Evaluation of The Association of Lipid Profile With IL-6 Levels in an Acute Myocardial Infarction Scenario
Downloads
Acute myocardial infarction (AMI) is a global health burden that targets the heart muscle and causes metabolic disorders as well as leads to increased inflammatory responses, and interleukin-6 (IL-6) is an axonal and anti-inflammatory cytokine that affects the stability of plaques, atherosclerosis, as well as endothelial damage, and cardiovascular outcomes. Therefore, the relationship between IL-6 and lipid disorders in AMI remains unclear, as it is in the Middle East community. This study aimed to clarify the levels of IL-6 in arterial tissue in patients with acute myocardial infarction and to examine their relationship with lipid parameters, fasting serum glucose, and signs of cardiac vitality. Several 30 cases including acute myocardial infarction were studied, which were admitted to the coronary care unit at Azadi Teaching Hospital since November 2024 and April 2025 with a matching health group according to sex, age, and measurement of lipid markers in arterial serum IL-6 Evidence of lipids (total cholesterol, triglycerides, HDL-C, LDL-C, and VLDL-C), fasting serum glucose, cardiac troponin I, and CK-MB B, By a program for biochemical and immunological statistical analysis. SPSS v25, using independent t-tests and Pearson correlation analysis, < 0.01 is statistically significant. The results showed that AMI patients showed an increase in serum IL-6, total cholesterol, triglycerides, LDL-C, VLDL-C, FASTING SERUM GLUCOSE, CK-MB, and cardiac troponin I in addition to a decrease in HDL-C compared to the two controls (p < 0.01). Serum IL-6 is strongly associated with fractions of atherogenic fats, fasting serum glucose, evidence of heart injury, and a negative association with HDL-C. High IL-6 levels are associated with fat decay, increased blood sugar, and their effect on the heart muscle and acute retention, characterizing the direct interaction between inflammation and metabolic disorders. IL-6 is a valuable biomarker for cardiovascular analysis and disease severity in AMI patients.
[1] K. Thygesen, J. S. Alpert, A. S. Jaffe, B. R. Chaitman, J. J. Bax, and D. A. Morrow et al., “Fourth universal definition of myocardial infarction (2018),” Circulation, vol. 138, no. 20, pp. e618–e651, 2018.
[2] N. G. Frangogiannis, “Pathophysiology of myocardial infarction,” Compr. Physiol., vol. 5, no. 4, pp. 1841–1875, 2015, doi:10.1002/cphy.c150006.
[3] S. Mythili and N. Malathi, “Diagnostic markers of acute myocardial infarction,” J. Oral Maxillofac. Pathol., vol. 19, no. 3, pp. 345–351, 2015.
[4] K. Thygesen, J. S. Alpert, A. S. Jaffe, et al., “Fourth universal definition of myocardial infarction (2018),” Eur. Heart J., vol. 39, no. 2, pp. 119–177, 2018.
[5] F. S. Apple, “Cardiac troponin and acute myocardial infarction,” Clin. Chem., vol. 51, no. 6, pp. 1095–1101, 2005.
[6] G. W. Reed, J. E. Rossi, and C. P. Cannon, “Acute myocardial infarction,” Lancet, vol. 389, no. 10065, pp. 197–210, 2017.
[7] American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, “2014 AHA/ACC guideline for the management of patients with non–ST-elevation acute coronary syndromes,” Circulation, vol. 130, no. 25, pp. e344–e426, 2014.
[8] A. Shirvani, S. S. Maroufi, M. Salehi, et al., “The global prevalence of myocardial infarction: a systematic review and meta-analysis,” Curr. Probl. Cardiol., vol. 48, no. 6, p. 102106, 2023, doi:10.1016/j.cpcardiol.2022.102106.
[9] “Assessment of myocardial infarction knowledge, attitudes, and practices,” Sci. Rep., vol. 14, p. 10953, 2024, doi:10.1038/s41598-024-83169-x.
