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Background. Dual antiplatelet therapy (DAPT) is a standard treatment in non-ST-segment-elevation myocardial infarction (NSTEMI). However, the timing of initiation of DAPT in the Emergency Department (ED) is not well established. The purpose of this study is to demonstrate the correlation between the different timings of DAPT initiation in ED and the outcomes in patients with NSTEMI. Method. We retrospectively collected data of patients who were diagnosed as NSTEMI in the ED of China Medical University Hospital during 2016 to 2019. All NSTEMI patients who required coronary stenting or ballooning were enrolled into the study, which means NSTEMI patients who received percutaneous coronary intervention (PCI) were included. The time interval between ED arrival and DAPT given was recorded. Patients were divided into 2 groups according to whether they received DAPT within 6 hours after arrival to the ED. The primary outcomes were in-hospital major adverse cardiovascular events (MACE). The secondary outcomes were unexpected return to the ED within 72 hours, readmission within 14 days, and revascularization procedures performed within the first 30 days. Results. 938 NSTEMI patients with PCI were enrolled. Patients who received DAPT beyond 6 hours were relatively old (65.70 ± 14.13 versus 63.16 ± 13.31, p=0.014) and had relatively more comorbidities and higher Killip scores than those who received DAPT within 6 hours. The group that received DAPT within 6 hours had lower in-hospital MACE rate (3.52% versus 8.37%, p=0.009). Multivariate logistic regression showed the group beyond 6 hours was independently associated with higher risk for in-hospital MACE rate (OR : 2.09, 95% CI 1.07–4.07, p=0.030). Conclusion. Among patients with NSTEMI, DAPT beyond 6 hours after ED arrival have higher in-hospital MACE rate than those within 6 hours.

Platelet activation and its interaction with leukocytes play an important role in atherothrombosis. Cardiovascular diseases resulted from atherothrombosis remain the major causes of death worldwide. Gallic acid, a major constituent of red wine and tea, has been believed to have properties of cardiovascular protection, which is likely to be related to its antioxidant effects. Nonetheless, there were few and inconsistent data regarding the effects of gallic acid on platelet function. Therefore, we designed this in vitro study to determine whether gallic acid could inhibit platelet activation and the possible mechanisms. From our results, gallic acid could concentration-dependently inhibit platelet aggregation, P-selectin expression, and platelet-leukocyte aggregation. Gallic acid prevented the elevation of intracellular calcium and attenuated phosphorylation of PKCα/p38 MAPK and Akt/GSK3β on platelets stimulated by the stimulants ADP or U46619. This is the first mechanistic explanation for the inhibitory effects on platelets from gallic acid. [ABSTRACT FROM AUTHOR]