Specific carboxyl-tail fragments of L-type Ca²⁺ channel maybe responsible for the voltage-dependence of cardiac CICR.

Ca²⁺ signaling in human fibroblast-derived cardiomyocytes shows similar voltage-dependence of CICR and Ca²⁺ spark properties as those of adult mammalian cardiomyocytes.

CPVT mutants myocytes of N-terminal and cytoplasmic-domains show smaller Ca²⁺ stores but longer, wandering, and recurrent Ca²⁺ sparks.

Myocytes expressing different point mutations express varied Ca²⁺ signaling phenotypes and pharmacological sensitivity.