论文部分内容阅读
目的探讨房颤患者射频消融术后有无单个核细胞动员及机制。方法连续收集实施射频消融的持续性房颤和阵发性房颤患者共25例,采集射频消融术前及术后第1天外周血,使用流式细胞仪检测CD117~+单个核细胞、CXCR4~+单个核细胞、CD34~+CD133~+单个核细胞比例,采用酶联免疫法(ELISA)检测基质金属蛋白酶-9(MMP-9)、人生长调节致癌基因β/黑素瘤生长刺激因子(GR0β)、基质细胞衍生因子1(SDF-1)、白细胞介素6(IL-6)、白细胞介素8(IL-8)、粒细胞集落刺激因子(G-CSF)、血管生成素1(ANG1)、cTnT及CK-MB等。结果房颤患者射频消融术后cTnT明显增高(P<0.001),提示射频消融导致了非缺血性心肌损伤,而且术后MMP-9(P=0.001),GR0β(P=0.014)、G-CSF(P=0.04)和IL-6(P=0.011)等细胞因子均显著升高,但SDF-1较术前明显减少,IL-8无明显变化。房颤患者射频消融术后外周血CXCR4+单个核细胞(20.45%±12.32%vs 37.75%±17.00%,P<0.001)及CD34~+CD133~+单个核细胞(7.04%±4.91%vs 11.80%±4.26%,P=0.001)显著动员,但CD117+单个核细胞无明显变化(P>0.05)。房颤患者射频消融术后cTnT与MMP-9呈正相关(R=0.636,P=0.001),而且消融术后cTnT和MMP-9均与CXCR4~+单个核细胞比例(R=0.674,P<0.001;R=0.579,P=0.002)及CD34~+CD133~+单个核细胞比例(R=0.655,P<0.001;R=0.522,P=0.007)呈正相关,但与CD117~+单个核细胞比例无关(P均>0.05)。结论房颤患者射频消融术导致了非缺血性心肌损伤,进而发生CXCR4~+单个核细胞及CD34~+CD133~+单个核细胞动员,两者动员程度与心肌损伤程度呈正相关,其动员机制不依赖SDF-1α/CXCR4轴,而与MMP-9升高呈正相关,提示缺血性心肌损伤和非缺血性心肌损伤后外周单个核细胞的主要动员机制不同。
Objective To investigate the mobilization and mechanism of mononuclear cells after radiofrequency catheter ablation in patients with atrial fibrillation. Methods Totally 25 consecutive patients with persistent AF and paroxysmal atrial fibrillation who underwent radiofrequency catheter ablation were collected. Peripheral blood samples were collected before and after radiofrequency ablation. Flow cytometry was used to detect CD117 ~ + mononuclear cells, CXCR4 ~ + Mononuclear cells, the ratio of CD34 ~ + CD133 ~ + mononuclear cells were detected by enzyme-linked immunosorbent assay (ELISA). The levels of MMP-9 and human growth regulatory oncogene beta / melanoma growth stimulating factor (GR0β), SDF-1, IL-6, IL-8, G-CSF, (ANG1), cTnT and CK-MB. Results The cTnT was significantly increased in patients with AF after radiofrequency ablation (P <0.001), suggesting that radiofrequency catheter ablation led to non-ischemic myocardial injury. The postoperative MMP-9, GR0β, CSF (P = 0.04) and IL-6 (P = 0.011) were significantly increased, but SDF-1 was significantly reduced compared with preoperative, IL-8 had no significant change. The levels of CXCR4 + mononuclear cells (20.45% ± 12.32% vs 37.75% ± 17.00%, P <0.001) and CD34 + CD133 + mononuclear cells (7.04% ± 4.91% vs 11.80% ± 4.26%, P = 0.001), but there was no significant change in CD117 + mononuclear cells (P> 0.05). There was a positive correlation between cTnT and MMP-9 (r = 0.636, P = 0.001) after radiofrequency ablation in patients with atrial fibrillation, and the ratio of cTnT and MMP-9 to CXCR4 ~ + mononuclear cells after ablation ; R = 0.579, P = 0.002) and the proportion of CD34 ~ + CD133 ~ + mononuclear cells (R = 0.655, P <0.001; R = 0.522, P = 0.007), but not with the proportion of CD117 ~ + mononuclear cells (P> 0.05). Conclusions RFA leads to non-ischemic myocardial injury, which leads to the mobilization of CXCR4 ~ + mononuclear cells and CD34 ~ + CD133 ~ + mononuclear cells. The degree of mobilization is positively correlated with the degree of myocardial injury, and the mechanism of its mobilization Independent of the axis of SDF-1α / CXCR4, but positively correlated with the increase of MMP-9, suggesting that the main mobilization mechanism of peripheral mononuclear cells in ischemic myocardium and non-ischemic myocardium were different.