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.
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.