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Updated: Jun 1, 2026

A Murine Model of Stent Implantation in the Carotid Artery for the Study of Restenosis
Published on: May 14, 2013
High on treatment platelet reactivity and stent thrombosis
Saissan Rajendran1, Devang Parikh, Ibrahim Shugman
1University of NSW, Sydney, Australia.
Insights
High platelet reactivity to aspirin and clopidogrel is common in patients with stent thrombosis. Doubling antiplatelet dosage can improve platelet inhibition and reduce this risk.
Area of Science:
- Cardiology
- Pharmacology
- Thrombosis Research
Background:
- Stent thrombosis (ST) is a serious complication following percutaneous coronary intervention (PCI).
- High on-treatment platelet reactivity (HTPR) is a suspected risk factor for ST.
- Understanding the relationship between HTPR and ST is crucial for improving patient outcomes.
Purpose of the Study:
- To investigate the association between HTPR and the incidence of ST.
- To evaluate the efficacy of increased antiplatelet therapy dosage in overcoming HTPR.
Main Methods:
- Compared clinical characteristics and platelet reactivity (using VerifyNow assays) in patients with ST versus those without.
- Assessed platelet reactivity before and after a two-week course of double-dose antiplatelet therapy in patients with HTPR.
Main Results:
- Significantly higher prevalence of HTPR (aspirin and/or clopidogrel) in ST patients (75%) compared to controls (2.5%).
- ST patients were younger, had more coronary artery disease, and smaller reference vessel diameters.
- Double-dose therapy significantly improved platelet reactivity in most patients with initial HTPR.
Conclusions:
- HTPR is frequently observed in patients experiencing stent thrombosis.
- Increasing the dosage of aspirin and clopidogrel can effectively enhance platelet inhibition in non-responsive patients.
Background:
Stent thrombosis (ST) remains a major adverse outcome of percutaneous coronary intervention (PCI). We examined potential associations between high on treatment platelet reactivity and the risk of ST and assessed the effects of increased antiplatelet dosage on platelet inhibition.
Methods:
Differences in clinical characteristics and the effect of aspirin and clopidogrel on platelet reactivity were determined after angiographically proven ST in 16 patients and in 40 patients without ST. Platelet reactivity was determined using the VerifyNow assays (Accumetrics Inc., San Diego, CA). Patients found with high on treatment platelet reactivity (P2Y12 Reaction Units ≥ 235 and/or Aspirin Reaction Units ≥ 550) returned following two weeks of double dose antiplatelet therapy for further analyses.
Results:
High post aspirin and/or clopidogrel platelet reactivity was significantly more common in patients with ST versus controls (75% vs. 2.5%, p = < 0.001). Overall, ST patients were younger (52.8 ± 10.5 vs. 59 ± 9.6 years; p = 0.039), had more pre-existing coronary artery disease (75% vs. 42%; p = 0.028) and smaller reference vessel diameters (2.9 ± 0.36 vs. 3.2 ± 0.54 mm; p = 0.047) when compared to controls. After double dose therapy, antiplatelet reactivity improved significantly in ten out of 12 subjects on clopidogrel (83.3%) and the two patients on aspirin who initially had high on treatment platelet reactivity.
Conclusion:
This study demonstrates that high on treatment platelet reactivity with aspirin and/or clopidogrel is common amongst patients who develop stent thrombosis. Additionally this resistance can be improved with doubling the prior dose of antiplatelet therapy.
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