Differences in inflammatory and thrombotic markers between unstable angina and acute myocardial infarction

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Abstract

Background

Unstable coronary syndromes are characterised by increased inflammatory process and endothelial activation. However, the underlying mechanisms of the acute coronary syndromes are still obscure. We evaluated the differences of inflammatory and thrombotic markers, at the acute phase of unstable angina (UA) and acute myocardial infarction (AMI).

Methods

The population of the study consisted of 216 subjects: 136 patients with UA, 57 patients with AMI and 23 healthy controls. Blood samples were taken by their admission to the hospital. Inflammatory and thrombotic markers were measured by ELISA.

Results

Patients with UA had significantly higher levels of interleukin-6 (IL-6), soluble vascular cells adhesion molecule (sVCAM-1) and von Willebrand factor (vWF) (p < 0.05 vs controls), and lower levels of antithrombin III (ATIII) (p < 0.01 vs controls) and protein C (PrtC) (p < 0.05 vs controls). Similarly, patients with AMI had higher levels of IL-6, sVCAM-1, vWF and tissue plasminogen activator (tPA) (p < 0.01 vs controls) and lower levels of ATIII (p < 0.01 vs controls) and prtC (p < 005 vs controls). Patients with AMI had significantly higher levels of vWF, tPA and sVCAM-1 compared to UA patients (p < 0.05).

Conclusions

Patients with unstable coronary syndromes had increased levels of IL-6, sVCAM-1 and vWF as well as decreased levels of ATIII and PrtC by their admission. However, patients with AMI had higher levels of all the endothelium-derived inflammatory (e.g. sVCAM-1) of thrombotic/fibrinolytic (e.g. tPA and vWF) markers, compared to those with UA. These findings imply that patients with myocardial infarction show further increase of endothelium-derived inflammatory and thrombotic markers compared to patients with unstable angina, in response to a similar proinflammatory stimuli.

Introduction

Coronary thrombosis is now widely recognized as a major cause of sudden cardiac death, acute myocardial infarction and unstable angina pectoris. Focal arterial inflammatory activity is one of the most prominent characteristics of the atherosclerotic process [1], [2]. Inflammation is also implicated in the pathogenesis of acute coronary syndromes as suggested by histologic findings in unstable coronary plaques [3], [4], evidence of systemic release of thromboxanes and leukotrienes [5], [6] and the presence of activated circulating leukocytes [7], [8], [9], [10]. Acute phase proteins such as CRP are involved in the prognosis of coronary artery disease [11], [12]. Leukocyte count and a number of inflammatory proteins such as fibrinogen [13], [14] or von Willebrand factor (vWF) [15] and various cytokines and adhesion molecules have been found in various studies to be independently associated with cardiovascular end points [16], [17]. Increased levels of interleukin-6 (IL-6), the major cytokine responsible for the acute phase response, were common in unstable patients and also correlated closely with prognosis [18]. Although thrombus formation is the major mechanism in both unstable angina (UA) and acute myocardial infarction (AMI), their clinical manifestations are different. The different underlying mechanisms leading to UA or AMI are still unknown.

In the present study we sought to compare the inflammatory and thrombotic factors in patients with an acute coronary syndrome. We compared serum levels of proinflammatory cytokines (TNF-a and IL-6), vascular cells adhesion molecules (such as sVCAM-1), and thrombotic/fibrinolytic markers (such as tissue plasminogen activator (tPA), antithrombin III (ATIII), proteins C (PrtC) and S (PrtS), factor VII (fVII) and von Willebrand factor (vWF)) in UA and AMI.

Section snippets

Patients

A total number of 216 subjects was included in this study (Table 1). One hundred ninety three patients admitted with acute coronary event were recruited by their admission to the hospital, and blood samples were obtained before the official diagnosis or the application of any therapeutic intervention/medication. Among these patients, 136 had unstable angina [19] and 57 developed AMI [20] as defined by the guidelines. Patients with UA had troponin levels at admission < 0.4 ng/ml.

The control group

Results

All data are presented in the table. Serum cholesterol and triglyceride levels were not significantly different between the three groups.

Discussion

The results of this study indicate that serum levels of inflammatory markers IL-6 and sVCAM-1, and thrombotic marker vWF were significantly increased at the acute phase of both UA and AMI. Plasma levels of ATIII and prtC were also decreased in both UA and AMI. Myocardial infarction patients had higher levels of sVCAM-1, t-PA, and vWF compared to UA patients. These findings provide evidence that both unstable coronary syndromes are accompanied by an increased inflammatory process, increased

References (35)

  • J.A. Berliner et al.

    Atherosclerosis: basic mechanisms. Oxidation, inflammation and genetics

    Circulation

    (1995)
  • P. Libby et al.

    Macrophages and atherosclerotic plaque stability

    Curr Opin Lipidol

    (1996)
  • A.C. van der Wal et al.

    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)
  • K. Kohchi et al.

    Significance of adventitial inflammation of the coronary artery in patients with unstable angina: results at autopsy

    Circulation

    (1985)
  • M.E. Helmer et al.

    Characterization of a novel differentiation antigen complex recognized by a monoclonal antibody (A-1A5): unique activation-specific molecular forms on stimulated T-cells

    J Immunol

    (1983)
  • G.R. Burmester et al.

    Activated T-cells in vivo and in vitro: divergence in expression of Tac and Ia antigens in the non-blastoid small T-cells of inflammation and normal T-cells activated in vitro

    J Immunol

    (1984)
  • F.J. Neumann et al.

    Induction of cytokine expression in leukocytes by binding of thrombin-stimulated platelets

    Circulation

    (1997)
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