Bare metal stent thrombosis and in-stent neoatherosclerosis

Very late stent thrombosis (VLST) was reported to occur even in patients with bare metal stent (BMS) implantation, although the annual incidence of VLST after BMS was much lower than that after drug-eluting stent implantation. Pathophysiologic mechanisms of VLST after BMS implantation remain largely unknown.

From September 2002 to February 2010, we identified 102 patients with definite stent thrombosis (ST) of BMS and 42 control patients with acute coronary syndrome (ACS) unrelated to ST who underwent thrombus aspiration with histopathologic evaluation. There were 40 patients with early ST (EST, within 30 days), 20 patients with late ST (LST, between 31-365 days), and 42 patients with VLST (>1 year). Evidence for fragments of atherosclerotic plaques, such as foamy macrophages, cholesterol crystals, and thin fibrous cap, was more commonly seen in patients with EST (23%) and VLST (31%), whereas these findings were rarely observed in patients with LST (10%). Atherosclerotic fragments were predominantly seen in patients who had EST within 7 days or VLST beyond 3 years. The aspirated thrombi harvested from patients with ST and those with ACS were histologically indistinguishable from each other. Eosinophils were very rarely observed. Plasma level of total cholesterol and triglyceride were significantly higher in VLST cases with atherosclerotic fragments as compared with those without.

Fragments of atherosclerotic plaque were highly prevalent in patients with VLST beyond 3 years. Disruption of in-stent neoatherosclerosis could play an important role in the pathogenesis of VLST of BMS occurring beyond 3 years after implantation.