Cardiovascular devices and platelet interactions understanding the role of injury, flow, and cellular responses

Shear influences platelet adhesion and activation through mechanisms that include altering vWF binding and IIb3/ purinergic signaling interactions. Shear can potentially promote inflammation and atherogenesis through plateletmediated processes. New methods to study platelet function under shear conditions and in more physiological contexts should be incorporated to guide the design of future devices and drug therapies. Some of these methods include in vivo imaging, in vitro flow models, and in vitro modeling/ computer-assisted iterative device design. Improving currently used antiplatelet agents is not the sole answer for reducing vascular injury after PCI. Cilostazol and statins are promising examples of agents that have effects beyond inhibition of platelet activation. In addition, LST, which has been associated with both stent design and pathological changes (such as endothelialization and neoatherosclerosis within the neointima), is becoming a less critical issue with DES because of the use of DAPT and newer stent designs.