|Risk Factor||Effect on In-Stent ESS/Endothelial Response to ESS|
|Acute coronary syndrome|
|Incomplete endothelialization||→ Attenuation of physiologic ESS-induced endothelial production of PGI2, tPA, eNOS (2)|
|Hypersensitivity to the drug or polymer|
|Bifurcation stenting||→ Adverse hemodynamic impact on the inherently complex ESS environment (68–70)|
|Excessive stent length|
|Stent undersizing||→ Gaps between stent struts and arterial wall → increased flow resistance → low ESS (12)|
|Incomplete stent expansion (underexpansion)|
|Expansive vascular remodeling||→ Reduced flow rate → low ESS (2,4)|
Certain recognized risk factors of late stent thrombosis, indicated in bold, likely act in part by adversely modulating the in-stent ESS or by affecting the response of the endothelial substrate to the local ESS.
eNOS = endothelial nitric oxide synthase; ESS = endothelial shear stress; PGI2 = prostacyclin I2; tPA = tissue plasminogen activator.