Abstract 2569: Comparative Pathologic Studies of Chronic Tissue Responses to Repeated Bare-Metal versus Drug-Eluting Stent Implantation within the Same or Different Types of Stents
Although drug-eluting stents (DES) have been increasingly used for treatment of in-stent restenosis (ISR) after bare-metal stents (BMS) or DES implantation, little is known regarding the subsequent pathological findings. We conducted a postmortem investigation of the late vascular responses (3– 6 months after the final stenting) in 26 coronary artery lesions treated for post-BMS ISR with either BMS (group I; 13 lesions) or sirolimus-eluting stents (SES) (group II; 7 lesions) or for post-SES ISR using SES or paclitaxel-eluting stents (PES) (group III; 6 lesions). At autopsy, 5 lesions showed restenosis in group I, but there was no restenosis in groups II and III. In the restenotic lesions, significant proliferation of polymorphic smooth muscle cells (SMCs) and increase in extracellular matrix (ECM) were observed on the intimal side of the stented segment. Arteries without restenosis in group I featured reduced ECM and SMCs that were spindle-shaped and ordered along the luminal surface. Furthermore, >90% of the luminal surface was reendothelialized in both restenosis and non-restenosis lesions in group I. In contrast, only mild neointimal thickening with scarce endothelialization was observed around the circumference of the lumen at the DES-stented site in both groups II and III. Few SMCs were observed in these portions, but abundant fibrin deposits were present around the struts. There was an intense inflammatory reaction involving T lymphocytes, macrophages and multinucleated giant cells adjacent to the DES struts. There were no significant differences in the degree of poor endothelialization or peri-strut inflammatory response not only between groups II and III, but also between the lesions treated with SES and PES in group III. DES implantation is effective for treatment of both post-BMS and post-SES ISR due to remarkable inhibition of neointimal hyperplasia, but inflammation and lack of endothelialization occur at the DES implanted segment. Thus, these sites could be at the persistent risk for thrombosis.