Abstract
Blackwell et al (JCI Insight January 6, 2022;doi:10.1172/jci.insight.151893, PMID 34990403) investigated the sources of ventricular arrhythmia triggered by delayed afterdepolarizations (DADs) in catecholaminergic polymorphic ventricular tachycardia (CPVT) syndrome by using cardiac calsequestrin knockout mice. The authors demonstrated that loss of calsequestrin in only ventricular myocytes produced a full-blown CPVT phenotype whereas mice with loss of calsequestrin in only Purkinje cells were comparable to wild-type mice.
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