Effects of persistent platelet reactivity despite aspirin therapy on cardiac troponin I and creatine kinase-MB levels after elective percutaneous coronary interventions

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Creatinine kinase-MB (CK-MB) and cardiac troponin I (cTnI) elevations are highly specific for myonecrosis after percutaneous coronary intervention (PCI). Aspirin is used to prevent thrombotic complications. Several studies have shown that some individuals exhibit a reduced or completely missing antiplatelet response to aspirin. The aim of this study is to investigate the effects of platelet reactivity despite aspirin therapy on CK-MB and cTnI levels after elective percutaneous coronary interventions despite 600 mg loading dose of clopidogrel.


One hundred fourteen (mean age 61.2 ± 9.3 years, 78.1% male) patients receiving 300 mg daily enteric coated aspirin for at least 7 days with documented coronary artery disease were included in the study. Platelet reactivity despite aspirin was measured by platelet function analyzer (PFA)-100 collagen/epinephrine cartridge. Blood samples for CK-MB and cTnI were obtained before and at 6, 24, and 36 h after the PCI. Persistent platelet reactivity was defined when collagen/epinephrine closure time <165 s.


A total of 87 (76.4%) patients were noted to have normal platelet reactivity (Group A), and 27 (23.6%) had persistent platelet reactivity (Group B). The elevations of CK-MB and cTnI levels were statistically significant within the groups (both P < 0.001). However, there were no significant differences in the CK-MB and cTnI levels of the groups at baseline and after PCI for all studied hours.


Persistent platelet reactivity was not associated with increased risk of CK-MB, cTnI elevations in low-to-intermediate risk PCI patients.

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