Catecholaminergic polymorphic ventricular tachycardia (CPVT) is an inherited 
arrhythmogenic cardiac disorder characterized by life-threatening arrhythmias 
induced by physical or emotional stress, in the absence structural heart 
abnormalities. The arrhythmias may cause syncope or degenerate into cardiac 
arrest and sudden death which usually occurs during childhood. Recent studies 
have shown that CPVT is caused by mutations in the cardiac ryanodine receptor 
type 2 (RyR2) or calsequestrin 2 (CASQ2) genes. Both proteins are key 
contributors to the intracellular Ca(2+) handling process and play a pivotal 
role in Ca(2+) release from the sarcoplasmic reticulum to the cytosol during 
systole. Although the molecular pathogenesis of CPVT is not entirely clear, it 
was suggested that the CPVT mutations promote excessive sarcoplasmic reticulum 
Ca(2+) leak, which initiates delayed afterdepolarizations (DADs) and triggered 
arrhythmias in cardiac myocytes. The recent breakthrough discovery of induced 
pluripotent stem cells (iPSC) generated from somatic cells (e.g. fibroblasts, 
keratinocytes) now enables researches to investigate mutated cardiomyocytes 
generated from the patient's iPSC. To this end, in the present article we review 
recent studies on CPVT iPSC-derived cardiomyocytes, thus demonstrating in the 
mutated cells catecholamine-induced DADs and triggered arrhythmias.