可溶性黏附分子在冠状动脉粥样硬化不同临床表现中的水平

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Adhesion molecules play an important role in the development and course of cor onary atherosclerosis. In this study, soluble forms of vascular cell adhesion mo lecule (VCAM-1) intercellular adhesion molecule-1 (ICAM-1), E-selectin and P -selectin were evaluated in patients with various clinical presentations of cor onary atherosclerosis and compared them to those with angiographically documente d normal coronary arteries. Venous plasma samples were collected from 43 patient s with acute myocardial infarction (AMI), 45 with unstable angina pectoris (UAP) , 34 with stable angina pectoris (SAP) and 29 subjects with normal coronary arte ries (control). The VCAM-1 level was significantly higher in patients with AMI (mean±SEM; 799.8±26.3 ng/ml) than those with UAP (644.2±26.7 ng/ml) and SAP ( 526±32.5ng/ml) and controls (270±26.8 ng/ml). In patients with UAP, VCAM-1 wa s found to be significantly elevated as compared to the SAP group and controls. VCAM-1 level was also higher in SAP group than the controls. Serum levels ICAM -1 were similar among patients with AMI (424.1±15.2 ng/ml), UAP (403±12.3 ng/ ml) and SAP (381.2±16.2 ng/ml); however, levels of ICAM-1 was significantly el evated in these groups as compared to the controls (244.3±11). The mean level o f E-selectin was not different in AMI and UAP groups (47.2±2.2 vs. 42.6±2.1 n g/ml; respectively). However, it was significantly higher in acute coronary synd rome groups as compared to SAP (33.4±2.3 ng/ml) and control subjects (30.7±1.9 ng/ml). Serum levels of E-selectin were similar in SAP group and controls. For P-selectin, no significant difference was observed between AMI and UAP groups (187.5±7.2 vs. 181.7±4.7 ng/ml; respectively), however, i t was significantly higher in both groups as compared to SAP group (146.1±7.4 n g/ml) and controls (108±6.6 ng/ml). Serum level of P-selectin was significantl y higher in patients with SAP than the control group. In conclusion, determinati on of serum VCAM-1, E-selectin and P-selectin levels seems more useful for de tecting coronary plaque destabilization. Adhesion molecules play an important role in the development and course of cor onary atherosclerosis. In this study, soluble forms of vascular cell adhesion mo lecule (VCAM-1) intercellular adhesion molecule- 1 (ICAM- 1), E-selectin and P- selectin were evaluated in cor withary atherosclerosis and compared them to those with angiographically documente d normal coronary arteries. Venous plasma samples were collected from 43 patient s with acute myocardial infarction (AMI), 45 with unstable angina pectoris (UAP ) 34 with stable angina pectoris (SAP) and 29 subjects with normal coronary arte ries (control). The VCAM-1 level was significantly higher in patients with AMI (mean ± SEM; 799.8 ± 26.3 ng / ml) than those with UAP (644.2 ± 26.7 ng / ml) and SAP (526 ± 32.5 ng / ml) and controls (270 ± 26.8 ng / ml). In patients with UAP, VCAM-1 wass found to be significantly elevated as compared to the SAP group and controls. VCAM-1 level was also higher in SAP gro Serum levels of ICAM -1 were similar among patients with AMI (424.1 ± 15.2 ng / ml), UAP (403 ± 12.3 ng / ml) and SAP (381.2 ± 16.2 ng / ml); however, levels of ICAM -1 was significantly elvaged in these groups as compared to the controls (244.3 ± 11). The mean level of E-selectin was not different in AMI and UAP groups (47.2 ± 2.2 vs. 42.6 ± 2.1 ng / ml; respectively) However, it was significantly higher in acute coronary syndome than as SAP (33.4 ± 2.3 ng / ml) and control subjects (30.7 ± 1.9 ng / ml). Serum levels of E-selectin were similar in SAP group and controls For P-selectin, no significant difference was observed between AMI and UAP groups (187.5 ± 7.2 vs. 181.7 ± 4.7 ng / ml; respectively), however, it was significantly higher in both groups as compared to SAP group (146.1 ± 7.4 Serum level of P-selectin was significantly higher than patients with SAP than the control group. In conclusion, determinati on of serum VCAM-1 E-selectin andP-selectin levels seems more more for detecting coronary plaque destabilization.
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