Lipoprotein-associated phospholipase A2 and the risk of ischemic stroke
Authors:
Ľudovít 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:
https://doi.org/10.14735/amcsnn2018308
Práca bola podporená projektom Európskej únie Mechanizmy a nové markery vzniku a priebehu cirkulárnych porúch mozgu ITMS 26220220099.
Overview
Aim:
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.
Methods:
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.
Results:
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).
Conclusion:
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.
Sources
1. Stafforini DM. Biology of platelet-activating factor acetylhydrolase (PAF-AH, lipoprotein associated phospholipase A2). Cardiovasc Drugs Ther 2009; 23(1): 73– 83. doi: 10.1007/ s10557-008-6133-8.
2. Kollár J. (Bio)markery vulnerabilných plátov a prediktabilita ischemických príhod. In: Kollár J. Aterotrombóza-patofyziológia a epidemiológia. Košice: Equilibria 2016: 65– 85.
3. Franeková J, Jabor A. Fosfolipáza A2 asociovaná s lipoproteiny – nový marker kardiovaskulárního rizika. Postgraduální med 2010; 12 (Suppl 3): 32– 42.
4. Greenland P, Alpert JS, Beller GA et al. 2010 ACCF/ AHA guideline for assessment of cardiovascular risk in asymptomatic adults: a report of the American College of Car-diology Foundation/ American Heart Association Task Force on Practice Guidelines. Circulation 2010; 122(25): e584– e636. doi: 10.1161/ CIR.0b013e3182051b4c.
5. Piepoli MF, Hoes AW, Agewall S et al. 2016 European guidelines on cardiovascular disease prevention in clinical practice: The Sixth Joint Task Force of the European Society of Cardiology and other societies on cardiovascular disease prevention in clinical practice (constituted by representatives of 10 societies and by invited experts): developed with the special contribution of the European Association for Cardiovascular Prevention & Rehabilitation (EACPR). Eur J Prev Cardiol 2016; 23(11): NP1– NP96. doi: 10.1177/ 2047487316653709.
6. Prescott SM, Mcintyre TM, Zimmerman GA et al. Sol Sherry lecture in thrombosis. Molecular events in acute inflammation. Arterioscler Thromb Vasc Biol 2002; 22(5): 727– 733. doi: 10.1161/ 01.ATV.0000016153.47693.B2.
7. White HD, Held C, Stewart R et al. Darapladib for preventing ischemic events in stable coronary heart disease. N Engl J Med 2014; 370(18): 1702– 1711. doi: 10.1056/ NEJMoa1315878.
8. O‘Donoghue ML, Braunwald E, White HD et al. Effect on darapladib on major coronary events after an acute coronary syndrome: the SOLID-TIMI 52 randomized clinical trial. JAMA 2014; 312(10): 1006– 1015. doi: 10.1001/ jama.2014.11061.
9. Rosenson RS, Stafforini DM. Modulation of oxidative stress, inflammation, and atherosclerosis by lipoprotein-associatedphospholipase A2. J Lipid Res 2012; 53(9): 1767– 1782. doi: 10.1194/ jlr.R024190.
10. Massot A, Pelegri D, Panalba A et al. Lipoprotein-associatel phosholipase A2 testing usefulness among patients with symptomatic intracranial atherosclerotic disease. Atherosclerosis 2011; 218(1): 181– 187. doi: 10.1016/ j.atherosclerosis.2011.04.031.
11. U.S. Food and Drug Administration. 510 (k) Summary diaDexus PLAC TM Test. [online]. Available from URL: https: / / www.accessdata.fda.gov/ cdrh_docs/ pdf5/ k050523.pdf.
12. Lanman RB, Wolfert RL, Fleming JK et al. Lipoprotein-accociated phosholipase A2: review and recommendation of clinical cut of point for adults. Prev Cardiol 2006; 9(3): 138– 143.
13. McConnell JP, Hoefner DM. Lipoprotein-associated phospholipase A2. Clin Lab Med 2006; 26(3): 679– 697.
14. Davidson MH, Corson MA, Alberts MJ et al. Consensus panel recommendation for incorporating lipoprotein-associated phospholipase A2 testing into cardiovascular disease risk assessment guidelines. Am J Cardiol 2008; 101(12A): 51F– 57F. doi: 10.1016/ j.amjcard.2008.04.019.
15. U.S. Food and Drug Administration. 510 (k) Summary diaDexus PLAC Test for Lp-PLA2 Activity. [online]. Available from URL: https: / / www.accessdata.fda.gov/ cdrh_docs/ pdf14/ K141575.pdf.
16. Mayo Clinic. Mayo Medical Laboratories. Lipoprotein-assocated phosholipase A2 (Lp-PLA2) activity. Novel and effective testing for prediction of coronary heart disease.[online]. Available from URL: http: / / www.mayomedicallaboratories.com/ media/ mayo_client/ marketing/ cardiology/ lp-pla2-PLACA-brochure-1115b.pdf.
17. O‘Riordan M. FDA approves Lp-PLA2 test for patients without existing coronary disease. [online]. Available from URL: http: / / www.medscape.com/ viewarticle/ 836640.
18. Jabor B, Choi H, Ruel I et al. Lipoprotein-associated phospholipase A2 (Lp-PLA2) in acute coronary syndrome: relationship with low-density lipoprotein cholesterol. Can J Cardiol 2013; 29(12): 1679– 1686. doi: 10.1016/ j.cjca.2013.09.026.
19. Kara H, Akinci M, Degirmenci S et al. High-sensitivity C-reactive protein, lipoprotein-related phospholipase A2, and acute ischemic stroke. Neuropsychiatr Dis Treat 2014; 10: 1451– 1457. doi: 10.2147/ NDT.S67665.
20. Tai W, Garcia M, Mlynash M et al. Lipoprotein phospholipase A2 mass and activity are not associated with the diagnosis of acute brain ischemia. Cerebrovasc Dis 2014; 38(5): 324– 27. doi: 10.1159/ 000368218.
21. Elkind MSV, Leon V, Moon YP et al. High-sensitivity C-Reactive protein and lipoprotein-associated phospholipase A2 stability before and after stroke and myocardial infarction. Stroke 2009; 40(10): 3233– 3237. doi: 10.1161/ STROKEAHA.109.552802.
22. Kocak S, Ertekin B, Girisgin AS et al. Lipoprotein-associated phospholipase A2 activity and its diagnostic potential in patients with acute coronary syndrome and acute ischemic stroke. Turk J Emerg Med 2016; 17(2): 56– 60. doi: 10.1016/ j.tjem.2016.10.001.
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Paediatric neurology Neurosurgery NeurologyArticle was published in
Czech and Slovak Neurology and Neurosurgery
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