Vol 8, No 4 (2023)
Original article
Published online: 2023-11-27

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Serum pentraxin and E-selectin levels are associated with outcomes in patients with acute myocardial infarction who undergo percutaneous coronary intervention

Wiktoria Smyła1, Sebastian Krych1, Michał Jurkiewicz1, Zenon Czuba2, Michał Skrzypek3, Patrycja Piłat1, Mariusz Gąsior4, Bożena Szyguła-Jurkiewicz4
Medical Research Journal 2023;8(4):306-311.

Abstract

Introduction: Despite reperfusion by primary percutaneous coronary intervention (PCI) in acute myocardial infarction (AMI) some patients develop left ventricular dysfunction. The extent of cardiac injury is associated with the inflammation and the reperfusion damage. An overly long inflammatory phase can cause sustained myocardial damage and improper healing, leading to remodelling and ventricular dilatation. We sought to elucidate whether proinflammatory proteins, cytokines and adhesion molecules that participate in the processes of inflammation, ischaemia-reperfusion injury and postmyocardial left ventricular remodelling are associated with the major adverse cardiovascular events (MACE) (all-cause mortality or AMI) during the two-year follow-up.

Material and methods: It is a prospective analysis of patients with AMI admitted to the cardiology ward who underwent PCI between December 2018 and April 2019. The Luminex Multiplex Assay was used to measure serum biomarker concentrations (Bio-Plex System 200, Bio-Rad, USA), and the data were analysed using Bio-Plex Manager Software.

Results: The median age was 66 (58–74), and 31.8% were women. The end-point was reached in 53 (37.9%) patients. Multivariate analysis found that serum pentraxin-3 [odds ratio (OR) 1.295 (1.175–1.443), p < 0.001] and E-selectin [OR 1.539 (1.151–2.265), p = 0.03] concentrations were associated with MACE.

Conclusions: Higher pentraxin and E-selectin serum concentrations are independently associated with all-cause mortality or myocardial infarction in the analysed population during the two-year follow-up.

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References

  1. Thygesen K, Alpert JS, Jaffe AS, et al. Fourth universal definition of myocardial infarction (2018). Circulation. 2018; 138(20): e618–e651.
  2. Ibanez B, James S, Agewall S, et al. 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. Rev Esp Cardiol (Engl Ed). 2017; 70(12): 1082.
  3. Mullane K. Neutrophil and endothelial changes in reperfusion injury. Trends Cardiovasc Med. 1991; 1(7): 282–289.
  4. Ristagno G, Fumagalli F, Bottazzi B, et al. Pentraxin 3 in cardiovascular disease. Front Immunol. 2019; 10: 823.
  5. Pereira-da-Silva T, Ferreira V, Castelo A, et al. Soluble CD40 ligand expression in stable atherosclerosis: a systematic review and meta-analysis. Atherosclerosis. 2021; 319: 86–100.
  6. Saraiva M, Vieira P, O'Garra A. Biology and therapeutic potential of interleukin-10. J Exp Med. 2020; 217(1).
  7. Rose-John S. Interleukin-6 family cytokines. Cold Spring Harb Perspect Biol. 2018; 10(2): a028415.
  8. Lindsey S, Langhans SA. Epidermal growth factor signaling in transformed cells. Int Rev Cell Mol Biol. 2015; 314: 1–41.
  9. Ornitz DM, Itoh N. The fibroblast growth factor signaling pathway. Wiley Interdiscip Rev Dev Biol. 2015; 4(3): 215–266.
  10. McEver RP. Role of selectins in leukocyte adhesion to platelets and endothelium. Ann N Y Acad Sci. 1994; 714: 185–189.
  11. Chen H, Wang J, Xiang MX, et al. Cathepsin S-mediated fibroblast trans-differentiation contributes to left ventricular remodelling after myocardial infarction. Cardiovasc Res. 2013; 100(1): 84–94.
  12. Niccoli G, Lanza GA, Shaw S, et al. Endothelin-1 and acute myocardial infarction: a no-reflow mediator after successful percutaneous myocardial revascularization. Eur Heart J. 2006; 27(15): 1793–1798.
  13. Bruno S, Bussolati B, Scacciatella P, et al. Combined administration of G-CSF and GM-CSF stimulates monocyte-derived pro-angiogenic cells in patients with acute myocardial infarction. Cytokine. 2006; 34(1-2): 56–65.
  14. Idzik M, Poloczek J, Skrzep-Poloczek B, et al. The effects of 21-day general rehabilitation after hip or knee surgical implantation on plasma levels of selected interleukins, VEGF, tnf-α, PDGF-BB, and eotaxin-1. Biomolecules. 2022; 12(5): 605.
  15. Fan Yu, He R, Man C, et al. Utility of elevated pentraxin-3 level as inflammatory marker for predicting adverse outcomes in patients with acute coronary syndrome: a meta-analysis. Front Cardiovasc Med. 2021; 8: 736868.
  16. Karakas MF, Buyukkaya E, Kurt M, et al. Serum pentraxin 3 levels are associated with the complexity and severity of coronary artery disease in patients with stable angina pectoris. J Investig Med. 2013; 61(2): 278–285.
  17. Latini R, Maggioni AP, Peri G, et al. Lipid Assessment Trial Italian Network (LATIN) Investigators. Prognostic significance of the long pentraxin PTX3 in acute myocardial infarction. Circulation. 2004; 110(16): 2349–2354.
  18. Kotooka N, Inoue T, Fujimatsu D, et al. Pentraxin3 is a novel marker for stent-induced inflammation and neointimal thickening. Atherosclerosis. 2008; 197(1): 368–374.
  19. Davies MJ, Gordon JL, Gearing AJ, et al. The expression of the adhesion molecules ICAM-1, VCAM-1, PECAM, and E-selectin in human atherosclerosis. J Pathol. 1993; 171(3): 223–229.
  20. O'Brien KD, McDonald TO, Chait A, et al. Neovascular expression of E-selectin, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1 in human atherosclerosis and their relation to intimal leukocyte content. Circulation. 1996; 93(4): 672–682.
  21. Pigott R, Dillon LP, Hemingway IH, et al. Soluble forms of E-selectin, ICAM-1 and VCAM-1 are present in the supernatants of cytokine activated cultured endothelial cells. Biochem Biophys Res Commun. 1992; 187(2): 584–589.
  22. Smith CW. Potential significance of circulating E-selectin. Circulation. 1997; 95(8): 1986–1988.
  23. Galvani M, Ferrini D, Ottani F, et al. Soluble E-selectin is not a marker of unstable coronary plaque in serum of patients with ischemic heart disease. J Thromb Thrombolysis. 2000; 9(1): 53–60.
  24. Wenzel K, Felix S, Kleber FX, et al. E-selectin polymorphism and atherosclerosis: an association study. Hum Mol Genet. 1994; 3(11): 1935–1937.
  25. Hwang SJ, Ballantyne CM, Sharrett AR, et al. Circulating adhesion molecules VCAM-1, ICAM-1, and e-selectin in carotid atherosclerosis and incident coronary heart disease cases: the atherosclerosis risk in communities (ARIC) study. Circulation. 1997; 96(12): 4219–4225.
  26. Weil BR, Neelamegham S. Selectins and immune cells in acute myocardial infarction and post-infarction ventricular remodeling: pathophysiology and novel treatments. Front Immunol. 2019; 10: 300.