Review Article

Pathologic Etiologies of Late and Very Late Stent Thrombosis following First-Generation Drug-Eluting Stent Placement

Figure 5

Representative images of late/very late stent thrombosis in SES and PES. (A) Histologic sections from sirolimus-eluting stents (SES). A 40-year-old woman who received 2 SES in left anterior descending artery (LAD) and right coronary artery (RCA) 17 months antemortem died suddenly 4 days after surgical removal of melanoma (wide excision). Antiplatelet therapy (aspirin and clopidogrel) was discontinued 5 days before the surgery. Histologic sections of the SES in LAD showed total thrombotic occlusion and diffuse inflammation (a). Numerous inflammatory cells were observed within neointimal area (b). Inflammatory reaction predominantly consists of T-lymphocytes (c) (CD45Ro) and eosinophils (d) (Luna stain). Note, the same reaction was observed in the SES in RCA (e) and severe inflammation resulted in malapposition of stent struts (f). (B) Histologic sections from paclitaxel-eluting stent (PES) showing malapposition. A 69-year-old man who received a PES in a saphenous vein graft died suddenly 3 months after the stent placement. Histologic sections showed thrombotic occlusion in the PES (a, b); note the malapposition secondary to severe fibrin deposition (c). A 48-year-old man with PES implantation in the proximal LAD died suddenly at 40 months. Histologic sections showed thrombotic occlusion of the PES (d). Most struts are malapposed with fibrin deposition underneath the stent struts (e and f). Thr = thrombus. (Reproduced with permission from [49].)
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