Inexcitable anatomical obstacles in normal homogeneous myocardium can induce electrical turbulence and high-frequency excitation due to wave front curvature effects.
May explain arrhythmia triggers at vascular sites in normal hearts; hypothesis-generating for curvature-driven reentry mechanisms.
In cardiac tissue, the propagation of electrical excitation waves is dependent on the active properties of the cell membrane (ionic channels) and the passive electrical properties of cardiac tissue (passive membrane properties, distribution of gap junctions, and cell shapes). Initiation of cardiac arrhythmias is usually associated with heterogeneities in the active and/or passive properties of cardiac tissue. However, as a result of the effect of wave front geometry (curvature) on propagation of cardiac waves, inexcitable anatomical obstacles, like veins and arteries, may cause the formation of self-sustained vortices and uncontrolled high-frequency excitation in normal homogeneous myocardium.
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Cabo et al. (1998) studied this question.
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