Spinal and bulbar muscular atrophy (SBMA), also known as Kennedy’s disease, is a rare X-linked neurodegenerative disorder that affects men. A polyglutamine expansion in the first exon of the androgen receptor (AR) causes progressive muscle weakness and atrophy in the facial, bulbar, and limb muscles. AR is a steroid hormone nuclear receptor that dimerizes upon ligand binding and recruits co-factors to regulate androgen responsive elements. Approximately 50% of SBMA patients exhibit arrhythmia by electrocardiogram, and some patients are susceptible to sudden cardiac arrest. It is not clear whether these cardiac complications are caused by inherent problems with the heart or are a secondary outcome of co-morbidities, including hypertension and diabetes. In this study, we test whether the polyglutamine expansion in AR causes cell-intrinsic problems in cardiomyocytes. We use human induced pluripotent stem cells (iPSCs) bearing polyglutamine expansions in AR to model the disease. Immunostaining of AR in cardiomyocytes differentiated from iPSCs shows AR translocation to the nucleus upon treatment with 5α-dihydrotestosterone (DHT), a potent ligand and metabolite of testosterone. We observe differences in cell size and sarcomere density in SBMA cardiomyocytes compared to healthy controls. Calcium imaging reveals that SBMA iPSC-cardiomyocytes are susceptible to arrhythmic events and that this propensity is not dependent on ligand binding. These data demonstrate that mutant AR induces cell-intrinsic problems with calcium handling, suggesting that SBMA patients exhibit arrhythmias due to inherent deficits in cardiac function. This work provides insight into the mechanistic origins of heart complications in SBMA, highlighting the importance of cardiac care for SBMA patients.