Increasingly, the link between genetics and cardiac disease is being elucidated, opening new questions about the multiscale nature of disease development and potential avenues for treatment. In particular, the role of active and passive mechanics in myocardial damage, inflammation, and fibrotic remodeling remains an open challenge particularly when considering genetic cardiac diseases. Desmoplakin (DSP) cardiomyopathy is a genetic cardiomyopathy of the desmoplakin protein involved in the desmosomes - providing the primary mode for cell-to-cell force transduction. Deficiencies in this force transduction leads to hallmark phenotypic subepicardial fibrosis that spreads around the heart wall, degrading cardiac function and output. While thought to result from cellular damage and scaring - the rationale behind this distinct phenotype and the best avenues for treatment remain unclear. To study the active and passive biomechanics in DSP cardiomyopathy, we followed a mulitscale approach. Engineered heart tissues of DSP were constructed to study the impact of increased contractility on strain, stress, and active mechanics. A cohort of DSP patients - at varying states of disease - were then analyzed to look at distinctive patterns of mechanics across patient hearts. From this, we examine the causal links between disease development and inherent alterations in biomechanics.