Hypertrophic cardiomyopathy (HCM) is a prevalent hereditary cardiac disorder linked to arrhythmia and sudden cardiac death. Myosin heavy chain (MYH7) is one of the major gene associated for HCM when mutated. To explain the mechanisms underlying HCM development, we generated three induced pluripotent stem cells (iPSC) lines from patient's skin fibroblasts, harboring three different mutations (MYH7 R403L, R403W and R403Q). We corrected one mutated codon (MYH7 R403L) using CRISPR/Cas9 editing to obtain the isogenic control line preserving the genomic background of the patient, and we used also a control iPSC line (ICAN-403.3). All iPSC lines are differentiated in cardiomyocytes (iPSC-CMs) and characterized by RT-qPCR and immunostaining as a quality control. MYH7 mutations affecting the cardiac sarcomere, we examinated the electrophysiological properties of iPSC-CMs at two stages of maturation : early stage (21 days of differentiation) and late stage (beyond 40 days of differentiation). Optical mapping, using fluorescent probes, high-speed cameras and electrical stimulation, offers detailed insights into cardiac activity by analysing membrane potential (RH 237) and calcium transient (Rhod-2). We anticipate that these findings will demonstrate electrophysiological differences between control iPSC-CMs and HCM iPSC-CMs, exacerbated by inotropic stimulation (isoproterenol) or prevented by treatment of Ca2+ dysregulation (verapamil) on HCM iPSC-CMs.