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