Heart failure repeatedly ranks as one of the leading causes of death worldwide, and the most practical therapeutic strategy is plagued with thrombotic complications. Treatment options for these patients are heart transplantation—which is met with low supply—and heart-assist device implantation. One major characteristic yet undesired feature of heart-assist devices is elevated shear rates throughout the flow circuit. Blood components rely on deviations from physiological shear to sense bleedings events and trigger thrombosis. As a result, thrombotic complications are common in patients with circulatory support devices, and even more so when experiencing acute or chronic inflammation.The current state of knowledge regarding shear effects on thrombosis has largely been achieved through the ability of microfluidic devices. However, there remains a large gap in knowledge about the impact of historical features on thrombosis. The extremely large range of shear rates generated by heart-assist devices can greatly perturb platelets and thrombogenic agents from their resting state at any given moment of flow. Therefore, a locally restricted assessment of shear on thrombotic outcome is insufficient and incomplete, and a more accurate analysis of shear-driven thrombosis requires a device that considers an entire history of shear. This research sets the foundation for studying thrombosis while jointly controlling shear history and shear rates by discussing the theory and design behind a massively parallel microfluidic device. Furthermore, the initiation and evolution of early forming microthrombi is stressed in this work analysis, as these dynamics become muddled with longer perfusion times. These dynamics become resolved once individual thrombi are tracked with perfusion time and when the entire population of developing thrombi are viewed as an ensemble. These tools are highly applicable to the study of other thrombotic complications, and this thesis delves into the problem of immunothrombosis through elevated IL-6 in serum.