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Published on: November 8, 2024
Overcoming Clopidogrel Resistance in Carotid Artery Stenting: Experience with Ticagrelor and Ticlopidine
Pavol Vigláš1,2, Jan Raupach2,3, Aleš Hejčl4
1Department of Radiology, J. E. Purkyně University-Faculty of Health Studies and Krajská zdravotní-Masaryk Hospital, Sociální péče 3316/12A, 401 13 Ústí nad Labem, Czech Republic.
Insights
High on-treatment platelet reactivity to clopidogrel is common after carotid stenting. Ticagrelor effectively reduces platelet reactivity in these patients, suggesting tailored antiplatelet therapy is beneficial.
Area of Science:
- Cardiovascular Medicine
- Pharmacology
- Interventional Neurology
Background:
- Carotid stenting requires effective antiplatelet therapy.
- High on-treatment platelet reactivity (HTPR) to clopidogrel can compromise treatment efficacy.
- Identifying HTPR is crucial for preventing thromboembolic events.
Purpose of the Study:
- To determine the incidence of HTPR to aspirin and clopidogrel in patients undergoing carotid stenting.
- To assess the efficacy of ticagrelor and ticlopidine in patients with HTPR to clopidogrel.
Main Methods:
- Retrospective analysis of 216 consecutive patients undergoing carotid artery stenting.
- Platelet function testing using light transmission aggregometry and Multiplate®.
- Assessment of HTPR to aspirin, clopidogrel, ticlopidine, and ticagrelor.
Main Results:
- HTPR to clopidogrel was observed in 31.4% (68/216) of patients.
- No HTPR was observed with ticagrelor or ticlopidine.
- Ticagrelor and ticlopidine significantly reduced platelet reactivity in patients with HTPR to clopidogrel.
Conclusions:
- HTPR to clopidogrel is prevalent in patients undergoing carotid stenting.
- Ticagrelor is an effective alternative for patients with clopidogrel-induced HTPR.
- Platelet function testing can guide tailored antiplatelet strategies to reduce complications.
Abstract:
Objectives: The goal of this study is to establish the incidence of high on-treatment platelet reactivity (HTPR) to aspirin and clopidogrel in patients undergoing carotid stenting and to evaluate the efficacy of ticagrelor and ticlopidine in patients with HTPR to clopidogrel. Methods: In a single institutional setting spanning eight years, every consecutive patient who underwent carotid artery stenting was incorporated into a study. Subsequently, a retrospective analysis of their platelet function was executed. Prevalence of high on-treatment reactivity to aspirin, clopidogrel, ticlopidine and ticagrelor was assessed. Platelet function testing was conducted by light transmission aggregometry and Multiplate®. Results: A total of 216 patients were tested for antiplatelet therapy efficacy. The high on-treatment reactivity to clopidogrel was observed in 68 patients (31.4%). No patients with high on-treatment reactivity to ticagrelor or ticlopidine were observed. There was a significant reduction in platelet reactivity with ticagrelor (p < 0.000) and ticlopidine (p < 0.000) in patients with HTPR to clopidogrel. Conclusions: High on-treatment platelet reactivity to clopidogrel is common in patients undergoing carotid artery stenting. Ticagrelor is a viable alternative to overcome HTPR to clopidogrel. These findings suggest that platelet function testing can identify patients who may benefit from tailored antiplatelet therapy in reducing thromboembolic complications after carotid stenting.
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