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. 2019 Aug 19;6(20):1900856. doi: 10.1002/advs.201900856

Figure 2.

Figure 2

a) Schematic of a stent strut causing disruption of the laminar blood flow resulting in platelet aggregation and reduction in vasomotive signaling molecules. b) A histological cross section of a stent strut surrounded by atherosclerotic platelet legion; the blood flow here was left to right. c) Schematic of an ultrathin stent strut promoting laminar flow keeping an intact endothelial barrier and allowing vasodilation promoters to act. d) A histological cross section of an ultrathin stent strut with minimal platelet aggregation surrounding the strut. NO, nitric oxide; PGI2, prostacyclin; TF, tissue factor; TFPI, tissue factor pathway inhibitor; TM, thrombomodulin; tPA, tissue plasminogen activator; vWF, von Willebrand factor; X, coagulation factor X; and Xa, activated coagulation factor X. Reproduced with permission.20 Copyright 2018, Springer Nature GmbH.