Abstract 12072: Damage to Coating Polymer Can Cause Serious Complications After Drug-Eluting Stent Implantation: A Pathological Study in Human Coronary Arteries
Introduction: Polymer coating is indispensable to optimize controlled drug release kinetics following drug-eluting stent (DES) implantation. However, how it can be damaged during the stenting procedure and the subsequent clinico-pathological events are not well studied.
Hypothesis: We histopathologically assessed the hypothesis that damage to polymer coating can hinder DES efficacy.
Methods: The study sample comprised 32 DES-implanted lesions obtained by autopsy from 2.5 to 49 months after stenting: 27 with durable polymers (Cypher, 12; Taxus, 6; Endeavor, 4; and Xience, 5) and 5 with biodegradable polymers coated only on the abluminal surface (Nobori, 3 and Ultimaster, 2). Tortuous lesions accounted for 60% and calcified lesions for 88%. We examined microscopically at least six slices from each lesion.
Results: Polymer cracking or delamination was observed in about 6% of Cypher struts and 4% of Taxus struts. In two Cypher-implanted lesions with stent thrombosis occurring beyond one year after stent implantation, significant detachment of polymer fragments phagocytosed by giant cells was observed, and their arterial walls were aneurysmally dilated with extensive inflammatory infiltration of the intima, media, and adventitia, predominantly consisting of T cells, eosinophils, and considerable giant cells. In Xience-implanted lesions, polymer damage was little. In contrast, in most Endeavor-implanted lesions, large spallings of the polymer were found, and numerous phagocytosed polymer remnants scattered in the thickened neointima. In Nobori- or Ultimaster-implanted calcified lesions within 4 months after the procedure, remarkable detachment of polymer coating resulted in severe inflammatory reaction consisting of macrophages and lymphocytes.
Conclusions: Polymer disruption may result in nonuniform drug distribution that may allow neointimal hyperplasia in the DES-implanted lesions. Moreover, polymer cracking may induce adverse and interrelated effects such as local inflammation and amplified cellular response, followed by very late stent thrombosis. Compared with polymer around the stent struts, delamination of abluminal polymer might occurr more easily when it is delivered through a calcified coronary artery.
Author Disclosures: K. Inoue: None. M. Imai: None. T. Kimura: None.
- © 2016 by American Heart Association, Inc.