Rupture of sinus of Valsalva aneurysm: a case report in a child.

BACKGROUND: Sinus of Valsalva aneurysm (SVA) is a rare congenital disease that can cause severe clinical presentations when the aneurysm ruptures. Here, we report a rare case of a noncoronary sinus of Valsalva aneurysm with rupture into the right atrium. CASE PRESENTATION: A 14-year-old Chinese female patient presented viral myocarditis with acute heart failure at the local hospital, and she was finally diagnosed with a noncoronary sinus Valsalva aneurysm with rupture into the right atrium by digital subtraction angiography with cardiac catheterization angiography and echocardiography at our hospital (Children's Hospital of Chongqing Medical University). Percutaneous closure intervention was performed shortly after her diagnosis, and the patient showed good functional recovery. CONCLUSIONS: We report a case of ruptured sinus of Valsalva aneurysm successfully treated by percutaneous closure, which is an excellent alternative treatment.

The effect of melatonin on cardio fibrosis in juvenile rats with pressure overload and deregulation of HDACs.

The effect of melatonin on juveniles with cardio fibrosis is poorly understood. We investigated whether HDACs participate in the anti-fibrotic processes regulated by melatonin during hypertrophic remodeling. Abdominal aortic constriction (AAC) was employed in juvenile rats resulting in pressure overload-induced ventricular hypertrophy and melatonin was subsequently decreased via continuous light exposure for 5 weeks after surgery. AAC rats displayed an increased cross-sectional area of myocardial fibers and significantly elevated collagen deposition compared to sham-operated rats, as measured by HE and Masson Trichrome staining. Continuous light exposure following surgery exacerbated the increase in the cross-sectional area of myocardial fibers. The expression of HDAC1, HDAC2, HDAC3, HDAC4 and HDAC6 genes were all significantly enhanced in AAC rats with light exposure relative to the other rats. Moreover, the protein level of TNF-α was also upregulated in the AAC light exposure groups when compared with the sham. However, Smad4 protein expression was unchanged in the juveniles' hearts. In contrast, beginning 5 weeks after the operation, the AAC rats were treated with melatonin (10 mg/kg, intraperitoneal injection every evening) or vehicle 4 weeks, and sham rats were given vehicle. The changes in the histological measures of cardio fibrosis and the gene expressions of HDAC1, HDAC2, HDAC3, HDAC4 and HDAC6 were attenuated by melatonin administration. The results reveal that melatonin plays a role in the development of cardio fibrosis and the expression of HDAC1, HDAC2, HDAC3, HDAC4 and HDAC6 in cardiomyocytes.

Ventricular Septal Rupture After Blunt Chest Trauma in an Infant: A Case Report and Mini-Review.

Ventricular septal rupture (VSR) due to blunt chest trauma (BCT) is rare in infants. Traumatic VSR should be considered in infants with acute congestive cardiac failure following blunt trauma to the chest. Echocardiography is the method of choice for diagnosis and guiding the management of VSR. In this case report, we present a case of VSR caused by BCT in a 1-year and 9-month-old infant, who was diagnosed by emergency bedside echocardiography. We also provide a mini-review of literatures on BCT-induced VSR in children.

Cardiac Protection of Valsartan on Juvenile Rats with Heart Failure by Inhibiting Activity of CaMKII via Attenuating Phosphorylation.

Background. This study was undertaken to determine relative contributions of phosphorylation and oxidation to the increased activity of calcium/calmodulin-stimulated protein kinase II (CaMKII) in juveniles with cardiac myocyte dysfunction due to increased pressure overload. Methods. Juvenile rats underwent abdominal aortic constriction to induce heart failure. Four weeks after surgery, rats were then randomly divided into two groups: one group given valsartan (HF + Val) and the other group given placebo (HF + PBO). Simultaneously, the sham-operated rats were randomly given valsartan (Sham + Val) or placebo (Sham + PBO). After 4 weeks of treatment, Western blot analysis was employed to quantify CaMKII and relative calcium handling proteins (RyR2 and PLN) in all groups. Results. The deteriorated cardiac function was reversed by valsartan treatment. In ventricular muscle cells of group HF + PBO, Thr287 phosphorylation of CaMKII and S2808 phosphorylation of RyR2 and PLN were increased and S16 phosphorylation of PLN was decreased compared to the other groups, while Met281 oxidation was not significantly elevated. In addition, these changes in the expression of calcium handling proteins were ameliorated by valsartan administration. Conclusions. The phosphorylation of Thr286 is associated with the early activation of CaMKII rather than the oxidation of Met281.