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Review
. 2012 Apr;5(2):296-304.
doi: 10.1161/CIRCINTERVENTIONS.111.965426.

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

Jesse W Rowley  1 , Aloke V Finn, Patricia A French, Lisa K Jennings, Danny Bluestein, Peter L Gross, Jane E Freedman, Steven R Steinhubl, Guy A Zimmerman, Richard C Becker, Harold L Dauerman, Susan S Smyth; 2011 Platelet Colloquium Participants
Collaborators, Affiliations
Review

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

Jesse W Rowley et al. Circ Cardiovasc Interv. 2012 Apr.
No abstract available

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Figures

Figure 1
Figure 1
Complex interplay among shear stress, inflammation, and platelet–leukocyte activation. vWF indicates von Willebrand factor; RBC, red blood cell; PSGL, P-selectin glycoprotein ligand; GP, glycoprotein; PKC, protein kinase C; TGF, transforming growth factor; and ADP, adenosine diphosphate.
Figure 2
Figure 2
Device thrombogenicity emulator. “Hot spot” trajectories from numeric simulations (shown, blood flow through a bileaflet mechanical heart valve, top) are translated into shear stress–loading waveforms τ(t). These waveforms are then programmed into the hemodynamic shearing device (bottom left), platelets are repeatedly exposed to them, and the resultant activity is measured using a platelet activity state assay (bottom right). Adapted from Bluestein et al, with permission. VWF indicates von Willebrand factor.
See this image and copyright information in PMC

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