ABSTRACT: Aim: To assess platelet (PLT) function and bleeding risks in patients with acute coronary syndrome after tirofiban infusion. Methods: Patients diagnosed with acute coronary syndrome from May 2016 to February 2018 in the Department of Cardiac Intensive Care Unit, Zhongshan Hospital, were enrolled. They were symmetrically allocated into two groups: tirofiban treatment group or control group (without tirofiban treatment). Blood samples were collected 24 h postoperation for the evaluation of antiplatelet effect of tirofiban. We applied thromboelastography to detect on-treatment PLT reactivity and conducted laboratory tests to assess the risk of bleeding following tirofiban treatment. After discharge, telephone follow-up and outpatient interview were carried out. The primary clinical endpoint was major adverse cardiovascular events, including cardiovascular death, cardiovascular mortality, myocardial infarction, and revascularization for the targeted vascular lesion. Results: There were a total of 196 patients with acute coronary syndrome after screening with the inclusion criteria and the exclusion criteria. Ninety-eight patients were assigned to receive either tirofiban treatment or control treatment. Patients treated with tirofiban had more coronary lesions and stents implanted compared with the control group (P = 0.000). After tirofiban infusion, inhibition of platelet aggregation induced by thromboxane A2 and adenosine diphosphate was significantly higher compared to patients without tirofiban infusion (80.3% ± 19.6% vs. 72.6% ± 13.0%, P = 0.002; and 81.0% ± 19.8% vs. 75.4% ± 12.4%, P = 0.020, respectively). There was no significant difference in the reduction of hemoglobin (Hb), hematocrit (Hct), and PLT after administration of tirofiban, compared with baseline (P > 0.05). In addition, no significant differences were identified between the two groups with respect to Hb, Hct, and PLT after tirofiban infusion. However, C-reactive protein level, referred to as an inflammation marker, was significantly lowered after infusion tirofiban compared with the control group (11.9 ± 14.2 vs. 17.9 ± 21.2, P = 0.020). During the 1-year follow-up, the incidence rate of major adverse cardiovascular events remains indiscriminate between the two groups (P = 0.208). The assessments of cardiac biomarkers showed that tirofiban could decrease incidence of procedural myocardial infarction (odds ratio [OR] = 0.250, 95% confidence interval [CI] = 0.067-0.925, P = 0.027). At follow-up, the morbidity of left atrial dilation in tirofiban-treated patients, defined as enlargement of left atrial diameter >40mm, was lower compared to the control group (OR = 0.533, 95% CI = 0.301-0.945, P = 0.031). Conclusion: Tirofiban infusion could decrease PLT activation in patients with acute coronary syndrome without increasing the risk of bleeding. As a concomitant medication, tirofiban shows no benefit in reducing the occurrence of major adverse cardiovascular events.
