Does the Level of Soluble Intercellular Adhesion Molecule 1 Predict Myocardial Injury before Cardiac Markers Increase?
DOI:
https://doi.org/10.1532/HSF98.20081092Abstract
Background: The measurement of cardiac markers is still the gold standard for diagnosing myocardial infarction (MI), but there is always a transition period between the time of infarction and when a marker can be measured in the blood. Therefore, clinicians are shifting their focus to the identification of potential new analytes capable of predicting MIs before the standard cardiac markers increase. In this study, we tested whether measurement of the concentration of soluble intercellular adhesion molecule 1 (sICAM-1) in plasma can be used for this purpose.
Materials and Methods: In this prospective study, we included 60 male patients who had a left main coronary artery lesion or a left main equivalent and who underwent elective (group I, n = 20), urgent (group II, n = 20), or emergent (group III, n = 20) coronary artery bypass grafting (CABG). We excluded patients who had increased cardiac markers at admission, and drew blood samples for sICAM-1 measurements from other patients immediately after coronary angiography evaluations. We divided the patients into 3 groups according to their clinical characteristics and cardiac marker levels. Only patients with increased cardiac markers underwent emergent CABG (group III). We measured sICAM-1 concentrations immediately after coronary angiography and measured creatine kinase MB (CK-MB) and cardiac troponin I (cTnI) just before CABG. We then evaluated the results for correlations.
Results: CK-MB, cTnI, and sICAM-1 levels were significantly higher in group III than in groups I and II (P < .05 for all). Our analysis for correlations between the sICAM-1 level and cardiac marker levels revealed no significant correlations in group I (CK-MB, r = 0.241 [P = .15]; cTnI, r = -0.107 [P = .32]) and group II (CK-MB, r = -0.202 [P = .19]; cTnI, r = 0.606 [P = .002]), but our analysis did reveal highly significant correlations in group III (CK-MB, r = 0.584 [P = .003]; cTnI, r = 0.605 [P = .002]).
Conclusion: Measuring the plasma concentration of sICAM-1 before the concentrations of cardiac markers increase in patients with MI may provide clinicians with faster and reliable data for deciding on and administering the most appropriate procedures and/or therapies.
References
Anderson M, Castelli WP, Levy D. 1987. Cholesterol and mortality: 30 years of follow-up from the Framingham Study. JAMA 257:2176-80.nAntonino M, Stefano De S, Giovanni R. 1993. Increased expression of neutrophils and monocyte adhesion molecules in unstable coronary artery disease. Circulation 88:358-63.nBrogan GX, Friedman S, McCuskey C. 1994. Evaluation of a new rapid quantitative immunoassay for serum myoglobin versus CK-MB for ruling out acute myocardial infarction in the emergency department. Ann Emerg Med 24:665-71.nDavies MJ, Gordon JL, Pigott R, Woolf N, Katz D, Kyriakopoulos A. 1993. The expression of the adhesion molecules ICAM-1, VCAM-1, PECAM, and E-selectin in human atherosclerosis. J Pathol 171:223-9.nDemerath E, Towne B, Blangero J, Siervogel RM. 2001. The relationship of soluble ICAM-1, VCAM-1, P-selectin and E-selectin to cardiovascular disease risk factors in healthy men and women. Ann Hum Biol 28:664-78.nFuster V, Badimon L, Badimon JJ, Chesebro JH. 1992. The pathogenesis of coronary artery disease and the acute coronary syndromes (1). N Engl J Med 326:242-50.nFuster V, Badimon L, Badimon JJ, Chesebro JH. 1992. The pathogenesis of coronary artery disease and the acute coronary syndromes (2). N Engl J Med 326:310-8.nHamm CW, Goldmann BU, Heeschen C, Kreymann G, Berger J, Meinertz T. 1997. Emergency room triage of patients with acute chest pain by means of rapid testing for cardiac troponin T or troponin I. N Engl J Med 337:1648-53.nHwang S-J, Ballantyne CM, Sharrett R, et al. 1997. Circulating adhesion molecules VCAM-1, ICAM-1, and E-selectin in carotid atherosclerosis and incident coronary heart disease cases. Circulation 96:4219-25.nJordan JE, Zhao ZQ, Vinten-Johansen J. 1999. The role of neutrophils in myocardial ischemia-reperfusion injury. Cardiovasc Res 43:860-78.nKatz IA, Irwig L, Vinen JD, et al. 1998. Biochemical markers of acute myocardial infarction: strategies for improving their clinical usefulness. Ann Clin Biochem 35:393-9.nLi H, Cybulsky MI, Gimbrone MA Jr, Libby P. 1993. An atherogenic diet rapidly induces VCAM-1, a cytokine-regulatable mononuclear leukocyte adhesion molecule, in rabbit aortic endothelium. Arterioscler Thromb 13:197-204.nLi YH, Teng JK, Tsai WC, Tsai LM, Lin LJ, Chen JH. 1997. Elevation of the soluble adhesion molecules is associated with the severity of myocardial damage in acute myocardial infarction. Am J Cardiol 80:1218-21.nLind L. 2003. Circulating markers of inflammation and atherosclerosis. Atherosclerosis 169:203-14.nMair J, Morandell D, Genser N, Lechleitner P, Dienstl F, Puschendorf B. 1995. Equivalent early sensitivities of myoglobin, creatine kinase MB mass, creatine kinase isoform ratios, and cardiac troponins I and T for acute myocardial infarction. Clin Chem 41:1266-72.nMurohara T, Kamijikkoku S, Honda T. 2000. Increased circulating soluble intercellular adhesion molecule-1 in acute myocardial infarction: a possible predictor of reperfusion ventricular arrhythmias. Crit Care Med 2000 28:1861-4.nPearson TA, Mensah GA, Alexander RW, et al. 2003. Markers of inflammation and cardiovascular disease. Application to clinical and public health practice: a statement for healthcare professionals from the Centers for Disease Control and Prevention and the American Heart Association. Circulation 107:499-511.nPitt B, Rubenfire M. 1999. Risk stratification for the detection of preclinical coronary artery disease. Circulation 99:2610-2.nRohde LE, Hennekens CH, Ridker PM. 1999. Cross-sectional study of soluble intercellular adhesion molecule-1 and cardiovascular risk factors in apparently healthy men. Arterioscler Thromb Vasc Biol 19:1595-9.nRohde LE, Lee RT. 2003. Pathophysiology of atherosclerotic plaque development and rupture: an overview. Semin Vasc Med 3:347-54.nSimpson PJ, Todd RF III, Mickelson JK. 1990. Sustained limitation of myocardial reperfusion injury by a monoclonal antibody that alters leukocyte function. Circulation 81:226-37.nSmith SC Jr, Greenland P, Grundy SM. 2000. Prevention conference V. Beyond secondary prevention: identification of the high-risk patient for primary prevention. Circulation 101:111-6.nSpringer TA. 1994. Traffic signals for lymphocyte recirculation and leukocyte emigration: the multistep paradigm. Cell 76:301-14.nTucker JF, Collins RA, Anderson MS, et al. 1994. Value of serial myoglobin levels in the early diagnosis of patients admitted for acute myocardial infarction. Ann Emerg Med 24:704-8.nWeiss SJ. 1989. Tissue destruction by neutrophils. N Engl J Med 320:365-76.nWu AH, Apple FS, Gibler WB, Jesse RL, Warshaw MM, Valdes RJ Jr. 1999. National Academy of Clinical Biochemistry Standards of Laboratory Practice: recommendations for the use of cardiac markers in coronary artery diseases. Clin Chem 45:1104-21.n
