| Background: Most acute coronary syndromes (ACS) are caused by thromboses occurring over ruptured vulnerable plaques. Atherosclerotic plaque vulnerability to rupture depends at least partly on the size of the necrotic lipid core. Previous studies found that the lipids of the erythrocyte membranes had important role in the lipid core augmentation in the progress of plaque vulnerability. It was reported that there was a significant correlation between elevated total cholesterol content of erythrocyte membranes (CEM) levels and ACS. Sphingomyelin is also one of the major lipids in red blood cell membranes, which has been isolated from atherosclerotic plaques in both humans and animals. The contribution of sphingomyelin of erythrocyte membranes to the clinical presentation of CAD and the rapid progression of coronary atheroma has not been studied.Objective: To investigate the changes and clinical significance of sphingomyelin and total cholesterol content of erythrocyte membranes in patients with ACS. We sought to assess whether SEM levels are associated with CEM,and whether they are associated with serum lipids , and explore the pathogenic mechanism of ACS.Methods: 327 subjects with the main complaint of chest pain, according to clinical symptoms and the result of coronary artery angiography, were devided into three different groups. 215 had ACS and 57 had stable angina pectoris (SAP). 55 individuals with atypical chest pain and normal coronary artery were considered to represent a control group. The levels of SEM and CEM were measured using an enzymatic assay after preparing erythrocyte membranes of all the patients.Results: (1) SEM levels in the ACS group (121.68μg/mg, range 96.72 to 171.07μg/mg) were significantly higher(p <0.001)compared with the SAP group (96.97μg/mg, range 75.65 to 106.84μg/mg), and there had no significant difference (p=0.644) between SAP and Control groups (90.77μg/mg, range 70.70 to 109.63μg/mg). (2) CEM levels in the ACS group(125.75μg/mg, range 110.57 to 147.32μg/mg) were significantly higher(p<0.001) compared with the SAP group(84.12μg/mg, range 67.06 to 98.78μg/mg), and there had no significant difference(p=0.750) between SAP and Control groups(88.08μg/mg, range 70.22 to 95.74μg/mg).(3) Serum SM levels in the ACS group(14.00mg/dl, range 9.83 to 17.54 mg/dl) were significantly higher(p<0.001) compared with the SAP group(8.58 mg/dl, range 6.29 to 13.17 mg/dl), and there had no significant difference(p=0.735) between SAP and Control groups(8.17 mg/dl, range 5.67 to 13.58 mg/dl). (4) Multivariable logistic regression analyses according to different covariates revealed a significant independent relation between SEM levels and the presence of ACS (OR 6.678, 95%CI 2.516 to 17.722, P<0.001) and a significant independent relation between CEM levels and the presence of ACS (OR 13.181, 95%CI 5.461 to 31.817, p<0.001). (5) ROC analysis regarding predictive accuracy for patients'CAD status showed that for CEM, the area under the curve was 0.842 (0.722 to 0.912), p<0.001;for SEM 0.751 (0.690 to 0.812), p<0.001;and for hs-CRP was 0.641(0.566 to 0.716),p=0.001.(6) SEM levels were positively correlated with CEM levels (r=0.363; p<0.001). CEM levels were negatively correlated with serum Apo A-I levels (r =-0.184, p =0.002)and serum HDL-C (r =-0.127, p =0.036) , and positively correlated with LP(a) levels (r =0.214; p<0.001). and they may have a certain diagnostic value about ACS.These findings probably suggested that the increased levels of SEM and CEM may be involved in the progress of plaque instability of ACS. Correlation analysis showed that the increasing of SEM levels, and the decreasing of ApoA - I and HDL-C levels were the possible mechanisms of the increasing of CEM levels. But the mechanisms of the increasing of SEM levels are not clear.
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