【Abstract】Objective To analyze the effect of platelet miR-126 on the antiplatelet reactivity of ticagrelor and its regulatory mechanism, identify the factors that affect the efficacy of ticagrelor, provide evidence for individualized antiplatelet therapy with P2Y12 receptor antagonists. Methods ACS patients received aspirin combined with ticagrelor were recruited continuously in PLA General Hospital from January 2019 to January 2020. After three days of stable antiplatelet treatment, thromboelastogram (TEG) was used for the detection of platelet reactivity. We selected 50 patients with high ADP% (high antiplatelet reactivity, HAPR) and 50 patients with low ADP% (low antiplatelet reactivity, LAPR). Platelet RNA from peripheral blood was measured miR-126 expression by using quantitative PCR. Results This study included 272 ACS patients treated with ticagrelor, with 49 patients in both the HAPR and LAPR groups completing platelet miR-126 detection. Both groups had a skewed distribution of ADP% [HAPR: 94.50 (92.95, 97.42); LAPR: 67.40 (57.00, 75.05); Mann-Whitney U test: p < 0.001]. Univariate analysis revealed significantly higher miR-126 expression in platelets in the HAPR group [2.97 (0.16-31.37)] compared to the LAPR group [1.00 (0.17-3.31)] (Mann-Whitney U test: p < 0.001). Multivariate analysis identified platelet miR-126 as an independent factor for ticagrelor antiplatelet response (OR: 1.991, 95% CI: 1.265-3.135, P = 0.003). Conclusion Platelet miR-126 is independently correlated with ticagrelor antiplatelet reactivity in ACS patients. Keywords: platelet, miR-126, ticagrelor, acute coronary syndrome, antiplatelet reactivity
