Insufficient platelet inhibition is related to silent embolic cerebral infarctions after coronary angiography.
OBJECTIVE
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.
Department of Neurology, Asan Medical Center, University of Ulsan, College of Medicine, Seoul, Republic of Korea.
Bum Joon
BJ
Kim
Seung-Whan
SW
Lee
Seong-Wook
SW
Park
Dong-Wha
DW
Kang
Jong S
JS
Kim
Sun U
SU
Kwon
D000368:Aged; D001241:Aspirin / Q000627:therapeutic use; D050197:Atherosclerosis / Q000150:complications; D001488:Basilar Artery / Q000503:physiopathology; D002339:Carotid Arteries / Q000503:physiopathology; D002544:Cerebral Infarction / Q000188:drug therapy* / Q000209:etiology / Q000473:pathology; D000077144:Clopidogrel; D017023:Coronary Angiography / Q000009:adverse effects*; D003627:Data Interpretation, Statistical; D038524:Diffusion Magnetic Resonance Imaging; D004351:Drug Resistance; D005260:Female; D006454:Hemoglobins / Q000032:analysis; D006801:Humans; D020766:Intracranial Embolism / Q000150:complications / Q000188:drug therapy* / Q000473:pathology; D007958:Leukocyte Count; D016015:Logistic Models; D018810:Magnetic Resonance Angiography; D008297:Male; D008875:Middle Aged; D010975:Platelet Aggregation Inhibitors / Q000008:administration & dosage / Q000627:therapeutic use*; D012189:Retrospective Studies; D012307:Risk Factors; D013988:Ticlopidine / Q000031:analogs & derivatives / Q000627:therapeutic use; D014711:Vertebral Artery / Q000503:physiopathology
D006454:Hemoglobins; D010975:Platelet Aggregation Inhibitors; D000077144:Clopidogrel; D013988:Ticlopidine; D001241:Aspirin