Key result
Delayed very late stent thrombosis had more neoatherosclerosis (44.9% vs 24.5%; P=0.034) and fewer uncovered struts (14.3% vs 34.7%; P=0.019) compared with earlier presentation.
Why the study?
Do the pathological mechanisms of very late drug-eluting stent thrombosis differ between earlier and delayed presentations?
Observational (n=98)
Yes
Do the pathological mechanisms of very late drug-eluting stent thrombosis differ between earlier and delayed presentations?
Absolute Event Rate: 44.9% vs 24.5%
p-value: p=0.034
The mechanisms of very late DES thrombosis evolve over time, with neoatherosclerosis becoming more frequent in delayed cases, though delayed neointimal healing remains a significant factor.
Supports time-dependent mechanisms in very late stent thrombosis; extends observational data but leaves open targeted prevention strategies.
Background The pathophysiology underlying very late drug‐eluting stent ( DES ) thrombosis is not sufficiently understood. Using optical coherence tomography, we investigated characteristics of very late stent thrombosis ( VLST ) according to different onset times. Methods and Results A total of 98 patients from 10 South Korean hospitals who underwent optical coherence tomography for evaluation of very late DES thrombosis were retrospectively included in analyses. VLST occurred at a median of 55.1 months after DES implantation. All patients were divided into 2 equal groups of earlier versus delayed presentation of VLST , according to median onset time. In total, 27 patients were treated with next‐generation DES and 71 with first‐generation DES . Based on optical coherence tomography findings at thrombotic sites, main VLST mechanisms were as follows, in descending order: neoatherosclerosis (34.7%), stent malapposition (33.7%), and uncovered struts without stent malapposition or evagination (24.5%). Compared with patients with earlier VLST , patients with delayed VLST had lower frequency of uncovered struts without stent malapposition or evagination (34.7% versus 14.3%, respectively; P =0.019). Conversely, the frequency of neoatherosclerosis was higher in patients with delayed versus earlier VLST (44.9% versus 24.5%, respectively; P =0.034). The frequency of stent malapposition was not different between patients with earlier and delayed VLST (34.7% versus 32.7%, respectively; P =0.831). The frequency of stent malapposition, evagination, and uncovered struts was still half of delayed VLST . Conclusions The pathological mechanisms of very late DES thrombosis changed over time. Delayed neointimal healing remained a substantial substrate for VLST , even long after DES implantation.
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Lee et al. (2017) conducted an observational in Very late drug-eluting stent (DES) thrombosis (n=98). Delayed presentation of very late stent thrombosis vs. Earlier presentation of very late stent thrombosis was evaluated on Frequency of neoatherosclerosis (p=0.034). Delayed very late stent thrombosis had more neoatherosclerosis (44.9% vs 24.5%; P=0.034) and fewer uncovered struts (14.3% vs 34.7%; P=0.019) compared with earlier presentation.
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