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Abnormal intracellular calcium cycling and spontaneous calcium release are critical mechanisms underlying focal excitations that initiate triggered arrhythmias and fibrillation.
Clinical studies have shown that sudden death is initiated by an ill-timed propagated ectopic beat that leads to fibrillation.1-4 However, the mechanism underlying these focal excitations is not completely understood. Experimental studies have demonstrated that abnormal calcium (Ca2+) cycling is a critical factor in the development of focal excitations.5-9 These excitations can be caused by spontaneous Ca2+ release (SCR) in the form of intracellular Ca2+ waves. These waves are initiated when Ca2+ release from a few Ca2+ release units (CRUs) on the sarcoplasmic reticulum (SR) causes regenerative release in adjoining units via Ca2+-induced Ca2+ release (CICR), causing Ca2+ wave propagation. The resulting depolarizing inward current through the electrogenic Na+-Ca2+ exchanger (NCX) depolarizes the cell.
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Shiferaw et al. (2012) studied this question.
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