INTRODUCTION: The ventricular apex has a helical arrangement of myocardial fibers called the "vortex cordis." Experimental studies have demonstrated that the first postshock activation originates from the ventricular apex, regardless of the electrical shock outcome; however, the related underlying mechanism is unclear. We hypothesized that the vortex cordis contributes to the initiation of postshock activation. To clarify this issue, we numerically studied the transmembrane potential distribution produced by various electrical shocks. METHODS AND RESULTS: Using an active membrane model, we simulated a two-dimensional bidomain myocardial tissue incorporating a typical fiber orientation of the vortex cordis. Monophasic or biphasic shock was delivered via two line electrodes located at opposite tissue borders. Transmembrane potential distribution during the monophasic shock at the center of the vortex cordis showed a gradient high enough to initiate postshock activation. The postshock activation from the center of the vortex cordis was not suppressed, regardless of the initiation of spiral wave reentry. Spiral wave reentry was induced by the monophasic shock when the center area of the vortex cordis was partially excited by the nonuniform virtual electrode polarization. Postshock activation following the biphasic shock also originated from the center of the vortex cordis, but it tended to be suppressed due to the narrower excitable gap around the center of the vortex cordis. The electroporation effect, which was maximal at the center of the vortex cordis, is another possible mechanism of postshock activation. CONCLUSION: Our simulations suggest that the vortex cordis may cause postshock activation.
INTRODUCTION: The ventricular apex has a helical arrangement of myocardial fibers called the "vortex cordis." Experimental studies have demonstrated that the first postshock activation originates from the ventricular apex, regardless of the electrical shock outcome; however, the related underlying mechanism is unclear. We hypothesized that the vortex cordis contributes to the initiation of postshock activation. To clarify this issue, we numerically studied the transmembrane potential distribution produced by various electrical shocks. METHODS AND RESULTS: Using an active membrane model, we simulated a two-dimensional bidomain myocardial tissue incorporating a typical fiber orientation of the vortex cordis. Monophasic or biphasic shock was delivered via two line electrodes located at opposite tissue borders. Transmembrane potential distribution during the monophasic shock at the center of the vortex cordis showed a gradient high enough to initiate postshock activation. The postshock activation from the center of the vortex cordis was not suppressed, regardless of the initiation of spiral wave reentry. Spiral wave reentry was induced by the monophasic shock when the center area of the vortex cordis was partially excited by the nonuniform virtual electrode polarization. Postshock activation following the biphasic shock also originated from the center of the vortex cordis, but it tended to be suppressed due to the narrower excitable gap around the center of the vortex cordis. The electroporation effect, which was maximal at the center of the vortex cordis, is another possible mechanism of postshock activation. CONCLUSION: Our simulations suggest that the vortex cordis may cause postshock activation.
Authors: Partho P Sengupta; Vijay K Krishnamoorthy; Josef Korinek; Jagat Narula; Mani A Vannan; Steven J Lester; Jamil A Tajik; James B Seward; Bijoy K Khandheria; Marek Belohlavek Journal: J Am Soc Echocardiogr Date: 2007-05 Impact factor: 5.251