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Biomarkers of inflammation and matrix remodeling in patients with acute coronary syndrome and vulnerable plaque

https://doi.org/10.15829/1728-8800-2024-3997

EDN: HZFOYK

Abstract

Aim. To evaluate the relationship between markers of inflammation and matrix remodeling and criteria for a vulnerable plaque according to multislice computed tomography (MSCT) coronary angiography, as well as lipid profile parameters in patients with acute coronary syndrome (ACS).

Material and methods. This prospective single-center study included 125 patients admitted urgently with ACS. All patients underwent percutaneous coronary intervention of the infarct-related artery. In ad­dition, in all patients, there were plaques in one or two non-infarct-related arteries with stenosis <50%. ACS was treated according to clinical guidelines, including statin therapy at the maximum dosage. After 1 month, all patients underwent MSCT coronary angiography to detect vulnerable plaques, as well as assessment of the lipid profile, and following biomarkers of inflammation and matrix remodeling: metalloproteinase-9 with its inhibitor type 1 (MMP-9 and TIMP-1), galectin-3 (Gal-3), neutrophil gelatinase-associated lipocalin (NGAL).

Results. Of the 125 patients, myocardial infarction (MI) was diagnosed in 94 people (75%). Criteria for the plaque vulnerability according to MSCT were identified in 55 (44%) patients, of which positive remodeling was detected in 35 patients, a low-density area (LDA) in 30, and punctate calcifications (PCs) in 11. Gal-3 concentration was significantly higher without LDA — 35,4 (8,6; 65,0) ng/ml, in comparison with the group of patients in whom this criterion was detected and was 16,1 (5,9; 27,4) ng/ml (p=0,006). In the absence of PCs, the Gal-3 concentration was >34,0 (8,6; 61,0) vs 5,9 (2,8; 25,4) ng/ml in the group with PCs (p=0,046). The regression model including the MMP-9, TIMP-1, NGAL, Gal-3 in identifying vulnerable plaques was found to be significant (p<0,001).

Conclusion. Criteria for vulnerable plaque in patients after ACS have a significant relationship with markers of inflammation and matrix remo­deling.

About the Authors

A. N. Kovalskaya
Samara State Medical University
Russian Federation

Samara



D. V. Duplyakov
Samara State Medical University; Polyakov Samara Regional Clinical Cardiology Dispensary
Russian Federation

Samara



A. P. Kuritsyna
Samara State Medical University
Russian Federation

Samara



L. V. Limareva
Samara State Medical University
Russian Federation

Samara



References

1. Antropova ON, Sukmanova IA, Voloshina UYe. Biomarkers of ca­rotid vulnerable atherosclerotic plaque. Mediсal almanaс. 2023;3(76):119-24. (In Russ.)

2. Lynch M, Barallobre-Barreiro J, Jahangiri M, et al. Vascular pro­teomics in metabolic and cardiovascular diseases. J Intern Med. 2016;280(4):325-38. doi:10.1111/joim.12486.

3. Scherbak SG, Kamilova TA, Lebedeva SV. Biomarkers of Caro­tid Stenosis. Physical and rehabilitation medicine, medical re­ha­bilitation. 2021;3(1):104-30. (In Russ.) doi:10.36425/rehab64286.

4. Shioi A, Ikari Y. Plaque calcification during atherosclerosis pro­gression and regression. J Atheroscler Thromb. 2018;25(4):294-303. doi:10.5551/jat.rv17020.

5. Kumric M, Borovac JA, Martinovic D, et al. Circulating Biomarkers Reflecting Destabilization Mechanisms of Coronary Artery Plaques: Are We Looking for the Impossible? Biomolecules. 2021;11(6):881. doi:10.3390/biom11060881.

6. Kochergin NA, Kochergina AM. Potential of optical coherence to­mography and intravascular ultrasound in the detection of vulnerable plaques in coronary arteries. Cardiovascular Therapy and Prevention. 2022;21(1):2909. (In Russ.) doi:10.15829/1728-8800-2022-2909.

