Why the study?
Mutations in the cardiac ryanodine receptor Ca2+ release channel can cause deadly ventricular arrhythmias and AF, with the RyR2-P2328S mutation producing CPVT and AF in homozygous RyR2S/S mouse hearts.
The RyR2-P2328S mutation significantly alters Ca2+ activation and inactivation gating, correlating with altered Ca2+ homeostasis and the CPVT/AF phenotypes.
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Does not support changes in CPVT/AF management; leaves open the Ca2+-dependent effects of P2328S RyR2.
Salvage et al. (2019) studied this question.
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