Expression of Monocytes Subsets in Patients Diagnosed With Coronary Artery Atherosclerosis and Their Impact on Disease Severity

Overview

Journal Cureus

Specialty Biomedical Engineering

Date 2024 Dec 30

PMID 39734983

Authors

Asmaa Khalf Kamel

Naglaa M Farag

Emad Allam

Mohamed Khaled

Doaa Elzaeem Ismail

Affiliations

Soon will be listed here.

Abstract

Introduction Many studies have supported inflammation as a mediator of lipoprotein (a) (Lp(a)) induced increase in cardiovascular disease risk, as it has pro-inflammatory effects on endothelial cells and monocytes. Aim This study aims to correlate Lp(a) level with different monocyte subsets in coronary atherosclerotic patients with different severity. Method The study included 60 patients with a mean age of 53.1 ± 10.5 diagnosed as coronary atherosclerotic patients by coronary angiography. Lp levels were measured using enzyme-linked immunosorbent assay (ELISA), while blood counts and monocyte subsets were analyzed by flow cytometry, and 30 apparently healthy individuals were included as the control group. Results Patients showed significantly higher median monocytic %, Lp(a), and higher C-reactive protein (CRP) values than the control group. Patients were subdivided into two groups: normal Lp(a) < 6.2 mg/dL (n = 24) and hyperlipoproteinemia(a) (hyper Lp(a)) ≥ 6.2 mg/dL (n = 36). Patients with hyper Lp(a) had higher non-classical monocytes (31.5% vs. 20%). Coronary atherosclerosis severity was associated with higher Lp(a) levels as well as non-classical monocytes; patients with mild atherosclerosis showed the highest classical and intermediate subset levels. While for a non-classical subset, patients with severe atherosclerosis showed the highest median level. A significant moderate positive correlation between Lp(a) and monocyte counts, as well as monocyte-lymphocyte (M/L) index and non-classical monocytes, was found. Conclusions Hyper Lp(a) and increased count of non-classical monocytes are significantly increased with disease progression (triple-vessel coronary disease risk). These results suggest that the expansion of non-classical monocytes is a cardiovascular disease (CVD) risk and predictor for disease severity. Strategies targeting inflammatory monocytes may slow CVD progression.

References

Wen Y, Zhan X, Wang N, Peng F, Feng X, Wu X . Monocyte/Lymphocyte Ratio and Cardiovascular Disease Mortality in Peritoneal Dialysis Patients. Mediators Inflamm. 2020; 2020:9852507. PMC: 7048939. DOI: 10.1155/2020/9852507. View

Ozanska A, Szymczak D, Rybka J . Pattern of human monocyte subpopulations in health and disease. Scand J Immunol. 2020; 92(1):e12883. DOI: 10.1111/sji.12883. View

Patel V, Williams H, Li S, Fletcher J, Medbury H . Monocyte Subset Recruitment Marker Profile Is Inversely Associated With Blood ApoA1 Levels. Front Immunol. 2021; 12:616305. PMC: 7952433. DOI: 10.3389/fimmu.2021.616305. View

Williams H, Mack C, Li S, Fletcher J, Medbury H . Nature versus Number: Monocytes in Cardiovascular Disease. Int J Mol Sci. 2021; 22(17). PMC: 8430468. DOI: 10.3390/ijms22179119. View

Kong P, Cui Z, Huang X, Zhang D, Guo R, Han M . Inflammation and atherosclerosis: signaling pathways and therapeutic intervention. Signal Transduct Target Ther. 2022; 7(1):131. PMC: 9033871. DOI: 10.1038/s41392-022-00955-7. View

Jang A, Han S, Sohn I, Oh P, Kon Koh K . Lipoprotein(a) and Cardiovascular Diseases　- Revisited. Circ J. 2020; 84(6):867-874. DOI: 10.1253/circj.CJ-20-0051. View

Simantiris S, Antonopoulos A, Papastamos C, Benetos G, Koumallos N, Tsioufis K . Lipoprotein(a) and inflammation- pathophysiological links and clinical implications for cardiovascular disease. J Clin Lipidol. 2022; 17(1):55-63. DOI: 10.1016/j.jacl.2022.10.004. View

