[Clinical amalysis of left subclavian artery revascularization by stented trunk fenestration for acute Stanford type A aortic dissection].

OBJECTIVE: To summarize the results and methods of left subclavian artery revascularization by stented trunk fenestration for acute Stanford type A aortic dissection. METHODS: Clinical data of 67 patients (54 male and 13 female, mean age of (50±10) years) underwent surgical treatment of left subclavian artery fenestration for acute Stanford A aortic dissection in Department of Cardiothoracic Surgery, Changhai Hospital, Second Military Medical College between September 2008 and December 2014 were analyzed retrospectively. The origin of the left subclavian artery was in the true lumen and no dissection existed near the artery's starting. There were 18 cases of Marfan's syndrome. Preoperative echocardiography showed moderate to severe aortic regurgitation in 10 cases, and mitral regurgitation in 3 cases. Electrocardiogram showed myocardial ischemia in 5 cases. Three patients had acute impaired renal function. All the patients received total arch replacement combined with stented elephant trunk implantation. Left subclavian artery revascularization was performed by stented trunk fenestration as follows: firstly, stented elephant trunk was implanted to completely cover the left subclavian artery, then part of stented trunk's polyester lining was removed which is located at the origin of left subclavian artery. Aortic root procedures included aortic valve replacement in 2 cases, Bentall procedure in 21 cases and aortic valve sparing in 44 cases. Three patients received mitral valve repair and 6 patients received coronary artery bypass grafting. RESULTS: The cardiopulmonary bypass time, cross-clamp time, and circulatory arrest time were (179±32) minutes, (112±25) minutes, and (26±10) minutes, respectively. The in-hospital mortality was 7.5% (5/67): 2 patients died of multiple organ failure, 1 patient died of acute renal failure and another 2 patients died of severe infection shock. Two patients required reexploration for root bleeding. Transient neurology dysfunction developed in 6 patients. Six patients received tracheotomy and prolonged ventilation due to pulmonary infection. All patients discharged from the hospital were followed up for 1 to 5 years. During long-term follow-up, the survival rate was 100% and 89.8% at 1 and 5 years, respectively. CT angiography was performed once per year after discharged. The left subclavian artery perfusion was good. No dissection or anastomosis leakage was identified in any case. Stroke and left limb ischemia did not develope. CONCLUSION: For acute Stanford type A aortic dissection whose origin of the left subclavian artery is in the true lumen and no dissection existed near the artery's starting, the left subclavian artery revascularization by stented trunk fenestration technique during total arch replacement combined with stented elephant trunk implantation is reliable and effective.

Long noncoding RNA XIST regulates cardiomyocyte apoptosis by targeting miR-873-5p/MCL1 axis.

OBJECTIVE: The purpose of this study was to investigate the expression of miR-873-5p and long non-coding RNA X-inactive specific transcript (lncRNA-XIST) in myocardial infarction (MI), the interaction mechanism and the effect of target gene MCL1 on apoptosis in H9c2 cells. MATERIALS AND METHODS: quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was used to detect and compare the expressions of miR-873-5p and lncRNA XIST in 8 myocardial infarction rats and 8 normal rats tissues, respectively, and the correlation between the expressions of miR-873-5p and lncRNA XIST in the myocardial tissues was explored. Next, qRT-PCR and Western blot were used to detect the effects of upregulation of miR-873-5p and downregulation of lncRNA XIST, as well as the impacts of their interactions on the expression level of MCL1 in H9c2 cells and the apoptosis of cells. RESULTS: It was found that the downregulation of miR-873-5p protected the heart against apoptosis after AMI, and lncRNA XIST inhibited apoptosis in H9c2 cells after hypoxia. Besides, inhibiting lncRNA XIST could upregulate miR-873-5p and downregulate MCL1, thus increasing apoptosis in the H9c2 cells after hypoxia. CONCLUSIONS: LncRNA XIST can regulate cardiomyocyte apoptosis by targeting miR-873-5p.

Ghrelin inhibits inflammatory response and apoptosis of myocardial injury in septic rats through JAK/STAT signaling pathway.

