Platelet Activation Markers (beta-thromboglobulin and platelet factor 4) and Clopidogrel Drug Response in Patients with Myocardiac Infarction.
- Author:
Youngchun PARK
1
;
Jimyung KIM
;
Jinok JUNG
;
Kyechul KWON
;
Sunhoe KOO
Author Information
- Publication Type:Original Article
- Keywords: Beta-thromboglobulin; Clopidogrel; Myocardial infarction; Platelet factor 4
- MeSH: beta-Thromboglobulin; Blood Platelets*; Humans; Infarction*; Myocardial Infarction; Percutaneous Coronary Intervention; Plasma; Platelet Activation*; Platelet Factor 4
- From:Laboratory Medicine Online 2015;5(3):137-142
- CountryRepublic of Korea
- Language:Korean
- Abstract: BACKGROUND: Dual antiplatelet therapy (aspirin and clopidogrel) is used to prevent adverse cardiac events in patients undergoing percutaneous coronary intervention (PCI). Some patients do not respond adequately to clopidogrel. Beta-thromboglobulin (beta-TG) and platelet factor 4 (PF-4) can act as markers to detect platelet activation. We investigated the relationship between clopidogrel response and the dynamics of beta-TG and PF4 concentrations. METHODS: This study included 36 myocardial infarction (MI) patients, who underwent PCI and was indicated for dual antiplatelet therapy. Platelet reactivity, using the VerifyNow P2Y12 assay, was measured on the 3rd day of PCI. At the time of admission, and on the 3rd and 10th day of PCI, the plasma beta-TG and PF4 concentrations were quantified. RESULTS: Ten patients (27.8%) were clopidogrel non-responders displaying >208 P2Y12 reaction units. At the time of admission, levels of beta-TG in patients were elevated than that in the healthy controls (P<0.001). A similar trend was observed on the 3rd and 10th day of PCI (P<0.001). The beta-TG levels on the 10th day were reduced than those at the time of admission and on the 3rd day of PCI. PF4 levels were not different between patients and controls, and were not significantly reduced after PCI. Higher beta-TG levels were observed in clopidogrel non-responders on the 10th day, but not significant. CONCLUSIONS: Clopidogrel therapy in MI reduce beta-TG concentration, but the beta-TG and PF4 levels before and after therapy are not associated with the response to clopidogrel. Platelet-derived markers may not be suitable for distinguishing clopidogrel non-responders.
