Cardiovascular disease continues to be the leading cause of morbidity and mortality in the United States and the costs associated with the management of these diseases exceed 300 billion dollars [1]. The most common form of heart disease, coronary heart disease, results from a narrowing of the blood vessels due to the buildup of plaque in the arteries. Over time, coronary heart disease weakens the heart muscle and can lead to heart failure, a condition where the heart muscle can no longer generate enough force to efficiently deliver blood to the body. Despite recent advances in medical and device therapies, there are no effective treatment strategies for heart failure. Although the death rates of heart disease have declined in the last decade, the disease burden remains high [1]. The risk of cardiovascular disease also increases with age due to diminished cardiac function associated with age-related morphological and structural changes and loss of cardiomyocytes [2]. Treatment modalities have been hampered by the fact that the maintenance and repair mechanisms of the heart are limited. Thus, novel approaches and techniques to improve or restore cardiac function must be developed, including the development of cardiomyocyte (CM) models for in vitro disease modeling, drug screening, cell-based therapies, and toxicity studies. CM toxicity models are critically important because cardiotoxicity is a primary reason drugs fail pre-clinical studies or clinical trials and accounts for the majority of drug recalls [3].
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