Abstract
Objective: Little is known about the pharmacodynamic antiplatelet effects of clopidogrel loading in acute ischemic stroke. This study is aimed to evaluate the pharmacodynamic antiplatelet effects of clopidogrel loading dose in patients with acute ischemic stroke.
Methods: We evaluated 23 consecutive patients who received a loading dose of antiplatelets including ≥300 mg clopidogrel from June 2011 to December 2013 at our institution (13 with acute ischemic stroke and 10 with non-acute ischemic stroke undergoing elective neuroendovascular treatment). The VerifyNow system was used to assess antiplatelet effects in terms of aspirin reaction unit (ARU), P2Y12 reaction unit (PRU), and % inhibition at baseline, 6 h, 24 h, and 48–72 h after loading. We also evaluated the clinical and genetic factors associated with high on-treatment platelet reactivity at 24 h after antiplatelet administration.
Results: Aspirin provided a sufficient antiplatelet effect at 6 h after loading (ARU <550). In contrast, the antiplatelet effect of clopidogrel was insufficient even at 48 h after loading (PRU >230, % inhibition <26%). Significant differences were observed in PRU levels between elective and acute stroke patients at 6 h (338.4±49.9 vs 251.3±89.9, p=0.032) and 24 h (298.9±54.2 vs 224.1±83.4, p=0.028) after loading. Moreover, % inhibition levels were significantly lower in acute stroke patients at all points (p=0.025 at baseline, 0.020 at 6 h, 0.013 at 24 h, and 0.017 at 48 h). Acute stroke (p=0.0018) and body mass index (p=0.005) were identified as independent factors for clopidogrel resistance, which was observed in 15 (65.2%) patients.
Conclusion: The antiplatelet effect of clopidogrel given in a loading dose reached a sufficient level within 24 h in elective patients but not in acute stroke patients. Furthermore, acute stroke was found to be correlated with clopidogrel resistance.
