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

Özet

Objective: High-density lipoproteins (HDLs) are a very heterogeneous group of particles. Little is known about the impact of their subfractionsincluding 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), particularlyin the acute phase of ST-segment elevation myocardial infarction (STEMI). The aim of the study was to evaluate the relationship betweenserum 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 demographicdata were collected and HDL subfractions were measured by rocket immunoelectrophoresis. Platelet reactivity was assessed using light transmissionaggregometry 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. Comparedwith subjects with satisfactory platelet response to clopidogrel, patients with HPR had 32.44% higher serum level of LpA-I (p=0.021). Onthe 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 analysisshowed 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 levelof 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 functionsof HDL subfractions in acute STEMI.