Biochemical Parameters of Iron Metabolism and TG/HDL-C Ratio in Patients with Coronary Artery Disease

Document Type : Original Article (s)

Authors

1 Department of Clinical Biochemistry, Isfahan Pharmaceutical Sciences Research Center, School of Pharmacy, Isfahan University of Medical Sciences, Isfahan, Iran

2 Professor, Department of Clinical Biochemistry, Isfahan Pharmaceutical Sciences Research Center, School of Pharmacy, Isfahan University of Medical Sciences, Isfahan, Iran

3 Associate Professor, Department of Nutrition, School of Health, Isfahan University of Medical Sciences, Isfahan, Iran

4 Associate Professor, Department of Cardiovascular Medicine, School of Medicine, Isfahan University of Medical Sciences Isfahan, Iran

5 Associate Professor, Department of Epidemiology and Biostatistics, School of Health, Isfahan University of Medical Sciences, Isfahan, Iran

Abstract

Background: The morbidity and mortality associated with coronary artery diseases (CVD) make it a main public health problem and every year billions of Dollars are spent on treating such disease. There are many epidemiological evidences indicate that iron is an essential factor in the development of atherosclerosis. However, the mechanisms stimulating atherogenesis by iron is still unclear; but it is believed that the likely catalytic role of iron in lipid peroxidation could be an important factor in formation of atherosclerosis lesion.Methods: Serum level of ferritin, transferring and TG/HDL-C ratio were measured in a total of 140 male patients (age ≥ 45 years) who referred to have a diagnostic coronary angiography. Subjects were divided into two groups according to their angiographic results (case group with ≥ 75% and control group < 75% stenosis in one of the coronary arteries).Findings: Mean iron stores concentration were higher in cases (ferritin: 129.8 ± 99 vs 107.7 ± 75 ng/ml and transferrin: 288.8 ± 53.9 vs 285 ± 58.9 µg/dl); however these differences were not statistically significant, but after adjusting basic characteristics, the difference for ferritin was significant (P < 0.05). By grouping ferritin levels in 3 quintile (Q1 ≤ 126, 126 < Q2 ≤ 233, and Q3 > 233) and control of confounding factors, the relationship of ferritin and the number of involved vessels was not significant. Although, the ratio of TG/HDL-C in the case group was higher than controls, but the difference was not statistically significant (P < 0.05).  Conclusion: Our findings showed that ferritin, hemoglobin, and TG/HDL-C ratio can be important diagnostic indicators of coronary atherosclerosis progression. But applying the level of ferritin, as a prognostic indicator, in determining the number of involved vessels may be unreliable. 

