Relationship between dynamic changes in subpopulations of blood monocytes and the development of complications in patients with acute myocardial infarction

Main Article Content

T. V. Talayeva
O. M. Parkhomenko
I. V. Tretyak
O. V. Dovhan
O. V. Shumakov

Abstract

The aim – to determine the extent of different subpopulations of blood monocytes in acute myocardial infarction (AMI) with ST-segment elevation patients on day 1 and 7 and to evaluate the relationship between their content and the dynamics of changes and the risk of complications after AMI.
Materials and methods. The composition of individual subpopulations of monocytes in the peripheral venous blood (and general clinical and biochemical blood tests) was evaluated in 50 pts with STEMI (who were admitted within 6 hours after the onset of the disease) at admission (before primary PCI) and on day 7. All patients received standard recommended therapy. Dynamic heart echocardiography was also performed on the 1st and 7th day. All patients were divided into 2 groups depending on the dynamical increase (1 group – 21 pts) or decrease (2 group – 29 pts) of classical monocytes (CD14hiCD16–) subpopulation during 7 days of follow-up. The control group included 15 healthy subjects with no signs of coronary heart disease and 23 pts with chronic coronary heart disease without AMI.
Results and discussion. In subgroup 1, the percentage of the «classical» fraction of monocytes during the observation increased to 89.0±1.2 %, which was 4.2 % more than on the 1st day and 12.5 % more than in the control group (p<0.05), while the absolute amount of classic monocytes on day 7 increased by 48 % compared to initial value (p<0.01). The percentage of «intermediate» (CD14hiCD16+) blood monocytes in patients of this subgroup on the 1st day of hospitalization was 70 % higher than in the control group, and 42 % higher than in the 2nd subgroup of patients (p<0,001), however, on the 7th day it decreased by 30 % compared to baseline, although it remained by 8 % more than in the control group (the absolute number of «intermediate» monocytes did not change). The activation index (IA) of the «intermediate» monocytes on the first day did not differ between subgroups and was 40 % higher than in the control group (p<0.001). However, in the dynamics of observation, in patients of subgroup 1, this figure did not change, while in subgroup 2 IA decreased by 60 % (p<0.001). Despite the fact that the absolute number of anti-inflammatory («patrolling») (CD14+lowCD16++) monocytes did not change until the 7th day of observation (and their percentage decreased slightly), their IA was significantly lower than in the control group (95 %) and in patients of subgroup 2 (92 %, p<0,001). In patients of subgroup 2, the decrease of the percentage of «classic» monocytes was –7.7 % (from 90.4±0.8 to 83.4±1.2 %). Despite the fact that the number and percentage of intermediate monocytes increased in dynamics, their IA decreased almost 2 times, which may indicate a decrease in the pro-inflammatory ability these monocytes. The percentage and number of «patrolling» monocytes increased in dynamics by 37.4 % (p<0.0001) and by 268.3 % (p<0.01), respectively. IA of patrolling monocytes was almost 12 and 7 times higher than in patients of subgroup 1 on the 1st and 7th day of observation, respectively, which may indicate a significant activation of anti-inflammatory activity of patrolling monocytes. Intracardiac thrombosis was 3.3 times more common in patients of subgroup 1, in this subgroup was also more often noted (compared to the subgroup 2): dilatation of the left ventricle (almost 8 times), reduction of left ventricular ejection fraction (4 times), and pathological post-infarction remodeling of the left ventricle (almost 7 times).
Conclusions. The results of the study indicate the important role of different subpopulations of blood monocytes in the processes of myocardial damage and recovery (in particular, the pro-inflammatory role of increasing the number of classical monocytes and increasing the activity of intermediate monocytes, as well as the anti-inflammatory role of increasing the number, percentage and activity of patrolling monocytes) in patients with AMI and can be the basis for developing new approaches to the diagnosis and prevention of complications of this disease.

Article Details

Keywords:

acute myocardial infarction, reperfusion, monocytes, inflammation, complication

References

Матвеева В.Г., Григорьев Е.В. Проблемы и перспективы изучения субпопуляций моноцитов крови в патогенезе заболеваний, связанных с воспалением // Патологиче­­­ская физиология и экспериментальная терапия.– 2016.– Т. 60, № 4.– С. 154–159. doi: https://doi.org/10.25557/0031-2991.2016.04.154-159.

Frangogiannis N.G. Regulation of the inflammatory response in cardiac repair // Circ. Res.– 2012.– Vol. 110.– P. 159–173. doi: https://doi.org/10.1161/CIRCRESAHA.116.303577.

Gawdat K., Legere S., Wong C. et al. Changes in Circulating Monocyte Subsets (CD16 Expression) and Neutrophil-to-Lymphocyte Ratio observed in patients undergoing Cardiac Surgery // Front. Cardiovasc. Med.– 2017.– Vol. 4.–P. 1–12. doi: https://doi.org/10.3389/fcvm.2017.00012.

Ghattas A., Griffiths H.R., Devitt A. et al. Monocytes in coronary artery disease and atherosclerosis // J. Amer. Coll. Cardiol.– 2013.– Vol. 62.– P. 1541–1551. doi: https://doi.org/10.1016/j.jacc.2013.07.043.

Glezeva N., Voon V., Watson C. et al. Exaggerated Inflammation and Monocytosis Associate With Diastolic Dysfunction in Heart Failure With Preserved Ejection Fraction: Evidence of M2 Macrophage Activation in Disease Pathogenesis // J. Card. Fail.– 2015.– Vol. 21 (2).– P. 167–177. doi: https://doi.org/10.1016/j.cardfail.2014.11.004.

