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J Am Coll Cardiol Intv, 2009; 2:583-593, doi:10.1016/j.jcin.2009.04.017
© 2009 by the American College of Cardiology Foundation
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Drug-Eluting Stent Thrombosis

The Kounis Hypersensitivity-Associated Acute Coronary Syndrome Revisited

Jack P. Chen, MD*,*, Dongming Hou, MD, PhD*, Lakshmana Pendyala, MD*, John A. Goudevenos, MD, PhD{dagger}, Nicholas G. Kounis, MD, PhD{ddagger}

* Saint Joseph's Translational Research Institute, Saint Joseph's Heart and Vascular Institute, Atlanta, Georgia
{dagger} Cardiology Department, Ioannina University Medical School, Ioannina, Greece
{ddagger} Medical Sciences, Patras Highest Institute of Education and Technology, Patras, Greece


Figure 1
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Figure 1 Macroscopic Images of Porcine Coronary Luminal Surfaces After Overlapping DES and BMS Implantation

All drug-eluting stent (DES) segments revealed mild-to-severe mural thrombi and transparently visible stent struts, consistent with absent to sparse neointima. These features are particularly prominent in the central segments of DES overlap. Conversely, bare-metal stent (BMS)-treated vessels developed robust, white neointima, with virtual strut non-visualization. Reprinted, with permission, from Pendyala et al. (19). Cx = circumflex coronary artery; LAD = left anterior descending artery; RCA = right coronary artery; PES = paclitaxel-eluting stent(s).

 

Figure 2
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Figure 2 High Magnification (200x) Microscopic Images of Hematoxylin-Eosin Stained Porcine Coronary Sections

(A) Bare-metal stent (BMS) segments exhibited well-healed, thick fibrocellular neointima, completely covered with endothelial-like cells. For (B) drug-eluting stent (DES) (designated PES for paclitaxel-eluting stent), the neointima is attenuated, with thrombus and fibrinoid deposits juxtaposed to stent struts. Several large round mononuclear cells (inflammatory white blood cells; white arrows) as well as thrombus (black arrows) formations were observed. The media was necrotic and hemorrhagic in appearance (*), and inflammatory cell infiltrations (white arrows) were present in DES segments. As in Figure 1, the inflammatory changes were markedly amplified in the DES overlap segments. Reprinted, with permission, from Pendyala et al. (19).

 

Figure 3
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Figure 3 Pathophysiology of Drug-Eluting Stent Thrombosis

Many factors, including impaired neointimal formation, technical issues, possible hypersensitivity to drug-eluting stent components (Kounis-associated), impaired vasomotion, patient characteristics, and adjunct pharmacology, all potentially contribute to and modify platelet activity, the major determinant of stent thrombosis. Solid arrows = promotional factors. Dashed arrows with question marks = possible promotional factors. Crossed arrows = inhibitory factors. ADP = adenosine diphosphate; Ig = immunoglobulin.

 




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