Original article

Lymphocyte and monocyte subtypes in coronary artery ectasia patients

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  • Department of Cardiology, Beijing Friendship Hospital Affiliated to Beijing Capital Medical University, Beijing 100050, China

Received date: 2021-10-08

  Online published: 2022-11-04

Abstract

Objective To determine whether peripheral lymphocytes and monocytes were involved in the pathological processes of coronary artery ectasia (CAE). Methods This study included 34 patients who underwent coronary angiography and were diagnosed as CAE from January 2017 to January 2018. In addition, a total of 30 patients with coronary heart disease (CHD) and 32 subjects with relatively normal coronary arteries (control group) who underwent coronary angiography on the same period were included by lot. Three groups were balanced according to age, sex, and other baseline characteristics, and the lymphocyte and monocyte subtypes in their blood samples were examined via flow cytometry. Results Lymphocyte subtypes in CAE and CHD patients showed no significant differences. However, compared to the CHD and control groups, the inflammatory (non-classic type) monocytes were significantly increased [26.45% (16.90%-44.55%) vs 13.70%(9.33%-17.60%), or 7.00% (13.70%-29.40%), P=0.000], while the classic subtype monocytes were significantly decreased [66.35% (39.73%-78.83%) vs 82.90% (80.50%-89.40%) or 78.30% (56.70%-83.80%), P=0.000] in the CAE group. Multiple linear regression analysis further confirmed that the non-classic monocyte was related to CAE [CAE group=1, CHD group=2, control group=3, so the regression coefficient is negative as β=-0.371, P=0.000 ]. Conclusions CAE could be an inflammatory disease rather than an immune disease.

Cite this article

LIU Ruifeng, SHENG Qianqian, ZHANG Yue, ZHAO Huiqiang . Lymphocyte and monocyte subtypes in coronary artery ectasia patients[J]. Journal of Internal Medicine Concepts & Practice, 2022 , 17(05) : 373 -378 . DOI: 10.16138/j.1673-6087.2022.05.005

References

[1] Sheikh AS, Hailan A, Kinnaird T, et al. Coronary artery aneurysm: evaluation, prognosis, and proposed treatment strategies[J]. Heart Views, 2019, 20(3): 101-108.
[2] Eitan A, Roguin A. Coronary artery ectasia: new insights into pathophysiology, diagnosis, and treatment[J]. Coron Artery Dis, 2016, 27(5): 420-428.
[3] Markis JE, Joffe CD, Cohn PF, et al. Clinical significance of coronary arterial ectasia[J]. Am J Cardiol, 1976, 37(2): 217-222.
[4] Li JJ, He JG, Nan JL, et al. Is systemic inflammation responsible for coronary artery ectasia?[J]. Int J Cardiol, 2008, 130(2): e69-e70.
[5] Balta S, Demir M, Ozturk C, et al. The relation between inflammation and coronary artery ectasia[J]. Rev Port Cardiol, 2016, 35(10): 553-554.
[6] Huang W, Berube J, McNamara M, et al. Lymphocyte subset counts in COVID-19 patients[J]. Cytometry A, 2020, 97(8): 772-776.
[7] Cormican S, Griffin MD. Human monocyte subset distinctions and function[J]. Front Immunol, 2020, 11: 1070.
[8] Tamis-Holland JE, Jneid H, Reynolds HR, et al. Contemporary diagnosis and management of patients with myocardial infarction in the absence of obstructive coronary artery disease[J]. Circulation, 2019, 139(18): e891-e908.
[9] Lin JP, Vitek L, Schwertner HA. Serum bilirubin and genes controlling bilirubin concentrations as biomarkers for cardiovascular disease[J]. Clin Chem, 2010, 56(10): 1535-1543.
[10] Tsai WN, Wang YY, Liang JT, et al. Serum total bilirubin concentrations are inversely associated with total white blood cell counts in an adult population[J]. Ann Clin Biochem, 2015, 52 Pt2: 251-258.
[11] Turhan H, Erbay AR, Yasar AS, et al. Impaired coronary blood flow in patients with metabolic syndrome[J]. Am Heart J, 2004, 148(5): 789-794.
[12] 李彭军, 韩慧文, 葛兰, 等. 健康体检者循环单核细胞亚群与性别及年龄的关系[J]. 武警医学, 2014, 25(1): 5-8.
[13] Chen J, Zhang Y, Liu J, et al. Role of lipoprotein(a) in predicting the severity of new on-set coronary artery disease in type 2 diabetics[J]. Diab Vasc Dis Res, 2015, 12(4): 258-264.
[14] Matta AG, Yaacoub N, Nader V, et al. Coronary artery aneurysm[J]. World J Cardiol, 2021, 26, 13(9): 446-455.
[15] Sheikh AS, Hailan A, Kinnaird T, et al. Coronary artery aneurysm: evaluation, prognosis, and proposed treatment strategies[J]. Heart Views, 2019, 20(3): 101-108.
[16] Virmani R, Robinowitz M, Atkinson JB, et al. Acquired coronary arterial aneurysms[J]. Hum Pathol, 1986, 17(6): 575-583.
[17] Sarli B, Baktir AO, Saglam H, et al. Neutrophil-to-lymphocyte ratio is associated with severity of coronary artery ectasia[J]. Angiology, 2014, 65(2): 147-151.
[18] Li JJ, Nie SP, Qian XW, et al. Chronic inflammatory status in patients with coronary artery ectasia[J]. Cytokine, 2009, 46(1): 61-64.
[19] Iwańczyk S, Borger M, Kamiński M, et al. Inflammatory response in patients with coronary artery ectasia and coronary artery disease[J]. Kardiol Pol, 2019, 77(7-8): 713-715.
[20] Lamblin N, Bauters C, Hermant X, et al. Polymorphisms in the promoter regions of MMP-2, MMP-3, MMP-9 and MMP-12 genes as determinants of aneurysmal coronary artery disease[J]. J Am Coll Cardiol, 2002, 40(1): 43-48.
[21] Finkelstein A, Michowitz Y, Abashidze A, et al. Temporal association between circulating proteolytic, inflammatory and neurohormonal markers in patients with coronary ectasia[J]. Atherosclerosis, 2005, 179(2): 353-359.
[22] Lee NY, Park HY, Park CK, et al. Analysis of systemic endothelin-1, matrix metalloproteinase-9, macrophage chemoattractant protein-1, and high-sensitivity C-reactive protein in normal-tension glaucoma[J]. Curr Eye Res, 2012, 37(12): 1121-1126.
[23] Liu R, Chen L, Wu W, et al. Neutrophil serine proteases and their endogenous inhibitors in coronary artery ectasia patients[J]. Anatol J Cardiol, 2016, 16(1): 23-28.
[24] Katritsis DG, Zografos T, Korovesis S, et al. Antiendothelial cell antibodies in patients with coronary artery ectasia[J]. Coron Artery Dis, 2010, 21(16): 352-356.
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