Gómez-Olarte S., Bolaños N., Echeverry M. et al. Interme­­­diate monocytes and cytokine production associated with severe forms of chagas disease // Front. Immunol.– 2019.– Vol. 10.– P. 1671. doi: https://doi.org/10.3389/fimmu.2019.01671.

Goyert S.M., Cohen L., Gangloff S.C. et al. CD14 Workshop panel report, 1997, Leucocyte Typing VI, White Cell Differentiation Antigens // Garland Publishing, Inc.– 1997.– P. 963–965.

Heidt T., Courties G., Dutta P. et al. Differential contribution of monocytes to heart macrophages in steady-state and after myocardial infarction // Circ. Res.– 2014.– Vol. 115.– P. 284–295. doi: https://doi.org/10.1161/CIRCRESAHA.115.303567.

Hernandez-Rodrigues J., Seggara M., Vilardell C. et al. Elevated production of interleukin-6 is associated with a low incidence of disease-related ischemic events in patients with giant-cell arteritis // Circulation.– 2003.– Vol. 107 (19).– P. 2428–2434. doi: https://doi.org/10.1161/01.CIR.0000066907.83923.32.

Hilgendorf I., Gerhardt L.M.S., Tan T.C. et al. Ly-6Chi monocytes depend on Nr4a1 to balance both inflammatory and reparative phases in the infarcted myocardium // Circ. Res.– 2014.– Vol. 114.– P. 1611–1622. doi: https://doi.org/10.1161/CIRCRESAHA.114.303204.

Hopfner F., Jacob M., Ulrich C. et al. Subgroups of monocytes predict cardiovascular events in patients with coronary heart disease. The PHAMOS trial (Prospective Halle Monocytes Study) // Hellenic J. Cardiology.– 2019.– Vol. 60 (5).– P. 311–321. doi: https://doi.org/10.1016/j.hjc.2019.04.012.

Ibanez B., James S., Agewall S. et al. ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation: The Task Force for the management of acute myocardial infarction in patients presenting with ST-segment elevation of the European Society of Cardiology (ESC) // Eur. Heart J.– 2018.– Vol. 39 (2).– P. 119–177. doi: https://doi.org/10.1093/eurheartj/ehx393.

Nahrendorf M., Swirski F.K., Aikawa E. et al. The healing myocardium sequentially mobilizes two monocyte subsets with divergent and complementary functions // J. Exp. Med.– 2007.– Vol. 204.– P. 3037–3047. doi: https://doi.org/10.1084/jem.20070885.

Park H.J., Chang K., Park C.S. et al. Coronary collaterals: the role of MCP-1 during the early phase of acute myocardial infarction // Int. J. Cardiol.– 2008.– Vol. 130.– P. 409–413. doi: https://doi.org/10.1016/j.ijcard.2007.08.128.

Prabhu S.D. It takes two to tango: monocyte and macrophage duality in the infarcted heart // Circ. Res.– 2014.– Vol. 114.– P. 1558–1560. doi: https://doi.org/10.1161/CIRCRESAHA.114.303933.

Schmidt R.E., Perussia B. Cluster report: CD16, 1989, Leucocyte Typing IV, White Cell Differentiation Antigens // Oxford University Press.– 1989.– P. 574–578.

Schwarz E.R., Meven D.A., Sulemanjiee N.Z. et al. Monocyte chemoattractant protein 1-induced monocyte infiltration produces angiogenesis but not arteriogenesis in chronically infarcted myocardium // J. Cardiovasc. Pharmacol. Ther.– 2004.– Vol. 9.– P. 279–289. doi: https://doi.org/10.1177/107424840400900408.

Shantsila E., Lip G.Y.H. Monocytes in Acute Coronary Syndromes // Arterioscler. Thromb. Vasc. Biol.– Vol. 29.– P. 1433–1438. doi:https://doi.org/ 10.1161/ATVBAHA.108.180513.

Swirski F.K., Robbins C.S. Neutrophils usher monocytes into sites of inflammation // Circ. Res.– 2013.– Vol. 112.– P. 744–745. doi: https://doi.org/10.1161/CIRCRESAHA.113.300867.

Tallone T., Turconi G., Soldati G. et al. Heterogenity of human monocytes: an optimized four-color flow cytometry protocol for analysis of monocyte subsets // J. Cardiovasc. Trans. Res.– 2011.– Vol. 4 (2).– P. 211–219. doi: https://doi.org/10.1007/s12265-011-9256-4.

Tapp L.D., Shantsila E., Wrigley B.J. et al. The CD14++CD16+ monocyte subset and monocyte-platelet interactions in patients with ST-elevation myocardial infarction // J. Thromb. Haemost.– 2012.– Vol. 10.– P. 1231–1241. doi: https://doi.org/10.1111/j.1538-7836.2011.04603.x.

Tsujioka H., Imanishi T., Ikejima H. et al. Impact of heterogeneity of human peripheral blood monocyte subsets on myocardial salvage in patients with primary acute myocardial infarction // J. Am. Coll. Cardiol.– 2009.– Vol. 54 (2).– P. 130–138. doi: https://doi.org/10.1016/j.jacc.2009.04.021.

Most read articles by the same author(s)

1 2 3 > >>