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The Pathology of Neoatherosclerosis in Human Coronary Implants: Bare-Metal and Drug-Eluting Stents
Study Questions:
How common is the formation of atheromatous lesions within different types of coronary stents?
Methods:
Cases from the CVPath stent registry, which includes a total of 406 lesions from 299 autopsies—197 bare-metal stents (BMS), 209 drug-eluting stents (DES) (103 sirolimus-eluting stents [SES] and 106 paclitaxel-eluting stents [PES])—with implant duration >30 days, were examined. Neoatherosclerosis was recognized as clusters of lipid-laden foamy macrophages within the neointima with or without necrotic core formation.
Results:
The incidence of neoatherosclerosis was greater in DES lesions (31%) than BMS lesions (16%; p < 0.001). The median stent duration with neoatherosclerosis was shorter in DES than BMS (DES, 420 days; BMS, 2,160 days, p < 0.001). Unstable lesions characterized as thin-cap fibroatheromas or plaque rupture were more frequent in BMS (4%) than in DES (1%; p = 0.17), with relatively shorter implant durations for DES (1.5 ± 0.4 years) compared to BMS (6.1 ± 1.5 years). Independent determinants of neoatherosclerosis identified by multiple logistic regression included younger age (p < 0.001), longer implant durations (p < 0.001), SES usage (p < 0.001), PES usage (p = 0.001), and underlying unstable plaques (p = 0.004).
Conclusions:
Neoatherosclerosis is a frequent finding in DES and occurs earlier than in BMS.
Perspective:
DES markedly reduce restenosis rates, but have higher rates of late stent thrombosis, which is thought to occur because of lack of stent strut endothelialization. Contrary to the belief that neointima formation within stents is only fibromuscular and therefore ‘stable,’ the current study demonstrates that typical atheromatous lesions are not uncommon within stented segments. Thus, plaque disruption with occlusive thrombosis may explain some cases of late stent thrombosis. These findings may also explain the occasional patient (after BMS or DES) that comes in with acute coronary syndrome thought to be due to tight in-stent ‘restenosis.’
Keywords: Neointima, Registries, Acute Coronary Syndrome, Macrophages, Coronary Restenosis, Metals, Thrombosis, Drug-Eluting Stents, Stents
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