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  • 1
    Digitale Medien
    Digitale Medien
    350 Main Street , Malden , MA 02148-5018 , USA , and 9600 Garsington Road , Oxford OX4 2DQ , UK . : Blackwell Science Inc
    Journal of cardiovascular electrophysiology 15 (2004), S. 0 
    ISSN: 1540-8167
    Quelle: Blackwell Publishing Journal Backfiles 1879-2005
    Thema: Medizin
    Notizen: Introduction: It has been reported that electrical stimulation can control spiral wave (SW) reentry. However, previous research does not account for the effects of stimulus-induced virtual electrode polarization (VEP) and the ensuing cathode-break (CB) excitation. The aim of the present study was to examine the interaction of VEP with SW reentry in a bidomain model of electrical stimulation and thus provide insight into the mechanistic basis of SW control. Methods and Results: We conducted 3,168 simulations of localized stimulation during SW reentry in an anisotropic bidomain sheet. Unipolar cathodal 2-ms stimuli of strengths 4, 8, 16, and 24 mA were delivered at 99 locations in the sheet. The interaction between stimulus-induced VEP and SW reentry resulted in 1 of 3 possible outcomes: SW shift, SW breakup, or no effect. SW shift, which could be instrumental in SW termination at an anatomic or functional line of block, resulted from CB rather than cathode-make excitation. Stimulus timing, site, and strength all were important factors in VEP-mediated SW control. Furthermore, we found that the number of episodes of SW shift across the fibers was more sensitive to stimulus strength than that of SW shift along the fibers. SW shift can be explained by the interaction between the four VEP-induced wavebreaks and the wavebreak of the SW, ultimately resulting in termination of the original SW and the survival of one of the VEP-induced wavebreaks. This establishes a new SW reentry. Conclusion: This study provides new mechanistic insight into SW control. (J Cardiovasc Electrophysiol, Vol. 15, pp. 226-233, February 2004)
    Materialart: Digitale Medien
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 2
    ISSN: 1540-8167
    Quelle: Blackwell Publishing Journal Backfiles 1879-2005
    Thema: Medizin
    Notizen: Electroporation in a Model of Cardiac Defibrillation. Introduction: It is known that highstrength shock disrupts the lipid matrix of the myocardial cell membrane and forms reversible aqueous pores across the membrane. This process is known as “electroporation.” However, it remains unclear whether electroporation contributes to the mechanism of ventricular defibrillation. The aim of this computer simulation study was to examine the possible role of electroporation in the success of defibrillation shock. Methods and Results: Using a modified Luo-Rudy-1 model, we simulated two-dimensional myocardial tissue with a homogeneous bidomain nature and unequal anisotropy ratios. Spiral waves were induced by the S1-S2 method. Next, monophasic defibrillation shocks were delivered externally via two line electrodes. For nonelectroporating tissue, termination of ongoing fibrillation succeeded; however, new spiral waves were initiated, even with high-strength shock (24 V/cm). For electroporating tissue, high-strength shock (24 V/cm) was sufficient to extinguish ongoing fibrillation and did not initiate any new spiral waves. Weak shock (16 to 20 V/cm) also extinguished ongoing fibrillation; however, in contrast to the highstrength shock, new spiral waves were initiated. Success in defibrillation depended on the occurrence of electroporation-mediated anodal-break excitation from the physical anode and the virtual anode. Some excitation wavefronts following electrical shock used a deexcited area with recovered excitability as a pass-through point; therefore, electroporation-mediated anodal-break excitation is necessary to block out the pass-through point, resulting in successful defibrillation. Conclusion: The electroporation-mediated anodal-break excitation mechanism may play an important role in electrical defibrillation.
    Materialart: Digitale Medien
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 3
    ISSN: 1540-8167
    Quelle: Blackwell Publishing Journal Backfiles 1879-2005
    Thema: Medizin
    Notizen: Tissue Structure and VF. Introduction: It is unclear how the patterns of wavelet propagation during ventricular fibrillation (VF) vary between structurally different tissues. We hypothesized that the structural complexities of septal tissue influence the maintenance of reentrant wavelets in the ventricle. Methods and Results: Endocardial activation patterns during VF were analyzed in the isolated, perfused canine right ventricular (RV) free wall (n = 9), interventricular septum (n = 5), and left ventricular (LV) free wall (n = 6) using a computerized mapping system (2-mm resolution) with 120-msec consecutive windows. Each tissue sample was cut progressively to reduce the tissue mass until the VF was terminated. More wavelets were seen in the septa than in the RV and LV free walls at baseline (P = 0.004), and VF in the septa displayed a shorter cycle length than in the RV and LV free walls (P = 0.017). As the tissue mass decreased, VF became successively more organized in all regions: the number of wavelets decreased and the cycle length of VF lengthened. Single and “figure-of-eight” stationary, reentrant wavelets often were mapped after tissue mass reduction in the RV free walls and rarely in the LV free walls, but they were not observed in the septa. Less critical mass was required to maintain VF in the septa than in the RV and LV free walls (P = 0.0006). Gross anatomic and histologic examinations indicated that the tissue structure of the septa is more complex than that of the RV and LV free walls. Conclusion: VF activation patterns with progressive reduction of tissue mass differ for the septum and the ventricular free walls. The structural complexities of the septal tissue influence the maintenance of fibrillation in the ventricle.
    Materialart: Digitale Medien
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 4
    Digitale Medien
    Digitale Medien
    350 Main Street , Malden , MA 02148 , USA , and 9600 Garsington Road , Oxford OX4 2DQ , UK . : Blackwell Science Inc
    Journal of cardiovascular electrophysiology 14 (2003), S. 0 
    ISSN: 1540-8167
    Quelle: Blackwell Publishing Journal Backfiles 1879-2005
    Thema: Medizin
    Notizen: 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)
    Materialart: Digitale Medien
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 5
    ISSN: 1540-8167
    Quelle: Blackwell Publishing Journal Backfiles 1879-2005
    Thema: Medizin
    Notizen: Breakthroughs in VF Depend on Rotational Anisotropy. Introduction: The left ventricle (LV) and right ventricle (RV) are characterized by specific fiber orientation known as “rotational anisotropy.” However, it remains unclear whether the LV and RV are different with regard to the effect of rotational anisotropy on the dynamics of scroll waves during ventricular fibrillation (VF). To resolve this issue, we used a computation-based model to study scroll wave behavior. Methods and Results: We composed an environment of simulated three-dimensional ventricular wall slabs, with optional ratios of fiber rotation to wall thickness (0°, 6°, and 12°/mm thickness; LV 10 mm, RV 5 mm), using Luo-Rudy phase I equations. When rotational anisotropy was not incorporated into the LV wall slab (θendo˜θepi= 0°), most scroll waves rotated around the filaments perpendicular to the tissue surface, with only a few accompanying breakthrough waves. In a twisted LV model (θendo˜θepi= 60° and 120°), the scroll waves were demonstrated as multiple wavelets scattered spatiotemporally, frequently accompanied by breakthrough waves that were promoted by rotational anisotropy. In a twisted RV model (θendo˜θepi= 30° and 60°), single scroll waves and/or figure-of-eight reentrant waves appeared, with comparatively few breakthrough waves, regardless of the degree of fiber twist. Conclusion: The proportion of electrical effects of rotational anisotropy and tissue boundaries plays an important role in the genesis of breakthrough waves during VF, and the difference in wave propagating patterns and frequency spectrum of the ventricles may arise, in part, from the number of breakthrough waves promoted by rotational anisotropy.
    Materialart: Digitale Medien
    Standort Signatur Einschränkungen Verfügbarkeit
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