Key result
Unfavorable platelet reactivity on clopidogrel linked to ~616% greater risk of significant ischemic infarct volume.
Why the study?
With the increasing use of clopidogrel for secondary stroke prevention, the impact of clopidogrel resistance on the size and extent of acute and chronic ischemic lesions remained to be evaluated.
Does unfavorable platelet reactivity dynamics on clopidogrel therapy increase the volume of acute ischemic lesions in ischemic stroke subjects?
Observational (n=74)
No
Does unfavorable platelet reactivity dynamics on clopidogrel therapy increase the volume of acute ischemic lesions in ischemic stroke subjects?
Effect estimate: OR 7.16 (95% CI 1.69-30.31)
p-value: p=0.008
Unfavorable dynamics of platelet reactivity during clopidogrel therapy in the acute phase of stroke is associated with larger acute infarct volumes and more severe chronic vascular lesions.
Associated with larger infarcts on clopidogrel in acute stroke; hypothesis-generating for reactivity monitoring, prospective trials needed.
Background: High on-treatment platelet reactivity or its equivalent—resistance to the antiplatelet agent—significantly reduces the efficacy of the therapy, contributing to a negative impact on stroke course. Previous studies demonstrated that aspirin resistance is associated with a larger size of acute ischemic infarct. Due to the increasing use of clopidogrel in the secondary prevention of stroke, we aimed to assess the impact of clopidogrel resistance on the size and extent of ischemic lesions, both acute and chronic. Methods: This prospective, single-center and observational study involved 74 ischemic stroke subjects, treated with 75 mg of clopidogrel. We used impedance aggregometry to determine platelet reactivity 6–12 h after a dose of clopidogrel as a first assessment and 48 h later as the second measurement. A favorable dynamics of platelet reactivity over time was the decrease in the minimum value equal to the median in the entire study. The volume of acute ischemic infarct was estimated within 48 h after onset in diffusion-weighted imaging and fluid-attenuated inversion recovery sequences of magnetic resonance and the severity of chronic vascular lesions by Fazekas scale. Results: Subjects with mild severity of chronic vascular lesions (Fazekas 1) exhibited a significant decrease of platelet reactivity over time (p = 0.035). Dynamics of platelet reactivity over time differed between subjects with large, moderate, mild and insignificant size of acute ischemic lesion (Kruskall-Wallis H = 3.2576; p = 0.048). In multivariate regression models, we reported unfavorable dynamics of platelet reactivity alone and combined with a high initial value of platelet reactivity as independent predictors of higher risk of a significant ischemic infarct volume (OR 7.16 95%CI 1.69–30.31, p = 0.008 and 26.49 95%CI 1.88–372.4, p = 0.015, respectively). Conclusions: We emphasized that unfavorable dynamics of platelet reactivity over time during clopidogrel therapy in acute phase of stroke affect the volume of acute infarct and the severity of chronic vascular lesions.
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Wiśniewski et al. (2021) conducted an observational in Ischemic stroke (n=74). Clopidogrel was evaluated on Significant ischemic infarct volume (OR 7.16, 95% CI 1.69-30.31, p=0.008). Unfavorable dynamics of platelet reactivity during clopidogrel therapy independently predicted a higher risk of significant ischemic infarct volume (OR 7.16; 95% CI 1.69-30.31; p=0.008).
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