Zhonghua xin xue guan bing za zhi · 2005
[Serum inflammatory related cytokines and circulating endothelial cells in patients with acute coronary syndrome].
Аннотация на английскомСтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Wang Chun-ling, Li Hong-wei, Fu Pan-feng, Zhang Shu-yang, Gao Run-lin, Xiu Rui-juan
Аннотация
OBJECTIVE: To study the number of CECs in patients with acute myocardial infarction (AMI) and unstable angina (UA), and to investigate its relationship with inflammatory related cytokines.
METHODS: 37 patients with AMI, 12 patients with UA, and 42 health controls were studied. CECs were isolated from peripheral blood by using of immunomagnetic beads coated with antibodies against CD146. Their endothelial origin was confirmed by the positive labelling of von Willebrand Factor (vWF), CD31 and electron microscope. Annexin V-FITC/PI kit was used to measure the apoptosis of CECs. Inflammatory related cytokines were analyzed turbidimetrically or ELISA using of commercially available testing kit.
RESULTS: CECs number was significantly higher in AMI and UA patients [medians (interquartile range) were 52 (28 approximately 81.5) cells/ml and 29 (18 approximately 61) cells/ml respectively] compared with health control [10.5 (6-16.5)cells/ml, P < 0.001]. After excluding diabetes patients, the number of CECs and CRP in AMI and UA group (n = 26) were still significantly higher than controls. The necrotic rate of CECs in AMI and UA was significantly higher than controls (P < 0.01). Correlation analysis revealed a significant positive correlation between CECs and CRP, or IL-6 (r = 0.677, 0.316, P = 0.000, 0.002). The multivariate linear regression analysis showed that CRP and Diabetes increased the number of CECs significantly (OR = 0.620, 0.164, 95% CI 3.985-6.751, 0.301-21.877, P = 0.000, 0.044).
CONCLUSION: The mechanism responsible for the increase of CECs in acute coronary disease may be due to the vessel injury caused by inflammation.
METHODS: 37 patients with AMI, 12 patients with UA, and 42 health controls were studied. CECs were isolated from peripheral blood by using of immunomagnetic beads coated with antibodies against CD146. Their endothelial origin was confirmed by the positive labelling of von Willebrand Factor (vWF), CD31 and electron microscope. Annexin V-FITC/PI kit was used to measure the apoptosis of CECs. Inflammatory related cytokines were analyzed turbidimetrically or ELISA using of commercially available testing kit.
RESULTS: CECs number was significantly higher in AMI and UA patients [medians (interquartile range) were 52 (28 approximately 81.5) cells/ml and 29 (18 approximately 61) cells/ml respectively] compared with health control [10.5 (6-16.5)cells/ml, P < 0.001]. After excluding diabetes patients, the number of CECs and CRP in AMI and UA group (n = 26) were still significantly higher than controls. The necrotic rate of CECs in AMI and UA was significantly higher than controls (P < 0.01). Correlation analysis revealed a significant positive correlation between CECs and CRP, or IL-6 (r = 0.677, 0.316, P = 0.000, 0.002). The multivariate linear regression analysis showed that CRP and Diabetes increased the number of CECs significantly (OR = 0.620, 0.164, 95% CI 3.985-6.751, 0.301-21.877, P = 0.000, 0.044).
CONCLUSION: The mechanism responsible for the increase of CECs in acute coronary disease may be due to the vessel injury caused by inflammation.