Outcomes of Transcatheter Closure in Outlet-Type Ventricular Septal Defect after 1 Year

Background: Ventricular septal defect (VSD) is the most common congenital heart disease. Transcatheter VSD closure is an effective treatment for patients with muscular and perimembranous VSD. However, there is a limit data for outlet VSD, especially impact to the aortic valve leaflet after transcatheter closure. This study aims to assess the outcomes of transcatheter closure of the outlet-type ventricular septal defect (OVSD) after 1 postoperative year. Methods: A retrospective study was performed including 50 patients who underwent transcatheter (n = 25) and surgical (n = 25) OVSD closure during the exact time frame at two medical centres. Results: The median age and body weight of patients in the transcatheter group were significantly higher than those of patients in the surgical group (7.0 vs. 2.8 years; 27.0 vs. 11.4 kg; p < 0.01). The defect size in the surgical group was significantly larger than that in the transcatheter group (5.0 vs. 3.0 mm; p < 0.01). All OVSD patients have successful transcatheter closure (100%) as effective as surgical closure. Less than small residual shunt was present 20% and 8% immediately after the procedure in the transcatheter and surgical groups (p = 0.50), which decreased to 12% and 4% at the 1-year follow-up (p = 0.61), respectively. No incidence of complete atrioventricular block and other complications was observed in both groups, and no significant differences were noted in the new onset or worsening of the aortic regurgitation in both groups (p = 1.0). Conclusions: Transcatheter treatment could be effectively and safely achieved for OVSD closure at 1-year follow-up.     

Ischemic acute tubular necrosis models and drug discovery: a focus on cellular inflammation

Acute renal failure (ARF) is a common cause of mortality and morbidity in hospitalized patients. Ischemia is an important cause of ARF, and ARF caused by ischemic injury is referred to as ischemic acute tubular necrosis (ATN). There is growing evidence from models that ischemic ATN is associated with intrarenal inflammation. Consequently, intrarenal inflammation is an attractive target for the development of novel drug therapies for ARF. This review outlines ischemic ATN models, the pathophysiological roles of inflammatory cells such as T and B cells in ischemic ATN models, and effective T and B cell therapeutic reagents.     

The Protective Effect of Radicicol Against Renal Ischemia–Reperfusion Injury in Mice

Overexpression of heat shock protein 70 kDa (HSP70) is known to confer cellular protection against ischemia–reperfusion (I/R) injury. Radicicol, a HSP90 inhibitor, has been reported to induce the expression of HSP70 protein. Here we studied whether radicicol attenuated renal I/R injury in vivo. Treatment of mice with radicicol ameliorated renal I/R injury and increased renal HSP70 mRNA and protein. Administration of radicicol with quercetin, an inhibitor of HSP70 induction, eliminated the renoprotective effect of radicicol. Our results suggest that the up-regulation of renal HSP70 protein by radicicol leads to a novel drug therapy against renal I/R injury.