Key result
DES linked to ~20-fold more uncovered struts than BMS in very late stent thrombosis.
Why the study?
Very late stent thrombosis remains an unresolved problem occurring in patients treated with both drug-eluting and bare metal stents, with unclear causes.
What are the OCT-derived causes of very late stent thrombosis in DES compared to BMS?
Observational (n=22)
Yes
What are the OCT-derived causes of very late stent thrombosis in DES compared to BMS?
Absolute Event Rate: 4.5% vs 0.2%
p-value: p=0.004
Very late stent thrombosis in bare metal stents is primarily caused by neoatherosclerosis, whereas in drug-eluting stents it has more complex causes including neoatherosclerosis, uncovered struts, and malapposition.
OCT reveals neoatherosclerosis as main VLST driver in BMS but heterogeneous causes in DES; leaves open mechanism-specific prevention strategies.
OBJECTIVE: Very late stent thrombosis (VLST) remains an unresolved problem, and recent reports have indicated that VLST onset can occur in patients treated with both drug-eluting stents (DES) and bare metal stents (BMS). We evaluated the causes of VLST using optical coherence tomography (OCT). METHODS: OCT was performed in 22 patients (12 DES-treated patients, 10 BMS-treated patients). Because two instances of VLST occurred simultaneously in one case in the DES group, the DES group comprised 13 lesions, while the BMS group comprised 10 lesions. All struts were counted in each frame, and the proportion of uncovered or malapposed struts was calculated based on the overall number of struts in the stent. RESULTS: The interval from stent implantation to VLST onset was significantly longer in the BMS group. The proportion of uncovered struts and the ratio of malapposed struts were significantly higher in the DES group than in the BMS group. The OCT analysis demonstrated intimal hyperplasia or intimal disruption in all patients in the BMS group. However, in the DES group, severe hyperplasia and/or neoatherosclerosis was observed in only eight lesions (61.5%), while uncovered and malapposed struts were involved in the other lesions. CONCLUSION: In most BMS-treated lesions, it appeared that VLST was caused by the occurrence of neoatherosclerosis after stent implantation. The causes of VLST in DES-treated lesions are more various and complicated than those observed for BMS-treated lesions.
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Amioka et al. (2014) conducted an observational in Very late stent thrombosis (VLST) (n=22). Drug-eluting stents (DES) vs. Bare-metal stents (BMS) was evaluated on Overall proportion of uncovered struts (p=0.004). In patients with very late stent thrombosis, drug-eluting stents exhibited a significantly higher proportion of uncovered struts (4.5% vs 0.2%, p=0.004) and malapposed struts (6.4% vs 0.3%, p=0.002) compared to bare-metal stents.
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