Myosin is the molecular motor that drives muscle contraction. Alterations that affect the motor's kinetic and mechanical properties are associated with the pathogenesis of human cardiomyopathies. We investigated the influence of Drosophila melanogaster myosin mutations on the structure and function of fly hearts. Beating hearts expressing D45 (hypoactive) or Mhc5 (hyperactive) myosins were imaged using direct immersion DIC optics in conjunction with a high‐speed digital camera. Cardiac movements were monitored via edge tracings obtained from processed movies. Our novel image and computational analysis revealed that depressed motor function in D45 flies produced a dilatory cardiac response, similar to that found in vertebrates expressing myosin with specific dilated cardiomyopathy mutations. This suggests an apparently conserved pathological response to impaired motor function. Mhc5 hearts with enhanced myosin function showed phenotypes analogous to those seen in restrictive cardiomyopathy, suggesting the human disease could have similar origins. Our data suggest Drosophila is a valuable system for modeling and identifying mutations analogous to those associated with human cardiac disorders. We are currently exploiting the power of Drosophila to manipulate genetic interactions between sarcomeric components. Our goal is to suppress defects in hearts with distinct myofibrillar mutations.