Lipoprotein-as­sociated phospholipase A2 and the risk of ischemic stroke

Authors: Ľ. Danihel 1,2;  Š. Madarász 2,3;  P. Blažíček 4,5;  A. Lacko 2,6;  J. Luha 7;  V. Lehotská 8,9
Authors‘ workplace: Rádiologická klinika ÚVN SNP Ružomberok – FN, Ružomberok 1;  Fakulta zdravotníctva, Katolícka univerzita, Ružomberok 2;  Neurologická klinika ÚVN SNP Ružomberok – FN, Ružomberok 3;  Ústav chémie, klinickej biochémie a labo­ratórnej medicíny, LF SZU v Bratislave 4;  Laboratórium 4vive, Bratislava 5;  Interná klinika, Kardiologická ambulancia, ÚVN SNP Ružomberok – FN, Ružomberok 6;  Ústav lekárskej biológie, genetiky a klinickej genetiky, LF UK a UN, Bratislava 7;  II. Rádiologická klinika, LF UK A UN, Bratislava 8;  Onkologický ústav svätej Alžbety, Bratislava 9
Published in: Cesk Slov Neurol N 2018; 81(3): 308-313
Category: Original Paper
doi: 10.14735/amcsnn2018308

Práca bola podporená projektom Európskej únie Mechanizmy a nové markery vzniku a priebehu cirkulárnych porúch mozgu ITMS 26220220099.


Lipoprotein-associated phospholipase A2 (Lp-PLA2) is an enzyme accumulated in atherosclerotic plaques and causes plaques inflammation that can induce plaque rupture. The aim of this work is to compare serum Lp-PLA2 concentration in healthy subjects and in patients with arterial hypertension (AH), ischemic heart disease (IHD) and ischemic stroke (IS) so that we could assess utility of Lp-PLA2 as a biomarker for IS risk. AH and IHD are considered risk factors for IS, therefore we measured serum Lp-PLA2 concentration also in patients with these diseases.

Serum Lp-PLA2 concentration was determined by diaDexus PLAC® Test ELISA Kit (Diadexus, Inc., San Francisco, USA), a sandwich enzyme immunoassay. The statistical analysis was performed with IBM SPSS Statistics 24 (IBM Corp., New York, USA) using the Fisher’s exact test and non-parametric correlations.

Our cohort comprised of 401 subjects in total (43% males), 80 subjects in the group of healthy individuals (35% males), 96 subjects in the group with AH (43% males), 85 subjects in the group with IHD (39% males) and 140 subjects in the group with IS (49% males). Serum Lp-PLA2 concentration in the group of healthy individuals was significantly lower than that in the group with AH (p = 0 × 10–3), IHD (p = 0 × 10–3) and IS (p = 0 × 10–3).

Our study confirmed the assumption that people with AH, IHD and IS have higher levels of serum Lp-PLA2 concentration than healthy people hence a higher incidence of inflamed atherosclerotic plaques and higher risk of rupture of these plaques, but a higher level of serum Lp-PLA2 persisted in people with AH, IHD and IS in our cohort despite the statin therapy, leading us to conclude that the role of Lp-PLA2 in the development and intensification of atherosclerotic plaque inflammation may be more complicated than only the hydrolysis of oxidized LDL in atherosclerotic plaque.

Key words:
lipoprotein-associated phospholipase A2 – atherosclerosis – ischemic stroke

The authors declare they have no potential conflicts of interest concerning drugs, products, or services used in the study.

The Editorial Board declares that the manuscript met the ICMJE “uniform requirements” for biomedical papers.


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