Key result
Alternans develops when decreased L-type channel opening and altered SR Ca2+ content cause spatially fragmented SR Ca2+ release, provided SR Ca2+ is sufficient to sustain wave propagation.
Systolic Ca2+ alternans in ventricular myocytes is driven by spatially fragmented SR Ca2+ release resulting from decreased L-type Ca2+ channel opening and altered SR Ca2+ content.
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Does not support clinical translation to arrhythmia management; leaves open mechanistic role of depolarization amplitude in intact hearts.
Li et al. (2009) studied Systolic Ca2+ alternans. Changes in depolarizing pulse amplitude, caffeine, and Cd2+ was evaluated on Systolic Ca2+ alternans magnitude and Ca2+ wave propagation. Alternans develops when decreased L-type channel opening and altered SR Ca2+ content cause spatially fragmented SR Ca2+ release, provided SR Ca2+ is sufficient to sustain wave propagation.
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