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J. Thromb. Thrombolysis · Jul 2014
Clinical TrialDecreased circulating microRNA-223 level predicts high on-treatment platelet reactivity in patients with troponin-negative non-ST elevation acute coronary syndrome.
- Ying-Ying Zhang, Xin Zhou, Wen-Jie Ji, Rui Shi, Rui-Yi Lu, Jin-Long Li, Guo-Hong Yang, Tao Luo, Jian-Qi Zhang, Ji-Hong Zhao, Tie-Min Jiang, and Yu-Ming Li.
- Graduate School of Medicine, Tianjin Medical University, Tianjin, China.
- J. Thromb. Thrombolysis. 2014 Jul 1; 38 (1): 65-72.
AbstractTo investigate the relationship between circulating microRNA 223 (miR-223) levels and clopidogrel responsiveness in patients with coronary heart disease. A total of 62 consecutive patients with troponin-negative non-ST elevation acute coronary syndrome (NSTE-ACS) scheduled for elective percutaneous coronary intervention were enrolled. The plasma circulating miR-223 levels were quantified by real-time PCR, and platelet reactivity was determined by platelet reactivity index (PRI), measured by vasodilator-stimulated phosphoprotein (VASP) phosphorylation flow cytometry after 300 mg (for at least 24 h) or 75 mg clopidogel (for at least 5 days) plus aspirin treatment. All subjects were dichotomized according to PRI median (normal-responders: PRI ≤ 56.3%, n = 31 and low-responders: PRI > 56.3%, n = 31). Compared with normal-responders, circulating miR-223 level was significantly decreased in low-responders (P = 0.007). In addition, miR-223 level was statistically correlated with PRI (Spearman r = -0.379, P = 0.002). Stepwise binary logistic regression analysis revealed that among factors that potentially influence platelet reactivity (CYP2C19*2/*3 loss-of-function genotypes, use of calcium channel blockers/proton-pump inhibitors, age, diabetes and smoking), decreased circulating miR-223 level was the only independent predictor for the presence of PRI-determined lower responders (OR 0.111, 95% CI 0.018-0.692, P = 0.019). Our data suggest that circulating miR-223 may serve as a novel biomarker for assessment of clopidogrel responsiveness in troponin-negative NSTE-ACS patients.
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