Auditory Working Memory Mediates the Relationship Between Musical Sophistication and Speech-In-Noise Perception.

Cardiomyopathies cause significant morbidity and mortality worldwide, yet therapeutic development is hindered by inadequate human disease models. This comprehensive review synthesizes advances in induced pluripotent stem cell-derived cardiac three-dimensional (3D) disease models, demonstrating their transformative potential for cardiovascular research. The sophisticated 3D models successfully recapitulate patient-specific disease phenotypes, enabling mechanistic investigation, high-throughput drug screening, and gene editing approaches impossible with conventional systems. By bridging the translational gap between animal models and human disease, cardiac models are revolutionizing precision medicine approaches for genetic cardiomyopathies. This review provides critical insights for researchers, clinicians, and pharmaceutical developers advancing therapeutic strategies from bench to bedside in cardiovascular medicine. Cardiomyopathies constitute a heterogeneous group of myocardial disorders affecting an estimated 10 million individuals worldwide and represent a major cause of heart failure, arrhythmias, and sudden cardiac death, particularly among younger and working-age populations. The prevalence of cardiomyopathies is estimated at approximately 1:250-1:500 individuals for common forms such as dilated and hypertrophic cardiomyopathy, with a substantial proportion attributable to genetic causes. In the United States, dilated cardiomyopathies (DCM) contribute significantly to the burden of heart failure and are a leading indication for advanced therapies including transplantation and mechanical circulatory support. In broader heart failure cohorts, 1-year case fatality has been reported to range from 4% to 45%, with a pooled average of approximately 33%. Dilated cardiomyopathy, in particular, is often progressive and may lead to advanced heart failure and death in the absence of definitive therapy. Device-based therapies such as implantable cardioverter-defibrillators and cardiac resynchronization therapy reduce arrhythmic risk and improve cardiac function but do not address the underlying disease biology. For patients with advanced disease, left ventricular assist devices serve as bridge-to-transplant or destination therapy, although their use is limited by significant complications. Cardiac transplantation remains the definitive treatment but is severely constrained by donor organ scarcity, restricting access to a small proportion of eligible patients. Moreover, lifelong immunosuppression exposes recipients to infection, malignancy, and allograft vasculopathy. Collectively, these limitations point to an urgent need for human disease models that can reveal truly disease-modifying therapies and reliably predict individual disease trajectories and treatment responses, while accurately reflecting the complexity of cardiac physiology and the substantial genetic and phenotypic heterogeneity of cardiomyopathies. Traditional research models, including transgenic animals and heterologous cell cultures, have provided valuable insights but often fail to fully recapitulate the complexity and specificity of human cardiac pathophysiology.