Insufficient platelet inhibition is related to silent embolic cerebral infarctions after coronary angiography

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Abstract

BACKGROUND AND PURPOSE-: Considering that insufficient platelet inhibition is related to thrombotic complications after coronary angiography, we hypothesized that the extent of platelet inhibition by antiplatelet agents is related to the occurrence of silent embolic cerebral infarction (SECI) after coronary angiography. METHODS-: Among the patients scheduled for coronary artery bypass surgery, we retrospectively analyzed the location of SECI on diffusion-weighted imaging of 272 patients, which was performed after coronary angiography, as a presurgical evaluation in Phase 1 study. In Phase 2 study, we have prospectively recruited 102 patients to compare the extent of platelet inhibition measured by the VerifyNow system among patients with and without SECI. RESULTS-: SECI is observed in 45 patients (16.5%) in Phase 1 and 17 (16.7%) in Phase 2. The lesions were slightly more frequent in the right hemisphere. In the Phase 2 study, aspirin reaction units and P2Y12 reaction units were higher in the patients with SECI than those without (aspirin reaction units: 490±72 versus 446±53, P=0.03; P2Y12 reaction units: 352±65 versus 300±77, P=0.009). The incidence of SECI increased with the number of resistant antiplatelets; resistance to both antiplatelet agent (50%), resistance to 1 antiplatelet agent (22%), and no resistance (4%; P=0.023). From the result of logistic regression, higher aspirin reaction units, white blood cell count, low hemoglobin, and nonresponsiveness to antiplatelet agents were independent risk factors. CONCLUSIONS-: Insufficient platelet inhibition after administration of antiplatelet agents is related with SECI appearing after coronary angiography. © 2012 American Heart Association, Inc.

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Kim, B. J., Lee, S. W., Park, S. W., Kang, D. W., Kim, J. S., & Kwon, S. U. (2012). Insufficient platelet inhibition is related to silent embolic cerebral infarctions after coronary angiography. Stroke, 43(3), 727–732. https://doi.org/10.1161/STROKEAHA.111.641340

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