Keywords

References

  1. Thom T, Haase N, Rosamond W, Howard VJ, Rumsfeld J, Manolio T, et al. Heart disease and stroke statistics--2006 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation 2006; 113(6): e85-151.
  2. Morita T. Heme oxygenase and atherosclerosis. Arterioscler Thromb Vasc Biol 2005; 25(9): 1786-95.
  3. Witztum JL, Steinberg D. Role of oxidized low density lipoprotein in atherogenesis. J Clin Invest 1991; 88(6): 1785-92.
  4. Berliner JA, Heinecke JW. The role of oxidized lipoproteins in atherogenesis. Free Radic Biol Med 1996; 20(5): 707-27.
  5. de VB, Marx JJ. Iron, atherosclerosis, and ischemic heart disease. Arch Intern Med 1999; 159(14): 1542-8.
  6. Balagopalakrishna C, Paka L, Pillarisetti S, Goldberg IJ. Lipolysis-induced iron release from diferric transferrin: Possible role of lipoprotein lipase in LDL-Coxidation. J Lipid Res 1999; 40(7): 1347-56.
  7. Smith C, Mitchinson MJ, Aruoma OI, Halliwell B. Stimulation of lipid peroxidation and hydroxyl-radical generation by the contents of human atherosclerotic lesions. Biochem J 1992; 286(Pt 3): 901-5.
  8. Eichner JE, Qi H, Moore WE, Schechter E. Iron measures in coronary angiography patients. Atherosclerosis 1998; 136(2): 241-5.
  9. Heinecke JW, Rosen H, Chait A. Iron and copper promote modification of low density lipoprotein by human arterial smooth muscle cells in culture. J Clin Invest 1984; 74(5): 1890-4.
  10. Halliwell B, Chirico S. Lipid peroxidation: its mechanism, measurement, and significance. Am J Clin Nutr 1993; 57(5): 715-24.
  11. Zheng H, Cable R, Spencer B, Votto N, Katz SD. Iron Stores and Vascular Function in Voluntary Blood Donors. Arteriosclerosis, Thrombosis, and Vascular Biology 2005; 25: 1577-83.
  12. Tietz NB. Clinical guide to laboratory tests. W B Saunders Co 1995.
  13. Haidari M, Javadi E, Sanati A, Hajilooi M, Ghanbili J. Association of increased ferritin with premature coronary stenosis in men. Clin Chem 2001; 47(9): 1666-72.
  14. Nozari Y, Nabati M. Assessment of iron stores in candidates for coronary angiography. Tehran University Medical Journal 2007; 65(7): 47-51.
  15. Ford ES, Cogswell ME. Diabetes and serum ferritin concentration among U.S. adults. Diabetes Care December 1999; 22(12): 1978-83.
  16. Shi Z, Hu X, Yuan B, Pan X, Meyer HE, Holmboe-Ottesen G. Association between serum ferritin, hemoglobin, iron intake, and diabetes in adults in Jiangsu, China. Diabetes Care 2006; 29(8): 1878-83.
  17. Acton RT, Barton JC, Passmore LV, Adams PC, Speechley MR, Dawkins FW, et al. Relationships of serum ferritin, transferrin saturation, and HFE mutations and self-reported diabetes in the Hemochromatosis and Iron Overload Screening (HEIRS) study. Diabetes Care 2006; 29(9): 2084-9.
  18. Auer J, Rammer M, Berent R, Weber T, Lassnig E, Eber B. Body iron stores and coronary atherosclerosis assessed by coronary angiography. Nutr Metab Cardiovasc Dis 2002; 12(5): 285-90.
  19. Balla G, Vercellotti GM, Eaton JW, Jacob HS. Iron loading of endothelial cells augments oxidant damage. J Lab Clin Med 1990; 116(4): 546-54.
  20. Balla G, Vercellotti GM, Muller-Eberhard U, Eaton J, Jacob HS. Exposure of endothelial cells to free heme potentiates damage mediated by granulocytes and toxic oxygen species. Lab Invest 1991; 64(5): 648-55.
  21. Bunn HF, Jandl JH. Exchange of heme among hemoglobins and between hemoglobin and albumin. J Biol Chem 1968; 243(3): 465-75.
  22. Vercellotti GM, Asbeck BSV, Jacob HS. Oxygen radical-induced erythrocyte hemolysis by neutrophils. Critical role of iron and lactoferrin. J Clin Invest 1985; 76(3): 956-62.
  23. Dallegri F, Ballestrero A, Frumento G, Patrone F. Augmentation of neutrophil-mediated erythrocyte lysis by cells derived in vitro from human monocytes. Blood 1987; 70(6): 1743-9.
  24. Sadrzadeh SM, Graf E, Panter SS, Hallaway PE, Eaton JW. A biologic fenton reagent. The Journal of Biological Chemistry 1984; 259: 14354-6.
  25. Javid J. Human haptoglobins. Current topics in hematology 1978; 1: 151-92.
  26. Libby P. Current concepts of the pathogenesis of the acute coronary syndromes. Circulation 2001; 104(3): 365-72.
  27. Robinson D, Ferns GA, Bevan EA, Stocks J, Williams PT, Galton DJ. High density lipoprotein subfractions and coronary risk factors in normal men. Arterioscler Thromb Vasc Biol 1987; 7: 341-6.
  28. Gaziano JM, Hennekens CH, O'Donnell CJ, Breslow JL, Buring JE. Fasting triglycerides, high-density lipoprotein, and risk of myocardial infarction. Circulation 1997; 96(8): 2520-5.
  29. Jeppesen J, Hein HO, Suadicani P, Gyntelberg F. Triglyceride concentration and ischemic heart disease: an eight-year follow-up in the Copenhagen Male Study. Circulation 1998; 97(11): 1029-36.
  30. Packard CJ, Shepherd J. Lipoprotein heterogeneity and apolipoprotein B metabolism. Arterioscler Thromb Vasc Biol 1997; 17(12): 3542-56.
  31. Brinton EA, Eisenberg S, Breslow JL. Increased apo A-I and apo A-II fractional catabolic rate in patients with low high density lipoprotein-cholesterol levels with or without hypertri-glyceridemia. J Clin Invest 1991; 87(2): 536-44.
  32. da Luz PL, Cesena FH, Favarato D, Cerqueira ES. Comparison of serum lipid values in patients with coronary artery disease at <50, 50 to 59, 60 to 69, and >70 years of age. Am J Cardiol 2005; 96(12): 1640-3.
  33. Kiechl S, Willeit J, Egger G, Poewe W, Oberhollenzer F. Body Iron Stores and the Risk of Carotid Atherosclerosis. Circulation 1997; 96: 3300-7.
Journal of Isfahan Medical School
Volume 29, Issue 159 - Serial Number 159
September and October 2011
Pages 1680-1689

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History

  • Receive Date: 12 June 2011
  • Revise Date: 01 November 2024
  • Accept Date: 06 April 2022

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