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Cardiac Tissue Analysis

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The conductive properties of cardiac tissue are an important part of an arrhythmogenic substrate. In a healthy heart rapid transmission of excitation and the refractory period, in which tissues remain unexcitable immediately following activation, work in concert to prevent reentry and arrhythmogenesis. Various diseases alter the conductive properties of myocardium, e.g. ischemia, creating favorable conditions for ectopy and reentry (Janse et al. 1980, Schalij et al. 1992, Wilders et al. 2000). Specifically, cardiomyopathies that cause a decrease in conduction velocity (CV), the rate of activation propagation through the myocardium, favor arrhythmogenesis by decreasing the critical wavelength necessary to foster reentry (Mines 1914). However, …show more content…
1988, Sawa et al. 2002). For example, invasive plaque electrode recordings from the epicardium of patients with long-standing persistent atrial fibrillation (AF), who are undergoing open heart surgery, suggest that conduction pathways become longitudinally dissociated (Allessie et al. 2013). This dissociation of muscle bundles, creates a substrate in which reentry can take root and perpetuate AF. Dissociation of the atrial muscle bundles would presumably have a differential effect on longitudinal and transverse CVs in the affected regions. However, existing techniques for assessing CV in the clinical setting currently lack the ability to differentiate longitudinal from transverse …show more content…
In the experimental laboratory multidetector arrays, e.g, plaque electrodes or optical mapping systems, facilitate the creation activation maps that track the spread of activation through the myocardium(Ideker et al. 1989). Such approaches allow calculation of longitudinal CV, traverse CV, and anisotropy ratios (Bayly et al. 1998). However, these techniques typically require invasive procedures that have not been readily translatable for routine clinical use. Furthermore, even in controlled laboratory environments the creation of activation maps from plaque electrode arrays, with dense spatial sampling of electrograms (EGMs), is hampered by the necessity of computing activation times for multiple channels that may contain

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