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Insufficient platelet inhibition is related to silent embolic cerebral infarctions after coronary angiography
Bum Joon Kim1, Seung-Whan Lee, Seong-Wook Park
1Department of Neurology, Asan Medical Center, University of Ulsan, College of Medicine, Seoul, Republic of Korea.
Insights
Insufficient platelet inhibition from antiplatelet agents is linked to silent embolic cerebral infarction (SECI) after coronary angiography. Higher resistance to these medications increases SECI risk, highlighting the importance of adequate platelet inhibition.
Area of Science:
- Cardiology
- Neurology
- Pharmacology
Background:
- Insufficient platelet inhibition is a known risk factor for thrombotic complications.
- Coronary angiography procedures carry a risk of embolic events.
Purpose of the Study:
- To investigate the relationship between the extent of platelet inhibition and silent embolic cerebral infarction (SECI) after coronary angiography.
- To determine if inadequate platelet inhibition by antiplatelet agents is associated with SECI.
Main Methods:
- Retrospective analysis of 272 patients undergoing coronary angiography (Phase 1).
- Prospective study of 102 patients measuring platelet inhibition using the VerifyNow system (Phase 2).
- Diffusion-weighted imaging used to detect SECI.
Main Results:
- SECI occurred in 16.5% (Phase 1) and 16.7% (Phase 2) of patients.
- Patients with SECI had higher aspirin and P2Y12 reaction units, indicating poorer platelet inhibition.
- Increased SECI incidence correlated with resistance to antiplatelet agents.
Conclusions:
- Inadequate platelet inhibition following antiplatelet therapy is associated with SECI after coronary angiography.
- Nonresponsiveness to antiplatelet agents is an independent risk factor for SECI.
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 P(2)Y(12) reaction units were higher in the patients with SECI than those without (aspirin reaction units: 490±72 versus 446±53, P=0.03; P(2)Y(12) 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.
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