Key result
Cerebral arterial stenting significantly increased platelet reactivity, with median Aspirin Reaction Units rising from 418 to 469 (p=0.045) and P2Y12 Reaction Units from 256 to 274 (p=0.018).
Why the study?
Does the stenting procedure itself increase platelet reactivity in patients undergoing cerebral artery stenting on dual antiplatelet therapy?
Observational (n=30)
No
Does the stenting procedure itself increase platelet reactivity in patients undergoing cerebral artery stenting on dual antiplatelet therapy?
Absolute Event Rate: 469% vs 418%
p-value: p=0.045
The stenting procedure itself significantly increases platelet reactivity in patients undergoing cerebral arterial stenting on dual antiplatelet therapy, suggesting that the timing of blood sampling is crucial when assessing antiplatelet response.
Stenting-associated platelet reactivity rise may affect DAPT monitoring timing; leaves open clinical impact in neurointerventional cohorts.
PURPOSE: VerifyNow antiplatelet assays were performed before and after stenting for various cerebral artery stenoses to determine the effect of the procedure itself to the function of dual antiplatelets given. MATERIALS AND METHODS: A total of 30 consecutive patients underwent cerebral arterial stenting procedure were enrolled. The antiplatelet pretreatment regimen was aspirin (100 mg daily) and clopidogrel (300 mg of loading dose followed by 75mg daily). VerifyNow antiplatelet assay performed before and right after stenting. The two test results were compared in terms of aspirin-reaction unit (ARU), P2Y12 reaction units (PRU), baseline (BASE), and percentage inhibition. We evaluated occurrence of any intra-procedural in-stent thrombosis or immediate thromboembolic complication, and ischemic events in 1-month follow-up. RESULTS: The median Pre-ARU was 418 (range, 350-586). For clopidogrel the medians of the pre-BASE, PRU, and percent inhibition were 338 (279-454), 256 (56-325), and 27% (0-57%). The medians of the post-ARU, BASE, PRU, and percent inhibition after stenting were 469 (range, 389-573), 378 (288-453), 274 (81-370), and 26% (0-79%). There was a significant increase of ARU (p=0.045), BASE (p=0.026), and PRU (p=0.018) before and after stenting. One immediate thromboembolic event was observed in poor-response group after stenting. There was no in-stent thrombosis and ischemic event in 1-month follow-up. CONCLUSION: We observed a significant increase of platelet reactivity to dual antiplatelet therapy right after stenting procedure for various cerebral arterial stenoses.
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Lee et al. (2012) conducted an observational in Cerebral artery stenosis (n=30). Cerebral arterial stenting procedure vs. Pre-stenting baseline was evaluated on Aspirin-reaction unit (ARU) (p=0.045). Cerebral arterial stenting significantly increased platelet reactivity, with median Aspirin Reaction Units rising from 418 to 469 (p=0.045) and P2Y12 Reaction Units from 256 to 274 (p=0.018).
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