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Soluble E-Selectin is Not a Marker of Unstable Coronary Plaque in Serum of Patients with Ischemic Heart Disease

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Abstract

Increased level of soluble cell adhesion molecules may be a marker for atherosclerosis and/or reflect complication of the atherosclerotic plaque. To test whether expression of cell adhesion molecules is more pronounced in unstable versus stable coronary plaques, we measured the serum level of soluble E-selectin (sE-selectin) in 99 consecutive patients admitted to the hospital for acute coronary syndromes (ACS) and in 61 patients with chronic coronary artery disease (CAD) using a commercially available ELISA kit. We also measured the sE-selectin concentration in 20 sex- and age-matched subjects without clinical evidence of atherosclerosis, who served as controls. The mean sE-selectin level was higher in both groups of patients compared with controls (ACS, 35.0 ± 23.4 ng/mL; chronic CAD, 32.9 ± 21.0 ng/mL; controls, 14.5 ± 6.6 ng/mL; one-way ANOVA, P = 0.001), but there was no difference between patients with ACS and chronic CAD. Furthermore, there was a trend (P = 0.08) toward a decrease in sE-selectin with an increase in the extent and severity of CAD. In patients with ACS, the in-hospital cardiac event rate was 8%. Although mean sE-selectin concentration tended to be higher in patients with (49.2 ± 42.1 ng/mL) than in those without (33.8 ± 21.3 ng/mL) in-hospital cardiac events, the difference was not significant. In 53 patients with ACS, C-reactive protein was measured and showed no correlation with the sE-selectin concentration. These findings show that although sE-selectin concentration is elevated in the presence of clinically relevant atherosclerosis, it does not further increase during the unstable phase of the disease, indicating that sE-selectin is not a reliable indicator of a complicated atherosclerotic plaque.

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References

  1. Ross R. The pathogenesis of atherosclerosis: A perspective for the 1990s. Nature 1993;362:801–809.

    Google Scholar 

  2. Davies MJ, Gordon JL, Gearing AJH, Pigott R, Woolf N, Katz D, Kyriakopoulos A. The expression of adhesion molecules ICAM-1, VCAM-1, PECAM, and E-selectin in human atherosclerosis. J Pathol 1993;171:223–229.

    Google Scholar 

  3. O'Brien KD, McDonald TO, Chait A, Allen MD, Alpers CE. Neovascular expression of E-selectin, intracellular adhesion molecule-1, and vascular cell adhesion molecule-1 in human atherosclerosis and their relationship to intimal leukocyte content. Circulation 1996;93:672–682.

    Google Scholar 

  4. Gearing AJH, Newman W. Circulating adhesion molecules in disease. Immunol Today 1993;14:506–512.

    Google Scholar 

  5. Cowley HC, Heney D, Gearing AJH, Hemingway I, Wester NR. Increased circulating adhesion molecule concentrations in patients with the systemic inflammatory response syndrome: A prospective cohort study. Crit Care Med 1994;22: 651–657.

    Google Scholar 

  6. Liuzzo G, Biasucci LM, Gallimore R, Grillo RL, Rebuzzi AG, Pepys MB, Maseri A. The prognostic value of C-reactive protein and serum amyloid A protein in severe unstable angina. N Engl J Med 1994;331:417–424.

    Google Scholar 

  7. Gundel RH, Wegner CD, Torcellini CA, et al. Endothelial leukocyte adhesion molecule-1 mediates antigen-induced acute airway inflammation and late phase airway obstruction in monkeys. J Clin Invest 1991;88:1407–1411.

    Google Scholar 

  8. Baj Z, Kowalski J, Kantorski J, Pokoca L, Kosmider M, Pawlicki L, Tchorzewski H. The effect of short-term myocardial ischemia on the expression of adhesionmolecules and the oxidative burst of coronary sinus blood neutrophils. Atherosclerosis 1994;106:159–168.

    Google Scholar 

  9. Blann A, McCollum C. Circulating endothelial cell/leukocyte adhesion molecules in atherosclerosis. Thromb Haemost 1994;72:151–154.

    Google Scholar 

  10. Hackman A, Abe Y, Insull W Jr., et al. Levels of soluble cell adhesion molecules in patients with dyslipidemia. Circulation 1996;93:1334–1338.

    Google Scholar 

  11. Sugama Y, Tiruppathi C, Offakidevi K, Andersen T, Fenton J, Malik A. Thrombin-induced expression of endothelial Pselectin and intercellular adhesion molecule-1: A mechanism for stabilizing neutrophil adhesion. J Cell Biol 1992;119: 935–944.

    Google Scholar 

  12. Youker K, Smith CW, Anderson DC, et al. Neutrophil adherence to isolated adult cardiacmyocytes. Induction by cardiac lymph collected during ischemia and reperfusion. J Clin Invest 1992;89:602–609.

    Google Scholar 

  13. Norris P, R.N., P., Thomas DS, Thornill M, Hawk J, Haskard DO. The expression of endothelial leukocyte adhesion molecule-1(ELAM-1), intracellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) in experimental cutaneous inflammation: A comparison of ultraviolet B erythema and delayed hypersensitivity. J Invest Dermatol 1991;96:763–760.

    Google Scholar 

  14. Pigott R, Dillon LP, Hemingway IH, Gearing AJH. 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;187:584–589.

    Google Scholar 

  15. Smith CW. Potential significance of circulating E-selectin. Circulation 1997;95:1986–1988.

    Google Scholar 

  16. Willerson JT, Campbell WB, Winniford MD, et al. Conversion from chronic to acute coronary artery disease: Speculation regarding mechanisms. Am J Cardiol 1984;54: 1349–1353.

    Google Scholar 

  17. Fuster V, Badimon L, Cohen M, Ambrose JA, Badimon JJ. Insights into the pathogenesis of acute ischemic syndromes. Circulation 1988;77:1213–1220.

    Google Scholar 

  18. Buja LM, Willerson JT. Role of inflammation in coronary plaque rupture. Circulation 1994;89:503–505.

    Google Scholar 

  19. van derWal AC, Becker AE, van der Loos CM, Das PK. Site of intimal rupture or erosion of thrombosed coronary atherosclerotic plaques is characterized by an inflammatory process irrespective of the dominant plaque morphology. Circulation 1994;89:36–44.

    Google Scholar 

  20. Tenaglia A, Buda A, Wilkins R, et al. Levels of expression of P-selectin, E-selectin, and intercellular adhesion molecule-1 in coronary atherectomy specimens from patients with stable and unstable angina pectoris. Am J Cardiol 1997;79: 742–747.

    Google Scholar 

  21. Richardson M, Hadcook SJ, DeReske M, Cybulsky MI. Increased expression in vivo of VCAM-1 and E-selectin by the aortic endothelium of normolipemic and hyperlipemic diabetic rabbits. Arterioscler Thromb 1994;14:760–769.

    Google Scholar 

  22. Shyu KC, Chang H, Lin CC, Kuan P. Circulating intercellular adhesionmolecule-1 and E-selectin in patients with acute coronary syndrome. Chest 1996;109:1627–1630.

    Google Scholar 

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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 9, 53–60 (2000). https://doi.org/10.1023/A:1018656530541

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