The Relationship Between Inflammatory Mediators And Acute Coronary Syndrome

Acute coronary syndrome (ACS) is one of the emergent cardiovascular events that are threating people's health seriously. The pathophysiological mechanisms responsible for ACS including unstable angina (UA), acute non-Q wave myocardial infarction (NQMI) and acute Q wave myocardial infarction (QMI) are believed to involve an acute inflammatory stimulus that contribute to coronary plaque disruption and subsequent platelet aggregation and vessel thrombosis. There are growing evdience that local and systemic inflammation plays a role in the initiation and progression of atherosclerosis; patients with ACS had higher serum levels of C-reactive protein (CRP) and cellular adhesion molecules (CAMs) than those with stable angina. The inflammatory response is associated with the generation of CRP and other inflammatory mediators that induce increased expression of CAMs. These CAMs play a critical role in the adhesion and transendothelial migration of luekocytes from the blood to the arterial intima. Intercellular adhesion molecule- 1 (ICAM-1) and vascular cell adhesion molecule- 1(VC AM- 1) are expressed on activated endothelial cells and promote adhesion of neutrophils, monocytes and lymphocytes. The extracellular portion of these adhesion proteins can be cleaved by proeolytic enzymes to form a circulating molecule that can be detected in serum and refer to as the soluble cell adhesion molecules (sCAMs). Levels of soluble vascular cell adhesion molecule-1 (sVCAM-1) and soluble intercellular adhesion molecule-1 (sICAM-1) are elevated in patients with UA and NQMI throughout the first 72h of acute presentation. Alteration in concentrations of these sCAMs may relate activation or damage of2003various cell types including platelets and endothelial cells. However, the clinical implications of elevated CRP and sCAMs levels for improved early risk stratification of such patients remain controversial.Objective The objective of this study was to explore the role of inflammatory mediators in the pathogenesis of ACS and the predictive values of elevated inflammatory mediators for patients with ACS.Methods 96 subjects were divided into three groups. 48 patients presenting with UA and NQMI (29 men and 19 women, mean age 63.2±11.7 years) had serum samples taked on admission and when discharge, 28 patients with SA (16 men and 12 women, mean age 62.2 + 12.7 years) and 20 healthy controls group (13 men and 7 women, mean age 59.3 + 12.6 years) was used for comparison. Serum levels of soluble intercellular adhesion molecule (sICAM-1), vascular cell adhesion molecule (sVCAM-1) were measured using enzyme liked immunosorbent assay (ELISA). C-reactive protein was also measured by ultrasensitive immunoassay. Coronary angiogrography was performed in all patients with ACS, SA and normal control persons. The severity of coronary stenosis was evaluated by Gensini's score.Results CD Serum levels of sVCAM-1, sICAM-1 and CRP were significantly higher in patients with ACS than those with SA (P < 0.01) and normal controls (P < 0.01); but no difference between the latter two groups (P > 0.05); In ACS patients the levels of sICAM-1 and sVCAM-1 were both positively correlated with CRP ( respectively r =0.332, P < 0.01; r = 0.334, P < 0.01); Serum CRP level in ACS patients when admitted was markedly higher than that when discharged, Serum sVCAM-1 level in ACS patients when admitted was lower than that when discharged, but still higher than those in controls; Patients with ACS who had elevated sVCAM-1 level at the time of presentation had significantly higher MACE (863.68±56.88 vs 928.76 ± 91.18ug/L, P < 0.01); The incidence of MACE is higher in patients with serum sVCAM-1 > 870ug/L than those with serum sVCAM-1 < 870ug/L (P < 0.05); (2)Serum levels of Fig were significantly lower in normal controls than patients with ACS(P < 0.01) and thosewith SA (P < 0.01); but no difference between the latter two groups (P > 0.05); Concentration of Fig were also significantly raised in MACE group(mean (SEM) 4.20+1.81 vs 5.62±1.34g/L, P < 0.05); T...