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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 (STEMI). [Anatol J Cardiol]
Anatol J Cardiol. Ahead of Print: AJC-63549 | DOI: 10.14744/AnatolJCardiol.2018.63549  

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 (STEMI).

Aleksander Siniarski1, Rafal Grzybczak2, Pawel Rostoff1, Jaroslaw Zalewski1, Urszula Czubek1, Jadwiga Nessler1, Grzegorz Gajos1
1Department of Coronary Disease and Heart Failure, Faculty of Medicine, Jagiellonian University Medical College, John Paul II Hospital, Krakow, Poland
2Department of Cardiac Rehabilitation, John Paul II Hospital, Krakow, Poland

Background and Aims:
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 patients with STEMI.
Methods and Results: Fifty-two consecutive STEMI patients (26.9% women, mean age 60.69.1 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. We have found a positive correlation between platelet aggregation after both ADP-5 and ADP-20 stimulation, and serum LpA-I. When compared to subjects with satisfactory platelet response to clopidogrel, patients with HPR had 32.44% higher LpA-I concentration (p=0.021). On the other hand, patients with HPR assessed by ADP-5 stimulation had 22.13% lower LpA-I/A-II level (p=0.040). Regression analysis showed that LpA-I (OR 1.03; 95%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. In ROC curve analysis we have designated the cut-off point at 57.52 mg/dl for LpA-I concentration for predicting HPR (AUC=0.71, p=0.010).
Conclusion: This study showed that higher serum LpA-I concentration 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 which can prove pleiotropic and different functions of HDL subfractions in acute STEMI.

Keywords: high-density lipoproteins, HDL, lipoprotein A-I, platelets, high platelet reactivity; STEMI, ST-elevation, myocardial infarction.




Corresponding Author: Grzegorz Gajos, Poland


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