Association of serum levels of lipoprotein A-I and lipoprotein A-I/A-II with high on-treatment platelet reactivity in patients with ST-segment elevation myocardial infarction

Objective: High-density lipoproteins (HDLs) are a very heterogeneous group of particles. Little is known about the impact of their subfractions including lipoprotein A-I (LpA-I) and lipoprotein A-I/A-II (LpA-I/A-II) on platelet function and high on-treatment platelet reactivity (HPR), particularly in the acute phase of ST-segment elevation myocardial infarction (STEMI). The aim of the study was to evaluate the relationship between serum levels of LpA-I and LpA-I/A-II and HPR in STEMI patients. Methods: Fifty-two consecutive STEMI patients (26.9% women, mean age 60.6±9.1 years) were enrolled into this study. Clinical and demographic data were collected and HDL subfractions were measured by rocket immunoelectrophoresis. Platelet reactivity was assessed using light transmission aggregometry and quantitative flow cytometry. Results: We found a positive correlation between platelet aggregation after both ADP-5 and ADP-20 stimulation and serum level of LpA-I. Compared with subjects with satisfactory platelet response to clopidogrel, patients with HPR had 32.44% higher serum level of LpA-I (p=0.021). On the other hand, patients with HPR assessed by ADP-5 stimulation had 22.13% lower serum level of LpA-I/A-II (p=0.040). Regression analysis showed that LpA-I [odds ratio (OR) 1.03; 95% confidence interval (CI) 1-1.07; p=0.049] and current smoking (OR 0.18; 95% CI 0.04-0.81; p=0.025) were independent predictors of HPR. With receiver operating characteristic (ROC) curve analysis, we designated the cut-off point at serum level of 57.52 mg/dL for LpA-I for predicting HPR (AUC=0.71, p=0.010). Conclusion: This study showed that higher serum level of LpA-I measured in the acute phase of STEMI is an independent risk factor for HPR. Our study is the first to demonstrate an important and distinct activity of LpA-I and LpA-I/A-II that can prove pleiotropic and different functions of HDL subfractions in acute STEMI. (Anatol J Cardiol 2018; 19: 374-81