Vortex cordis as a mechanism of postshock activation:: arrhythmia induction study using a bidomain model.
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 m...
| Publicado en: | Journal of Cardiovascular Electrophysiology Vol. 14; no. 3; pp. 295 - 303 |
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| Autores principales: | , , , , , , , |
| Formato: | Journal Article |
| Publicado: |
Wiley-Blackwell
Mar2003
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| Acceso en línea: | Ver este registro en EBSCOhost |
| fields | @attributes: recordID: 1 pdfLink: plink: https://search.ebscohost.com/login.aspx?direct=true&db=ccm&AN=106102094&site=ehost-live header: @attributes: shortDbName: ccm uiTerm: 106102094 longDbName: CINAHL Complete uiTag: AN controlInfo: bkinfo: dissinfo: jinfo: jid: 10453873 GSB jtl: Journal of Cardiovascular Electrophysiology issn: 10453873 maglogo: Y pubinfo: dt: Mar2003 vid: 14 iid: 3 pid: 480 pub: Wiley-Blackwell place: Malden, Massachusetts artinfo: ui: 106102094 2009472116 NLM12716113 106102094 ppf: 295 ppct: 8 formats: fmt: @attributes: type: P tig: atl: Vortex cordis as a mechanism of postshock activation:: arrhythmia induction study using a bidomain model. aug: au: Ashihara T Namba T Yao T Ozawa T Kawase A Ikeda T Nakazawa K Ito M sug: subj: Cardioversion Methods Heart Ventricle Physiology Membrane Potentials Physiology Arrhythmia Etiology Arrhythmia Physiopathology Arrhythmia Therapy Cardiovascular System Physiology Computer Simulation Models, Biological Myocardium ab: 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.(J Cardiovasc Electrophysiol, Vol. 14, pp. 295-302, March 2003). pubtype: Academic Journal doctype: Journal Article ougenre: Article language: English refInfo: holdings: @attributes: islocal: N |
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