Platelets play an essential role in thrombotic processes. Recent studies suggest a direct link between increased plasma
glucose,
lipids, and inflammatory
cytokines with platelet activation and aggregation, resulting in an increased risk of atherothrombotic events in cardiovascular patients. Antiplatelet
therapies are commonly used for the primary prevention of
atherosclerosis. Transitioning from a population-based strategy to patient-specific care requires a better understanding of the risks and advantages of antiplatelet
therapy for individuals. This proof-of-concept study evaluates the potential to assess an individual's risk of forming
atherothrombosis using a dual-channel microfluidic model emulating multiple atherogenic factors in vitro, including high
glucose, high
cholesterol, and inflammatory
cytokines along with
stenosis vessel geometry. The model shows precise sensitivity toward increased plasma
glucose,
cholesterol, and tumour
necrosis factor-alpha (TNF-α)-treated groups in
thrombus formation. An in vivo-like dose-dependent increment in platelet aggregation is observed in different treated groups, benefiting the evaluation of
thrombosis risk in the individual condition. Moreover, the model could help decide the effective dosing of
aspirin in multi-factorial complexities. In the high
glucose-treated group, a 50 μM dose of
aspirin could significantly reduce platelet aggregation, while a 100 μM dose of
aspirin was required to reduce platelet aggregation in the
glucose-TNF-α-treated group, which proves the model's potentiality as a tailored tool for customised
therapy.