Idzkowska E, Eljaszewicz A, Miklasz P, Musial W, Tycinska A, Moniuszko M . The Role of Different Monocyte Subsets in the Pathogenesis of Atherosclerosis and Acute Coronary Syndromes. Scand J Immunol. 2015; 82(3):163-73. DOI: 10.1111/sji.12314. View

Afanasieva O, Filatova A, Arefieva T, Klesareva E, Tyurina A, Radyukhina N . The Association of Lipoprotein(a) and Circulating Monocyte Subsets with Severe Coronary Atherosclerosis. J Cardiovasc Dev Dis. 2021; 8(6). PMC: 8228191. DOI: 10.3390/jcdd8060063. View

10.

Xiang Y, Liang B, Zhang X, Zheng F . Lower HDL-C levels are associated with higher expressions of CD16 on monocyte subsets in coronary atherosclerosis. Int J Med Sci. 2020; 17(14):2171-2179. PMC: 7484662. DOI: 10.7150/ijms.47998. View

11.

Sagris M, Theofilis P, Antonopoulos A, Oikonomou E, Paschaliori C, Galiatsatos N . Inflammation in Coronary Microvascular Dysfunction. Int J Mol Sci. 2021; 22(24). PMC: 8703507. DOI: 10.3390/ijms222413471. View

12.

Badimon L, Pena E, Arderiu G, Padro T, Slevin M, Vilahur G . C-Reactive Protein in Atherothrombosis and Angiogenesis. Front Immunol. 2018; 9:430. PMC: 5840191. DOI: 10.3389/fimmu.2018.00430. View

13.

Helgadottir A, Sulem P, Thorgeirsson G, Gretarsdottir S, Thorleifsson G, Jensson B . Rare SCARB1 mutations associate with high-density lipoprotein cholesterol but not with coronary artery disease. Eur Heart J. 2018; 39(23):2172-2178. PMC: 6001888. DOI: 10.1093/eurheartj/ehy169. View

14.

Fransen K, Pettersson C, Hurtig-Wennlof A . CRP levels are significantly associated with CRP genotype and estrogen use in The Lifestyle, Biomarker and Atherosclerosis (LBA) study. BMC Cardiovasc Disord. 2022; 22(1):170. PMC: 9013148. DOI: 10.1186/s12872-022-02610-z. View

15.

Murray C, Siddiqui T, Keller N, Chowdhury S, Nahar T . Physiology-Guided Management of Serial/Diffuse Coronary Artery Disease. Curr Cardiol Rep. 2019; 21(4):25. DOI: 10.1007/s11886-019-1105-0. View

16.

Kral B, Kalyani R, Yanek L, Vaidya D, Fishman E, Becker D . Relation of Plasma Lipoprotein(a) to Subclinical Coronary Plaque Volumes, Three-Vessel and Left Main Coronary Disease, and Severe Coronary Stenoses in Apparently Healthy African-Americans With a Family History of Early-Onset Coronary Artery Disease. Am J Cardiol. 2016; 118(5):656-61. PMC: 4991623. DOI: 10.1016/j.amjcard.2016.06.020. View

17.

Khodadi E . Platelet Function in Cardiovascular Disease: Activation of Molecules and Activation by Molecules. Cardiovasc Toxicol. 2019; 20(1):1-10. DOI: 10.1007/s12012-019-09555-4. View

18.

Kamstrup P . Lipoprotein(a) and Cardiovascular Disease. Clin Chem. 2020; 67(1):154-166. DOI: 10.1093/clinchem/hvaa247. View

19.

Pirro M, Bianconi V, Paciullo F, Mannarino M, Bagaglia F, Sahebkar A . Lipoprotein(a) and inflammation: A dangerous duet leading to endothelial loss of integrity. Pharmacol Res. 2017; 119:178-187. DOI: 10.1016/j.phrs.2017.02.001. View

20.

Man J, Beckman J, Jaffe I . Sex as a Biological Variable in Atherosclerosis. Circ Res. 2020; 126(9):1297-1319. PMC: 7185045. DOI: 10.1161/CIRCRESAHA.120.315930. View