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OCT detected common cause of very late stent thrombosis
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Advanced neoatherosclerosis with neointimal rupture and thrombosis detected by optical coherence tomography was the most common mechanism of definite very late stent thrombosis and was associated with a high frequency of STEMI, study results found.
Researchers reported on 33 patients — 27 treated with drug-eluting stents, six with bare-metal stents — with definite very late stent thrombosis defined by OCT images taken before either thrombus aspiration or IVUS. Among all patients, 94% showed intraluminal thrombi.
Very late stent thrombosis was associated with in-stent neointimal rupture in 23 patients (70%), and 22 had thrombi near the rupture site. Stent malapposition was observed in 14 (42%) lesions, but only nine of them showed thrombi at the site, whereas six (18%) stented segments with malapposition also had neointimal rupture. Only two (6%) of lesions had no evidence of neointimal rupture or malapposition. Stent fracture occurred in three lesions (all with DES), and all had concomitant neointimal rupture.
Lesions with neointimal rupture showed a higher frequency of STEMI (65% vs. 20%; P=.04) and a higher peak creatine kinase-myocardial band level (163.1 ng/mL vs. 15.7 ng/mL; P=.017) compared with lesions without neointimal rupture.
More than two-thirds of very late stent thrombi were associated with advanced neoatherosclerosis and neointimal rupture, the researchers wrote, suggesting that it is the primary mechanism. But the remaining one-third without neointimal rupture suggested a relationship between neoatherosclerosis, restenosis, very late stent thrombosis and stent fracture.
“The underlying mechanism of very late stent thrombosis was as important as the very late stent thrombosis event itself; neointimal rupture was associated with more intense clinical sequelae in the setting of stent thrombosis,” they wrote.
Disclosure: The researchers report no relevant financial disclosures.
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