Objective To summarize the experiences of surgical treatment for partial atrioventricular canal defect. Methods The data of 66 patients of surgical treatment for partial atrioventricular canal defect from January 1984 to December 2007 were analyzed retrospectively. The cleft of mitral valve presented in all of those patients. There were 52 cases with direct suture on cleft, 8 cases with direct suture with commissurroplasty, 1 case with posterior leaflet plasty, 3 cases with direct suture St.Jude ring and 2 cases mitral valve replacement. The ostium primum atrial septal defects were repaired with patches of Dacron in 12 cases and autologous pericardium in 54 cases. Coronary sinus was situated on the left atrium in 5 and ostium primum atrial septal defects were repaired in Kirklin’s way; the others in MeGoon’way. Meanwhile other heart abnormalities were done. Results There were two early deaths (3.03%), one patient died of heart arrhythmia and one patient died of respiratory failure. Complications of total A-V block was in 2 cases. Both of them were replanted with pace makers.52 cases were followed up, followup time was 5 months to 22 years(mean follow-up 15 years). All patients had better life. Four patients have been re -operated for different reasons post primary operation. One had good result after re-mitral valve replacement. One case died of acute renal failure and the other two died of low cardiac output syndrome. Conclusions Early operation is definitely recommended when the diagnosis is confirmed. Because the structure or function of mitral valve is saved, pulmonary hypertension is avoided and the mortality is lower in the future. The key points of operation are to rectify the mitral insufficiency, repair ostium primum atrial septal defects and avoid atrioventricular block. The patients of mild regurgitation of mitral valve have good results. Provided in those have more than middle regurgitation of mitral valve then their longterm results are poor.
Objective To explore the induction of cardiomyogenesis of microRNA-129 （mir-129） in rat bone marrowmesenchymal stem cells （BM-MSCs） and its mechanism. Methods BM-MSCs were isolated from Sprague-Dawley rats and cultured in vitro. Overexpression of mir-129 or both mir-129 and glycogen synthase kinase-3β （GSK-3β） in BM-MSCs was produced with a lentiviral vector system. All the BM-MSCs were divided into four groups: control group （MSCs），Lentiviral vectors＋MSCs group （Lv-MSCs），mir-129 transfection group （mir-129-MSCs），and mir-129＋GSK-3βdouble transfection group （mir-129＋GSK-3β-MSCs）. Five-Azacytidine （5-Aza） （10 μmol/L） was used to induce BM-MSCsdifferentiation into cardiomyocytes. On the 1st，5 th，10 th，15 th and 20 th day after induction，realtime-PCR was performedto detect mRNA levels of GATA-4，Nkx2.5 and MEF-2C. On the 10 th，15 th and 20 th day after induction，Western blottingwas performed to examine expression levels of cTnI，Desmin，GSK-3β，phosphorylated β-catenin and dephosphorylated β-catenin. Results Compared with the control group，at respective time points，mRNA levels of cardiomyogenic genes and expression levels of cardiomyocyte-related proteins of mir-129 transfection group were significantly elevated，theexpression level of GSK-3β was significantly decreased，and the ratio of dephosphorylated/phosphorylated β-catenin was significantly elevated. When both mir-129 and GSK-3β were overexpressed in BM-MSCs，mRNA levels of cardiomyogenicgenes and expression levels of cardiomyocyte-related proteins were significantly lower than those of mir-129 transfection group，and the ratio of dephosphorylated/phosphorylated β-catenin was significantly decreased. Conclusion Overexpression of mir-129 can promote cardiomyogenesis of rat BM-MSCs possibly via inhibiting GSK-3β production and thus decreasing the inhibition of phosphorylation of β-catenin which then enters the nucleus and activates downstream signaling pathways that regulate cardiomyogenic differentiation of BM-MSCs.