[10] Z. Al-Johar, “Prevalence and demographic characteristics of metabolic syndrome in Iraqi patients with acute coronary syndrome,” J. Fac. Med. Baghdad, vol. 65, no. 1, pp. 10–19, 2023.
[11] A. Allami, S. Ali, A. Omar, et al., “A cross-sectional study on the epidemiology and risk factors of acute coronary syndrome in Northern Iraq,” Int. J. Cardiol. Cardiovasc. Risk Prev., vol. 10, pp. 107–113, 2024.
[12] A. Allami, S. Ali, A. Omar, et al., “A cross-sectional study on the epidemiology and risk factors of acute coronary syndrome in Northern Iraq,” Cureus, vol. 16, no. 6, p. e42076, 2024.
[13] Z. S. Abulrahman Aldaggistany, et al., “Prevalence and demographic characteristics of the metabolic syndrome in Iraqi patients with acute coronary syndrome,” J. Fac. Med. Baghdad, vol. 65, no. 1, pp. 10–19, 2023.
[14] P. M. Ridker, “Inflammatory and thrombotic mechanisms in coronary atherosclerosis,” Cardiovasc. Res., vol. 56, no. 2, pp. 340–350, 2003.
[15] P. Libby, “Targeting inflammation in atherosclerosis: overview, strategy and directions,” EuroIntervention, vol. 21, pp. 89–101, 2025.
[16] J. M. Tarkin, F. R. Joshi, and J. H. F. Rudd, “Systemic atherosclerotic inflammation following acute myocardial infarction: mechanistic insights and clinical implications,” J. Am. Heart Assoc., vol. 4, no. 9, p. e001956, 2015.
[17] A. Gisterå and G. K. Hansson, “The immunology of atherosclerosis,” Nat. Rev. Nephrol., vol. 13, no. 6, pp. 368–380, 2017.
[18] Z. Wang and S. Yan, “Inflammation in atherosclerosis: pathophysiology and mechanisms,” Cell Death Dis., vol. 15, no. 11, p. 951, 2024.
[19] F. M. Van der Valk, et al., “Inflammation and cardiovascular disease: from mechanisms to therapeutics,” Eur. Heart J., vol. 41, no. 9, pp. 674–681, 2020.
[20] B. Ibanez, G. Heusch, M. Ovize, and F. Van de Werf, “Antiinflammatory therapy in acute myocardial infarction,” J. Am. Coll. Cardiol., vol. 72, no. 19, pp. 2231–2247, 2018.
[21] T. Anzai, “Inflammation in acute myocardial infarction: the good, the bad, and the ugly,” Circ. J., vol. 88, no. 2, pp. 89–95, 2024.
[22] L. C. Heather and K. Clarke, “Cardiac lipid metabolism, mitochondrial function, and heart failure,” Eur. Heart J., vol. 44, no. 26, pp. 2355–2369, 2023.
[23] D. K. Arnett, et al., “Impact of lipids on cardiovascular health,” J. Am. Coll. Cardiol., vol. 72, no. 24, pp. 3148–3161, 2018.
[24] Y. Wang, et al., “Lipid metabolism-associated metabolites and cardiovascular diseases,” Front. Cardiovasc. Med., vol. 12, p. 1445732, 2025.
[25] C. J. Packard and J. Borén, “Lipoproteins and lipids in cardiovascular disease,” Curr. Opin. Lipidol., vol. 31, no. 4, pp. 251–257, 2020.
[26] M. S. Sabatine, D. A. Morrow, J. A. de Lemos, et al., “Elevations of cardiac troponin I predict long-term mortality after acute coronary syndrome,” Circulation, vol. 106, no. 23, pp. 2906–2911, 2002.
[27] F. S. Apple, “Cardiac troponin assays for rapid diagnosis of myocardial infarction,” Clin. Chem., vol. 46, no. 9, pp. 1332–1335, 2000.
[28] M. Kosuge and K. Kimura, “Creatine kinase-MB isoenzyme in acute myocardial infarction,” Heart Vessels, vol. 19, no. 3, pp. 103–110, 2004.