7. Theofilis P, Sagris M, Antonopoulos AS, et al. Non-Invasive Modalities in the Assessment of Vulnerable Coronary Atherosclero­tic Plaques. Tomography. 2022;8(4):1742-58. doi:10.3390/tomography8040147.

8. Averkov OV, Duplyakov DV, Gilyarov MYu. Acute myocardial infarction with ST segment elevation electrocardiogram. Clinical guidelines 2020. Russian Society of Cardiology, Association of Cardiovascular Surgeons of Russia. Russian Journal of Cardio­logy. 2020;25(11):4103. (In Russ.) doi:10.15829/1560-4071-2020-4103.

9. Barbarash OL, Duplyakov DV, Zateishchikov DA, et al. Acute coronary syndrome without ST segment elevation electrocardiogram. Clinical guidelines 2020. Russian Journal of Cardiology. 2021;26(4):4449. (In Russ.) doi:10.15829/1560-4071-2021-4449.

10. Kovalskaya AN, Duplyakov DV. Biomarkers in assessing the vul­nerability of atherosclerotic plaques: a narrative review. Rational pharmacotherapy in cardiology. 2023;19(3):282-8. (In Russ.) doi:10.20996/1819-6446-2023-2878.

11. Li T, Li X, Feng Y, et al. The Role of Matrix Metalloproteinase-9 in Atherosclerotic Plaque Instability. Mediators Inflamm. 2020; 2020:3872367. doi:10.1155/2020/3872367.

12. Cheng Z, Cai K, Xu C, et al. Prognostic Value of Serum Galectin-3 in Chronic Heart Failure: A Meta-Analysis. Front Cardiovasc Med. 2022;9:783707. doi:10.3389/fcvm.2022.783707.

13. Agnello L, Bivona G, Lo Sasso B, et al. Galectin-3 in acute coronary syndrome. Clin Biochem. 2017;50(13-14):797-803. doi:10.1016/j.clinbiochem.2017.04.018.

14. Ozturk D, Celik O, Satilmis S, et al. Association between serum galectin-3 levels and coronary atherosclerosis and plaque burden/structure in patients with type 2 diabetes mellitus. Coron Artery Dis. 2015;26(5):396-401. doi:10.1097/MCA.0000000000000252.

15. Sygitowicz G, Maciejak-Jastrzębska A, Sitkiewicz D. The Dia­gnostic and Therapeutic Potential of Galectin-3 in cardiovascular diseases. Biomolecules. 2021;12(1):46. doi:10.3390/biom12010046.

16. Kume N, Kita T. New scavenger receptors and their functions in atherogenesis. Curr Atheroscler Rep. 2002;4(4):253-7. doi:10.1007/s11883-002-0001-y.

17. Eilenberg W, Stojkovic S, Piechota-Polanczyk A, et al. Neutrophil Ge­latinase-Associated Lipocalin (NGAL) is Associated with Symptomatic Carotid Atherosclerosis and Drives Pro-inflammatory State In Vitro. Eur J Vasc Endovasc Surg. 2016;51(5):623-31. doi:10.1016/j.ejvs.2016.01.009.


Supplementary files

What is already known about the subject?

  • Vulnerable plaques are the main cause of acute coronary artery disease.
  • Criteria for vulnerable plaque (positive remodeling, low-density area, punctuate calcifications) can be identified using multislice computed tomography.
  • One mechanism for preventing adverse cardiovas­cular events may be plaque stabilization and/or regression of its volume.

What might this study add?

  • The combined use of various serum and tissue bio­markers (MMP-9, Gal-3, TIMP-1, NGAL) and vulnerability criteria according to multislice com­puted tomography may be key to identifying vul­nerable plaque, which should facilitate accurate stratification of patients at risk of acute vascular events.

Review

For citations:


Kovalskaya A.N., Duplyakov D.V., Kuritsyna A.P., Limareva L.V. Biomarkers of inflammation and matrix remodeling in patients with acute coronary syndrome and vulnerable plaque. Cardiovascular Therapy and Prevention. 2024;23(6):3997. (In Russ.) https://doi.org/10.15829/1728-8800-2024-3997. EDN: HZFOYK

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ISSN 1728-8800 (Print)
ISSN 2619-0125 (Online)