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Comment
. 2016 Jul;8(7):1398-405.
doi: 10.21037/jtd.2016.05.69.

Coronary stent thrombosis: what have we learned?

Affiliations
Comment

Coronary stent thrombosis: what have we learned?

Carlos Collet et al. J Thorac Dis. 2016 Jul.
No abstract available

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Conflict of interest statement

Conflicts of Interest: Dr. Y. Sotomi is a consultant of GOODMAN and has received a grant from Fukuda Memorial Foundation for Medical Research and SUNRISE lab. Dr. P. W. Serruys and Y. Onuma are a members of the Advisory Board for Abbott Vascular. The other authors have no conflicts of interest to declare.

Figures

Figure 1
Figure 1
Optical coherence tomography images of stent thrombosis cases. Representative examples of stent thrombosis underlying mechanisms explored by optical coherence tomography imaging after optimal thrombus resorption in acute stent thrombosis with edge dissection (A); sub-acute stent thrombosis with major stent malapposition (B); late stent thrombosis with isolated uncovered struts (C); very late stent thrombosis with neoatherosclerosis lesion (D); ruptured neoatherosclerotic lesion (E and F); major stent underexpansion with stent area and reference lumen area measurements (G); coronary evaginations related to underlying positive remodeling (H). Reproduced with permission of Souteyrand et al.
Figure 2
Figure 2
Simulation of blood flow in the vicinity of stents struts. (A) Path-lines generated by 1 µm fluorescent particles in the vicinity of stent struts of increasing size (50 to 150 µm) demonstrate the formation of a range of recirculation zones by different geometries; (B) representative images of fibrin deposition near stent struts; (C) distal and proximal fibrin deposition near the stent strut of disturbed flow (DF) and undisturbed flow (UF); (D) WSS distribution for UF (grey) and DF (black) waveforms in the artery model. Reproduced with permission of Jimenez et al.

Comment on

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