Every 40 seconds someone in the United States experiences an acute myocardial infarction, or related disease. Cardiac disease models superior to current human and animal models are necessary to advance our understanding of cardiac diseases and biomarkers. This thesis offers a "proof of concept" disease model using induced cardiomyocytes differentiated from human induced pluripotent stem cells to mimic the ischemia and reperfusion stresses the human heart endures during an AMI. The cells were stressed both chemically and physically, and the cells were tested for the release of the cardiac stress microRNA biomarker, miRNA-499-5p using reverse transcription quantitative PCR. After 48 hours of hypoxia the released miRNA increased 40-fold and the increase was more than 80-fold after 3 hours. The levels peaked at 6 hours and remained high for 24 hours. With optimization, this disease model can be used to study the release pattern of miRNA biomarkers in various cardiac conditions.