Management of adolescent anorexia with symptomatic bradycardia and frequent premature ventricular contractions: a case report.

Syncope associated with bradycardia and ventricular arrhythmia is an indication of cardiac intervention. However, in adolescent patients with anorexia nervosa, the management of syncope and arrhythmia can be different. We present a case of a 17-year-old boy who was admitted to the hospital because of syncope during exercise. Electrocardiographic monitoring showed that his mean heart rate was 41 beats/minute, with many long pauses and frequent premature ventricular contractions. These results suggested that the syncope was probably caused by arrythmia. He had been on a diet and had lost 20 kg in the past 6 months, with a body mass index of only 15.3 kg/m2. He was diagnosed with anorexia nervosa. Pacemaker implantation or ablation was not performed. Refeeding therapy was performed with mirtazapine. A follow-up showed a stepwise increase in his heart rate and a stepwise decrease in premature ventricular contractions, with an increase in his body weight. The findings from this case show that vagal hyperactivity associated with anorexia nervosa might lead to multiple premature ventricular contractions and bradycardia.

Cardioprotective Action of Glycyrrhizin on Diabetic Rats with Myocardial Remodeling.

Introduction: Cardiovascular disorders are one of the prominent causes of risks of mortality which accounts for high rate of the deaths at a global level. The risk of deadly myocardial infraction grows because of diabetes which even causes the development of heart failure. Objective: The objective of this study was to understand and study the effect of glycyrrhizin on diabetes suffering rats with myocardial remodeling. Materials and Methods: Streptozotocin was used for induction of diabetes, and 8-12 weeks later, the assessment of inflammation, fibrosis, and cardiac damage was evaluated. Histopathological analysis and immunohistochemistry was performed to analyze the effect in various groups. Western blotting was performed to understand the proteins expressed in diabetes, and also, their expression was noted in treatment groups. Results: There was a significant rise in TNF-α, dense fibrosis, and collagen deposits in the STZ diabetes group. The effects of hyperglycemia were significantly improved in the glycyrrhizin-treated group. DAPI, BrDu, and caspase staining was also performed to understand apoptosis in tissues where the diabetic groups reported significant apoptosis, while the effects were significantly lower in the treated group. Conclusion: All the observations indicate that glycyrrhizin has cardioprotective action in diabetic rats with myocardial remodeling and is due to the inhibition of the NF-κB signaling pathway in the myocardial layer.

Improvements in the primary culture of neonate rat myocardial cells by study of the mechanism of endoplasmic reticulum stress.

We previously found that endoplasmic reticulum stress (ERS) might be exhibited in the conventional protocol of the primary culture of neonate rat myocardial cells (NRMCs) and that the high glucose concentration (25 mmol/L) in the culture medium might be the cause. Here, we investigated if the high concentration of glucose might influence ERS in myocardial cells during culture. GRP78 expression (ERS marker) was similar in groups with tunicamycin (TM) and without TM in high glucose cultured cells (p > 0.01). Different glucose concentrations elicited different GRP78 expressions according to analyses of protein and RNA levels, which showed ERS in H/H groups. Finally, we found that GRP78 expression was higher in TM groups compared with M/M groups (p < 0.01). The conventional high-glucose culture media during primary culture of NRMCs induced ERS. We propose that medium-glucose culture media should be used and describe an improved protocol for the primary culture of NRMCs.

Inhibition of TNF-α by cyclophosphamide reduces myocardial injury after ischemia-reperfusion.

PURPOSE: The purpose of this study was to determine whether cyclophosphamide (CP) can decrease myocardial and systemic TNF-α expression and thus protects myocardial I/R injury. METHODS: Open chest rats were subjected to 30 min of ischemia followed by 3h, 12h or 24h of reperfusion. Rats were divided into sham group, I/R group and CP group, and each group included 3 timepoint subgroups (3h, 12h and 24h). Plasma TNF-α was measured by cytometric bead array (CBA) and immunohistochemistry was used to detect TNF-α in myocardium. RESULTS: Compared with I/R group, rats treated with CP showed a significant difference with decreased plasma TNF-α (13.31 ± 2.62 vs 14.13 ± 5.95 pg/mL at 3 h reperfusion, 10.1 ± 2.73 vs 12.54 ± 5.00 pg/mL at 12 h reperfusion, 10.38 ± 5.59 vs 13.00 ± 3.59 pg/mL at 24 h reperfusion, p <0.05 respectively). Immunostaining was less intense with CP injection at each reperfusion time. The score of the intensity of myocardial TNF-α staining was down regulated. CONCLUSIONS: TNF-α is expressed in the myocardium and plasma after myocardial I/R injury. CP might be a feasible strategy for anti-TNF-α to protect myocardial I/R injury.