OBJECTIVE: The purpose of this study was to explore the influence of Ghrelin on myocardial injury of septic rats through the Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway. MATERIALS AND METHODS: A total of 36 Sprague-Dawley rats were randomly divided into normal group (n=12), model group (n=12), and Ghrelin group (n=12). The rats in the normal group were fed normally, while those in the model group were intraperitoneally injected with endotoxin to establish the sepsis model. The rats in the Ghrelin group were given intraperitoneal injection of Ghrelin solution to prepare the sepsis model. 9 h later, the specimens were obtained. Then, the expressions of interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) were detected via immunohistochemistry, and the protein expressions of phosphorylated JAK (p-JAK) and STAT3 were determined by Western blotting (WB). Next, enzyme-linked immunosorbent assay (ELISA) was performed to measure the content of IL-6 and TNF-α, and quantitative Polymerase Chain Reaction (qPCR) was applied to examine the messenger ribonucleic acid (mRNA) expressions of JAK and STAT3. Finally, the cell apoptosis was detected through terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay. RESULTS: The results of immunohistochemistry showed that compared with those in the normal group, the positive expression levels of IL-6 and TNF-α were markedly increased in other groups (p<0.05), while in comparison with those in the model group, the positive expression levels of IL-6 and TNF-α were decreased significantly in the Ghrelin group (p<0.05). The WB results indicated that the model group and Ghrelin group had remarkably higher protein expression levels of p-JAK and STAT3 than the normal group (p<0.05), and Ghrelin group exhibited notably lower protein expression levels of p-JAK and STAT3 than the model group (p<0.05). According to the results of qPCR, the relative mRNA expression levels of JAK and STAT3 were distinctly raised in the model group and Ghrelin group in comparison with those in the normal group (p<0.05), while they were reduced evidently in the Ghrelin group compared with those in the model group (p<0.05). Furthermore, it was manifested in the results of ELISA that the model group and Ghrelin group had prominently elevated content of TNF-α and IL-6 compared with normal group (p<0.05), and Ghrelin group displayed significantly lowered content of TNF-α and IL-6 in comparison with the model group (p<0.05). Moreover, the TUNEL results revealed that the apoptosis rate was remarkably higher in the other two groups than that in the normal group (p<0.05), while it was evidently lower in the Ghrelin group than that in the model group (p<0.05). CONCLUSIONS: Ghrelin can inhibit inflammatory response and apoptosis in the process of myocardial injury in septic rats by repressing the JAK/STAT signaling pathway.

[Effect of ICAM-1/LFA-1 on hypoxia/reoxygenation injury of cardiomyocytes mediated by neutrophils].

AIM: To observe the effect of hypoxia/reoxygenation on the adherence of neutrophils to cardiomyocytes and to investigate the effect of ICAM-1/LFA-1 on hypoxia/reoxygenation injury of cardiomyocytes mediated by neutrophils. METHODS: Count adhered neutrophils to cardiomyocytes suffering hypoxia, hypoxia/reoxygenation and normal culture, as well as adhered neutrophils that were blocked by anti ICAM-1 and LFA-1 monoclonal antibodies. Release of lactate dehydrogenase (LDH) was determined as injury index of cardiomyocytes. RESULTS: Adherence of with normal culture group (P < 0.01). The neutrophils to cardiomyocytes with hypoxia/reoxygenation were significantly increased compared lease of LDH by cardiomyocytes was also significantly increased (P < 0.01). There was no significant difference between hypoxia group and normal control (P > 0.05). The adherence of neutrophils to hypoxia/reoxygenation cardiomyocytes was significantly inhibited by anti-ICAM-1 and anti-LFA-1 antibody compared with normal culture group (P < 0.01). While release of LDH markedly decreased (P < 0.01). CONCLUSIONS: Hypoxia/reoxygenation increased the adherence of neutrophils to cardiomyocytes. ICAM-1 and LFA-1 mediated the enhanced adherence of neutrophils to hypoxia/reoxygenation cardiomyocytes. Anti-ICAM-1 and anti-LFA-1 antibody attenuated the cytotoxic effects of neutrophils on hypoxia/reoxygenated cardiomyocytes. These results suggested that the damage of neutrophils on cardiomyocytes is partly mediated by ICAM-1/LFA-1. Anti ICAM-1 and LFA-1 antibody are both beneficial in protecting hypoxia/reoxygenation cardiomyocytes from injury mediated by neutrophils.