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Congenital Heart Disease Interventional Treatment-induced Myocardial Injury In Immune Mechanisms

Posted on:2009-03-06Degree:MasterType:Thesis
Country:ChinaCandidate:R ChenFull Text:PDF
GTID:2204360245968889Subject:Immunology
Abstract/Summary:PDF Full Text Request
With the improvement of the materials and technology, interventional treatment of congenital heart disease(CHD) develops very quickly at home and abroad in recent years. However, the treatment is still one kind of traumatic methods, which may lead to clinical or subclinical myocardial damage and inflammatory reaction. In this regard, the treatment of CHD can cause myocardial damage and inflammatory reaction too, but it is unclear whether the damage is severe; and the mechanism is also not clear.Objective: To explore myocardial damage resulted from interventional treatment and its immunological mechanism.Methods: Including 28 atrial septal defects (ASD) , 32 ventricular septal defects(VSD) suitable for interventional treatment and 20 VSDS unsuitable for interventional treatment by evaluation of left ventricular angiography(as a control group), all patients were taken serial blood samples before and 2 hours after the procedures. Measuring the cTnI, IL-8 and MCP serum levels by ELISA; Checking blood routine test for counting of WBC and PMN, and expression of NF-κB in PBMC counting of WBC and PMN by immunocytochemistry.Results: 1.Basic information: The total of 60 occluders had been successfully implanted. 20 VSDs were only proformed left ventricular angiography and then were considered as control group. There was no significant difference of the age, gender, body weight between ASD/VSD group and control group (P>0.05). There is no significant difference of diameters and occluders size between ASD group and VSD group(P>0.05).2.Change of cTnI level in serum: all patients serum cTnI levels was at the normal range before intervention. The levels were significantly increased 2 hours after intervention in ASD group and VSD group in comparison with the levels before operation (P<0.05). Moreover, cTnI level in serum VSD group was higher than that of ASD group(P<0.01). No difference in control group was found with the levels before and after operation (P>0.05).3. counting of WBC and PMN counting of WBC and PMN: There was no difference in blood counting before operation among the three groups. Counting of WBC and PMN in VSD closure group after operation was higher than that before operation(P<0.05); But no difference was found in ASD group and control group preoperatively and postoperatively (P>0.05).4. Expression of NF-κB in peripheral blood: There is no difference of percentage of chromoscopy—positive cell among groups; But the percentage after procedures in ASD and VSD closure groups was higher than before procedures(P<0.05). The percentage VSD closure group was higher than ASD group(P<0.05). But no difference was found in control group preoperatively and postoperatively (P>0.05). 5.Coparasion of IL-8 and MCP serum levels among the groups: IL-8 and MCP serum levels in three groups were in normal range. There was no significant difference among the groups (P>0.05). In ASD group and VSD group, Serum IL-8 levels were significantly increased after operation in comparison with the levels before intervention (P<0.05); IL-8 and MCP serum levels in VSD closure group was significantly higher than ASD group(P<0.05). Control group was not associated with detectable IL-8 and MCP increase(P>0.05).Conclusion: After interventional closure of atrial septal defects and ventricular septal defects, there exists a mild myocardial damage and inflammatory reaction, which means that interventional treatment is one kind of safe, effective and microinvasive treatments. Moreover, the increasing of NF-κB p65 in peripheral blood after intervention is associated with increasing of expression of IL-8 and MCP serum levels and infiltration of Peripheral blood neutrophilic granulocyte, which indicates that mechanical stimulation caused by interventional damage probably activates intracellular NF-κB channel which may regulates expression of IL-8 and MCP-1, which accelerates aggregation of neutrophilic granulocyte and mononuclear phagocyte and so on, and leads to myocardial inflammatory damage eventually.
Keywords/Search Tags:congenital heart disease, intervention myocardial damage, immunological mechanism
PDF Full Text Request
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