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目的探讨炎性细胞因子与老年人急性冠脉综合征(ACS)的关系。方法应用夹心酶联免疫吸附法(ELISA)、单克隆荧光抗体标记法检测ACS组33例、稳定性劳力型心绞痛(SA)组24例及健康对照组20例外周血中单核细胞趋化因子-1(MCP-1)、可溶性细胞间黏附分子-1(sICAM-1)、单核细胞表面CD11b及P-选择素(CD62p)水平。结果(1)ACS组、SA组与对照组比较,MCP-1〔(85.78±33.79)(、56.96±22.47)μg/L对(39.16±14.17)μg/L〕、sICAM-1〔(561.29±93.16)(、496.49±73.55)μg/L对(359.19±110.78)μg/L〕、CD11b〔(227.17±67.13)(、118.05±24.19)MFI对(86.81±40.93)MFI〕、CD62p〔(36.03±9.30)、(14.19±6.49)对(4.25±2.59)%〕均值之间的差异均具有统计学意义(P<0.01),以ACS组中4种炎性因子水平最高,SA组次之,对照组最低。(2)不稳定型心绞痛(UA)组20例和急性心肌梗死(AMI)组13例的4种炎性因子检测指标,其均值之间的差异均无统计学意义(P>0.05)。(3)SA组、UA组和AMI组冠状动脉病变程度之间的差异均无统计学意义(P>0.05)。结论外周血中炎性细胞因子可能参与了ACS发病过程。
Objective To investigate the relationship between inflammatory cytokines and acute coronary syndrome (ACS) in the elderly. Methods Sandwich enzyme-linked immunosorbent assay (ELISA) was used to detect the expression of chemokines in 33 patients with ACS, 24 patients with stable angina pectoris (SA) and 20 patients with healthy controls 1, soluble intercellular adhesion molecule-1 (sICAM-1), monocyte CD11b and P-selectin (CD62p) levels were measured. Results (1) Compared with the control group, the levels of MCP-1 in the ACS group and the SA group were significantly higher than those in the control group (95.78 ± 33.79, 56.96 ± 22.47 μg / L vs 39.16 ± 14.17 μg / L, 93.16), (496.49 ± 73.55) μg / L vs 359.19 ± 110.78 μg / L], CD11b (227.17 ± 67.13) (118.05 ± 24.19) MFI vs (86.81 ± 40.93) MFI), CD62p (36.03 ± 9.30), (14.19 ± 6.49) vs. (4.25 ± 2.59)%, respectively) were statistically significant (P <0.01). In the ACS group, the highest levels of the four inflammatory cytokines were found, followed by the SA group The lowest group. (2) There was no significant difference among the four indexes of inflammatory cytokines detected in 20 cases of unstable angina pectoris (UA) and 13 cases of acute myocardial infarction (AMI). (3) There was no significant difference in the degree of coronary artery lesions between SA group, UA group and AMI group (P> 0.05). Conclusion Inflammatory cytokines in peripheral blood may be involved in the pathogenesis of ACS.