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In recent years, with the constant improvement of the materials and processes, interventional treatment of heart disease in the domestic and international clinical applications development soon. However, it is, after all, is a noninvasive means of examination and treatment, can cause clinical or subclinical myocardial injury and inflammatory response. Inferred interventional treatment of congenital heart disease (CHD), also cause myocardial injury and inflammatory response, but its cause myocardial injury is serious or not, how the mechanism is unclear. Objective To explore the interventional treatment of congenital heart disease caused by myocardial injury and related immune mechanisms. Methods 80 cases of children with congenital heart disease as the research object, which atrial septal defect (Atrial septal defects, ASD) closure group, 28 patients, ventricular septal defect (Ventricalar septal defect, VSD) occluder group of 32 patients, 20 patients the VSD patients due to the defect is too large or too small, the only line left ventricular angiography, set to the control group (angiography group). Preoperative and postoperative 2h, blood samples were collected from the cubital vein by ELISA detection of cTnI, IL-8 and MCP-1 serum concentrations, blood WBC of PMN counts, immunocytochemistry assay in PBMC of NF -κB expression. 1 basic situation: 60 cases of children with congenital heart disease were successfully implanted occluder ASD group, VSD group and the control group in terms of gender, age, weight and other, no significant difference (P gt; 0.05). ASD group, VSD group, no significant difference (P gt; 0.05) defect diameter, the size of the occluder. Serum cTnI concentration changes: all children with preoperative serum cTnI was no significant difference (P> 0.05). Elevated postoperative the 2h ASD group compared with the preoperative difference was statistically significant (P lt; 0.05) the VSD group also increased compared with the preoperative difference was statistically significant (P lt; 0.05), and the the VSD group after 2h cTnI concentration was significantly higher than the ASD group, the difference was statistically significant (P lt; 0.01), no difference (P> 0.05) in the control group with preoperative. WBC, PMN count: the group of patients with preoperative blood count was no difference in postoperative WBC, PMN count, VSD group than normal (P lt; 0.05); ASD group and the control group with preoperative differences. 4 in PBMC expression of NF-κB: preoperative group between PBMC positive cells percentage no difference in postoperative regardless of ASD or VSD group PBMC staining positive cell percentage was significantly higher than the preoperative (P lt; 0.05 ), and VSD group cells positive rate in the ASD group (P lt; 0.05), no difference (P> 0.05) in the control group with preoperative. 5 serum IL-8, MCP-1 concentration comparison: the group of children with preoperative serum IL-8, MCP-1 water in the normal range on average, among the groups did not change significantly, no significant (P gt; 0.05), the ASD group VSD serum IL-8, MCP-1 levels after surgery compared with the preoperative elevated (P lt; 0.05);, and the the VSD group postoperatively IL-8, MCP-1 levels above ASD group (P lt; 0.05), no difference (P> 0.05) in the control group with preoperative. Conclusions ASD, VSD children after interventional treatment, minor myocardial damage and inflammatory changes, interventional therapy is a safe, effective, minimally invasive treatment method. In addition, the interventional treatment of peripheral blood in NF-κB p65 increased along with the inflammatory mediators IL-8, MCP-1 expression increased peripheral blood inflammatory cell infiltration, the prompt intervention damage caused by the mechanical stimulation may activate NF-κB pathway regulation of intracellular expression of IL-8, MCP-1 and other cytokines, thus making neutrophils, monocytes - macrophages partial aggregation, eventually leading to the inflammatory injury.
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