Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a life threatening genetically inherited cardiac disease characterized by arrhythmias under adrenergic stress. Mutations in the cardiac ryanodine receptor (RYR2) are the leading cause for CPVT. The role of calcium in CPVT has been previously studied [1], but the association between membrane potential and contractile function in arrhythmia is not well understood. In this study, we characterized electrophysiological properties of CPVT patient-specific induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) carrying different mutations in RYR2. In addition, we evaluated effects of carvedilol and flecainide on action potential (AP) and contractile properties of hiPSC-CMs. Both drugs have been shown to directly affect RYR2. iPSC-CMs were generated from skin biopsies of CPVT patients carrying exon 3 deletion (E3D) and L4115 mutation in RYR2 and of a healthy individual. Cardiac differentiation was carried out by the END2 method and CMs were dissociated and plated as single or miniaggregates. APs and video were recorded simultaneously from the same hiPSC-CMs. Conventional perforated patch clamp technique was synchronized with imaging system to acquire membrane voltage and contractile dynamics. Only ventricular CMs (APD90/APD50 < 1.3) were analyzed. Differences in AP properties (Table1) were seen in CPVT and control CMs: APD90 of both E3D (n=37) and L4115F (n=57) CPVT CMs was shorter than control CMs (n=41). E3D-CPVT CMs had shortest APD90, lowest APA, dVdT and more positive MDP than control or L4115F CPVT CMs. Furthermore, more arrhythmic events, DADs, EADs and alternans were seen in CPVT CMs compared to controls. Adrenaline decreased APD10, 50 and 90 and increased beat rate in all hiPSC CMs. Carvedilol and flecainide increased APD10, 50 and 90 and decreased beat rate in all hiPSC CMs. Both drugs increased the APD90 the most in L4115F CPVT CMs. EADs were pronounced also in contractile profile unlike DADs. APD alternans was characterized by amplitude changes in contractile profile. iPSC-CMs provide a unique platform for disease modeling and testing drugs for CPVT. Combining electrophysiological measurements we can gain deeper insight into mechanisms of arrhythmias.