figure 8 reentry. A parameter AAR is introduced to increase the action potential duration and therefore simulate various Class III drugs. Simulations are ran under several conditions (phases of the reentry, values of AAR, durations). They show that a VT can be suppressed whatever the phase of the reentry but it strongly depends on the duration of the effect. It confirms that a drug which can suppress a reentry can also worsen it. It also shows a great variety of activation patterns and thus the complexity of antiarrhythmic drugs effects. Simulations also demonstrate that suppressing VT is an increasing function of AAR.
Maastro Lab, University of Maastricht, UNS 50/23, PO Box 616, 6200, MD Maastricht, The Netherlands. r.seigneuric@maastro.unimaas.nl
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Seigneuric
J-L
JL
Chassé
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Auger
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Bardou
D000200:Action Potentials / Q000187:drug effects; D000889:Anti-Arrhythmia Agents / Q000494:pharmacology / Q000627:therapeutic use*; D006801:Humans; D008954:Models, Biological; D014693:Ventricular Fibrillation / Q000188:drug therapy* / Q000503:physiopathology
D000889:Anti-Arrhythmia Agents