Cardiovascular disease has historically been the leading cause of death in the US [1], and coronary artery disease in particular accounts for over fifty percent of these deaths [1]. Since their approval in 1994, coronary stents have become one of the leading treatments for this disease. However, problems persist in both bare metal and drug-eluting stents (DESs) with long-term restenosis and thrombosis. It is well accepted that disruptions in arterial wall shear stress (WSS), especially low WSS, are linked to alterations in the endothelial cell layer, atherosclerosis, and thrombogenesis [2], although the exact mechanisms are still uncertain, and studies have shown that stent design is closely linked to clinical outcomes [3].

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