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Matteo Ghione, Kadriye Kilickesmez, Carlo Di Mario, Sealing old plaques, seeding new plaques, European Heart Journal - Cardiovascular Imaging, Volume 14, Issue 3, March 2013, Pages 203–204, https://doi.org/10.1093/ehjci/jes219
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In stent restenosis (ISR) is a heterogeneous phenomenon. The classical paradigm is neointimal proliferation in response to vessel wall injury often in combination with incomplete stent expansion. Drug-eluting stents (DES) have been designed to reduce or eliminate hyperplasia and in fact dramatically reduced restenosis and target lesion revascularization (TLR). The drawback of DES has been an increase in late and very late stent thrombosis, a potentially life-threatening complication considered a consequence of delayed and incomplete strut endothelialization.
The article of Habara et al.1 challenges this concept by analysing in-stent restenosis with optical coherence tomography (OCT) in the first generation DES at different time intervals from the implantation. In this study of 86 sirolimus-eluting Cypher and paclitaxel-eluting Taxus stents ISR they described different neointimal patterns and assessed their prevalence at various time intervals from DES implantation. They demonstrated that restenotic tissue changes its characteristics over time. In the first months after implantation a speckled pattern is frequent and they hypothesized this was caused by proteoglycan deposition and delayed arterial healing. Later after implantation neoatherosclerosis develops with a pattern of thin-cap fibroatheroma (TCFA) observed in >10% of 1–3 years old ISR and >30% IRS older than 3 years, some with plaque rupture and thrombus formation. The majority of these patients was identified with elective angiography and since restenosis is rare also in first generation DES they had to perform control angiography in 2666 patients to identify 91eligible ISR patients.
