Key result
Postprocedural oral anticoagulation fails to reduce 12-month TLR in femoropopliteal stent thrombosis.
Why the study?
The prognostic role of high on-treatment platelet reactivity and the optimal antithrombotic strategy, including adjunctive anticoagulation, after peripheral stent thrombosis remain unclear.
Does postprocedural oral anticoagulation reduce 12-month target lesion revascularization in patients with femoropopliteal stent thrombosis?
Cohort
Does postprocedural oral anticoagulation reduce 12-month target lesion revascularization in patients with femoropopliteal stent thrombosis?
Routine platelet function testing or intensified anticoagulation with OAC does not appear to provide clinical benefit in patients with a history of femoropopliteal stent thrombosis.
HTPR and post-ST OAC effects in femoropopliteal interventions remain unclear; hypothesis-generating for antithrombotic strategies.
Summary: Background: Stent thrombosis (ST) is a rare but serious complication following peripheral endovascular interventions. The prognostic role of high on-treatment platelet reactivity (HTPR) and the optimal antithrombotic strategy, including adjunctive anticoagulation, remain unclear. To evaluate (I) the prognostic value of ADP-induced platelet function in femoropopliteal ST compared to matched controls, and (II) the impact of post-ST oral anticoagulation (OAC) on clinical outcomes. Materials and methods: In this retrospective cohort study, 148 endovascular procedures in 67 patients with documented femoropopliteal ST were compared to 492 matched procedures without ST. Propensity-score-matching for age, sex, and lesion length/type yielded 113 pairs. ADP-induced platelet aggregation was assessed and compared between groups. Within the ST cohort, 12-month outcomes were additionally stratified according to the postprocedural antithrombotic regimen, with or without oral anticoagulation (OAC). Time-to-reintervention was analysed via Kaplan-Meier and Cox regression. Results: ADP-induced platelet reactivity did not differ significantly between ST and control groups (p = .58). Additionally, among ST patients, postprocedural OAC use had no significant impact on 12-month target lesion revascularization (TLR) rates (HR 0.96; 95% CI 0.57–1.62; p = .90), with consistent findings across subgroups (VKA, standard-/low-dose NOAC). Conclusions: In this matched cohort, ADP-induced platelet reactivity did not differ significantly in patients with femoropopliteal stent thrombosis compared to controls. Similarly, no consistent benefit of specific anticoagulation strategies on 12-month target lesion revascularization was observed. Therefore, these findings do not support routine platelet function testing or intensified anticoagulation solely based on a history of ST.
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Bradaric et al. (2026) conducted a cohort in Femoropopliteal stent thrombosis. Postprocedural oral anticoagulation (OAC) vs. No oral anticoagulation was evaluated on 12-month target lesion revascularization (TLR) (HR 0.96, 95% CI 0.57-1.62, p=.90). Postprocedural oral anticoagulation had no significant impact on 12-month target lesion revascularization in patients with femoropopliteal stent thrombosis (HR 0.96; 95% CI 0.57-1.62; p=.90).
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