OBJECTIVES: Endovascular procedures are one of the important treatment options for steno-occlusive arteries in ischemic stroke patients. However, embolic complications after such procedures are always a concern. The authors investigated the association between serial change of residual platelet reactivity and silent embolic cerebral infarction (SECI) after endovascular treatment., METHODS: Ischemic stroke patients undergoing stenting of intra- or extracranial arteries were recruited prospectively. Residual platelet reactivity, represented by aspirin reaction units (ARUs) and P2Y12 reaction units (PRUs), was measured serially (6 hours before, immediately after, and 24 hours after the procedure). A loading dosage of aspirin (500 mg) and/or clopidogrel (300 mg) was given 24 hours before the procedure to patients naive to antiplatelet agents, whereas the usual dosage (aspirin 100 mg and clopidogrel 75 mg) was continued for patients who had previously been taking these agents for more than a week. Diffusion-weighted MRI was performed before and 24 hours after the procedure to detect new SECIs. Clinical characteristics, baseline ARU and PRU values, and the change in ARU and PRU values after stenting were compared between patients with and without SECIs., RESULTS: Among 69 consecutive patients who underwent neurovascular stent insertion, 41 patients (59.4%) had poststenting SECIs. The lesion was located only at the vascular territory of the stented vessel in 21 patients (51.2%), outside the stented vessel territory in 8 patients (19.5%), and both inside and outside in 12 patients (29.3%). The occurrence of SECIs was not associated with the baseline ARU or PRU value, but was associated with PRU increase after stenting (36 +/- 73 vs -12 +/- 59, p = 0.007), deployment of a longer stent (31.1 +/- 16.5 mm vs 21.8 +/- 9.9 mm, p = 0.01), and stent insertion in extracranial arteries (78.1% vs 45.2%, p = 0.008). Stent length (OR 1.066, p = 0.01) and PRU change (OR 1.009, p = 0.04) were independently associated with the occurrence of SECI., CONCLUSIONS: Residual platelet reactivity after dual antiplatelet treatment measured before stenting did not predict poststenting SECI. However, the longer stent and the serial increase of PRU values after stenting were related to SECI. Continuous increase of platelet activation after endovascular procedure may be important in poststent cerebral infarction.
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