Heterogeneity of left ventricular signal characteristics in response to acute vagal stimulation during ventricular fibrillation in dogs.

Studies have shown that long-term vagal stimulation is protective against ventricular fibrillation; however, the effects of acute vagal stimulation during ventricular fibrillation in the normal heart have not been investigated. We examined the effects of acute vagal stimulation on ventricular fibrillation in a canine model. In 4 dogs, we induced 30-second periods of ventricular fibrillation by means of intraventricular pacing. During 2 of the 4 periods of fibrillation that we analyzed, vagal stimulation was delivered through electrodes in the caudal ends of the vagus nerves. Noncontact unipolar electrograms were recorded from 3 ventricular regions: the basal septum, apical septum, and lateral free wall. We then computed the most frequent cycle length, mean organization index, and mean electrogram amplitude for each region. During fibrillation, vagal stimulation shortened the most frequent cycle lengths in the basal septum (P=0.02) and apical septum (P=0.0001), but not in the lateral wall (P=0.46). In addition, vagal stimulation significantly reduced the mean organization indices in the apical septum (P <0.001) and lateral wall (P <0.001), but not in the basal septum (P=0.19). Furthermore, vagal stimulation raised the mean electrogram amplitude in the basal septum (P <0.01) but lowered it substantially in the apical septum (P=0.00005) and lateral wall (P=0.00003). We conclude that vagal stimulation acutely affects the characteristics of ventricular fibrillation in canine myocardium in a spatially heterogeneous manner. This nonuniformity of response may have implications with regard to manipulating the autonomic system as a means of modifying the substrate for ventricular dysrhythmias.

Analysis of electrically induced reentrant circuits in a sheet of myocardium.

Understanding the complex spatiotemporal dynamics of action potential propagation in the heart during arrhythmia is exceedingly difficult. This study applies nonlinear dynamics tools to simplify this task. Using the results of a simulation of an electrical induction of reentry in a sheet of myocardium represented as a bidomain, transmembrane voltage maps are processed to obtain: (i) spatial maps of phase angle and phase singularity trajectories, (ii) state scatter plots, and (iii) spatial maps of even phase resetting, wave fronts and wave tails. Tracking the phase singularities allows us to identify the "seeds" of reentry before the reentrant circuit is formed and to characterize the spatiotemporal evolution of the organizing center of the reentrant circuit. The state scatter plots demonstrate the effect of the shock on the instantaneous state of the system. The spatial maps of even phase resetting allow us to identify the shock-induced excitable gaps (regions of regenerative repolarization) as well as the regions directly activated by the shock. These nontraditional approaches to the analysis of electrophysiological phenomena greatly enhance our ability to conceptualize the dynamics of arrhythmias.