Objective: Early anti-platelet therapy is a cornerstone in the prevention of recurrent ischaemic stroke (IS) and transient ischaemic attacks (TIAs), although the responsiveness to anti-platelet medications varies among patients. Several studies have reported that patients with ischaemic stroke who exhibit high on-treatment platelet reactivity (HTPR) 5–10 days after antiplatelet medication onset, have an increased risk of vascular events. In this study we aim to determine the prevalence of HTPR in the hyper-acute stroke phase less than 48 h from symptom onset, after the administration of a 300 mg bolus of oral clopidogrel in a real-world setting in Danish IS and TIA patients.Material and Methods: In total, 219 Danish patients with acute IS or TIA received 300 mg of oral clopidogrel on admission. Blood samples from all patients were analyzed using the VerifyNow P2Y12 system at 8–24 h after clopidogrel intake. Concomitant therapy and the intervals between ictus and blood collection, clopidogrel intake and blood collection, and blood sampling and analysis were recorded for all patients.Results: HTPR in the hyper-acute stroke phase was observed in 28.8% (63/219) samples. After adjustment for age, sex, co-morbidities, and co-medications, none of the tested variables exhibited an association with HTPR or the platelet reaction unit value measured using the VerifyNow P2Y12 system.Conclusions: The recognition of HTPR to specific anti-platelet agents in the hyper-acute phase after stroke may be the first step toward interventions that may further minimize the early recurrent stroke risk. Further large randomized trials including clinical outcome assessments are necessary.

Background Antiplatelet therapy is a cornerstone of secondary stroke prevention, but the responsiveness to antiplatelet medication varies among patients. Clopidogrel is a pro-drug that requires hepatic transformation to reach its active metabolite. Single nucleotide polymorphisms (SNPs) in key enzymes or the target adenosine diphosphate (ADP) receptor on the platelet surface are believed to be involved in clopidogrel-mediated platelet inhibition and decreased antiplatelet effect with high-on-treatment platelet reactivity (HTPR). Objective This study investigated whether specific SNPs in key hepatic enzymes (CYP2C19*2, *3, *17, CYP3A4*1G, and NR1I2) or the ADP receptor (PR2Y12) are associated with HTPR to clopidogrel. Patients & methods This observational study included patients with ischemic stroke (IS) and transient ischemic attacks (TIAs) receiving clopidogrel at a dose of 75 mg/day. Patients were genotyped for eight different SNPs in the genes encoding CYP2C19, CYP3A4, NR1I2, and the P2Y12 receptor. Results Of the 103 patients that were included, 30.7% carried the CYP2C19*2 allele and had higher platelet reaction unit (PRU) values than non-carriers, but no patients showed HTPR. Carriers of the *17 allele had higher platelet inhibition but showed no difference in PRU values compared with non-carriers. The remaining SNPs were neither associated with PRU nor with platelet inhibition. Conclusions Patients with IS and TIAs treated with 75 mg clopidogrel/day do not have HTPR. A genetic analysis of CYP2C19*2, *3, *17, CYP3A4*1G, and NR1I2 revealed no associations with clopidogrel HTPR. CYP2C19*2 carriers and patients with HTPR in the acute phase after ischemic stroke or transient ischemic attacks exhibit higher PRU values, but not long-term treatment HTPR.

Stroke mimics, like attacks of hemiplegic migraine, are challenging in acute stroke evaluation. We present a 28-year-old woman with a suspected hemiplegic migraine attack with left-sided hemiparalysis. Brain CT with perfusion imaging 1 h 54 min after symptom onset revealed hypoperfusion in the right hemisphere. The patient was treated with intravenous recombinant tissue plasminogen activator (rtPA) with no effect. After a subsequent intravenous verapamil infusion, the patient gained full motor function within 10 min. Brain magnetic resonance imaging (MRI) performed 5 h 46 min after symptom onset revealed diffusion restriction in the same area as the hypoperfusion on CT. There were no notable changes on T2 images. The patient stayed clinically in remission, except for reduced sensation for all modalities on the extremities on the left side. Although brain CT 24 h after symptom onset revealed an edema in the same area, an MRI performed 17 days later showed no new infarctions. Young patients with a history of migraine with aura admitted with symptoms of acute ischemic stroke are at risk of insufficient treatment. Calcium antagonists might be considered if there is no effect of first-line treatment with rtPA.

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