The heart is a four-chambered organ that is responsible for pumping blood throughout the body. The organ is characterized by highly organized cardiac tissues coupled with intricate electrical and mechanical function to allow for efficient pumping function. Once injured, this organization is lost and maladaptive structural remodeling resulted in sarcomere disorganization and declined contractile function. To counteract this maladaptive remodeling, it is imperative to elucidate the behavior of cardiac muscle in order to predict its response to injury. In this thesis, the morphological and contractile changes in cardiomyocytes were studied using the scratch assay and the newly developed “physical injury on a cardiac chip” platform. From the morphology study, it was concluded that there was an effect on the cytoskeletal structures of cardiomyocytes exposed to the induced injury. Interestingly, this effect was local to the critical zone (0 – 250 m) immediately next to the wound border and there was no propagating effect to the farther surrounding cardiac cells. This conclusion was supported in the contractility study findings where cardiac cells outside of the critical zone displayed contractile stresses and cytoskeletal organization similar to those found in normal cardiac tissues unexposed to any kind of injury. Thus, a better in vitro cardiac injury model is needed to explore the morphological and functional changes in cardiomyocytes that further mimic the response in myocardial infarction and ischemic injuries.