Utility of cardiac MRI in paediatric myocarditis.

BACKGROUND: The diagnostic role of cardiac MRI in myocarditis is evolving, however with extremely limited data in paediatrics. The goal of this study was to assess the utility of cardiac MRI in paediatric myocarditis and present a new prognostic score for risk stratification. METHOD: The present study is a retrospective investigation of children with a clinical diagnosis of myocarditis, including analysis of demographics, clinical presentation, diagnostic studies, including cardiac MRI, and outcomes. RESULTS: A total of 44 patients met the inclusion criteria, of whom 20 had undergone cardiac MRI. Patients who underwent cardiac MRI were older (median 15.6 versus 11.1 years, p=0.004), had a shorter length of hospital stay (median 4.0 versus 12.5 days, p=0.004), had overall less-severe illness at presentation as evidenced by a higher left-ventricular ejection fraction on echocardiography, had lower peak brain-type natriuretic peptide, were less likely to require advanced mechanical support, and were less likely to experience cardiac death or transplant. In patients who had undergone cardiac MRI, the most common findings were increased early gadolinium enhancement (n=9) or late gadolinium enhancement (n=9). Cardiac MRI findings did not predict a worse outcome. Independent predictors of the need for heart-failure medications at 1-year follow-up included inotrope requirement, extracorporeal membrane oxygenator requirement, and antiarrhythmic requirement at presentation (p<0.05). CONCLUSION: In paediatric myocarditis, cardiac MRI is not used uniformly, has a low yield, and does not predict worse outcomes. Future research should evaluate clinical decision-making and the cost-benefit analysis of cardiac MRI in the diagnosis of paediatric myocarditis.

Prolonged feeding with green tea polyphenols exacerbates cholesterol-induced fatty liver disease in mice.

SCOPE: This study investigated the potential deleterious impact of dietary supplementation with green tea extract (GTE) on the progression of fatty liver disease, in a mouse model of cholesterol-induced steatohepatitis that represents chronic liver injury. METHODS AND RESULTS: Male C57BL mice (n = 32, 8-wk-old) were fed for 6 wk with one of the following diets: normal control diet (ND, Con), Con + 1% w/w polyphenols from GTE (Con + GTE); high cholesterol diet, Con + 1% cholesterol + 0.5% cholate w/w (HCD); HCD + 1% green tea polyphenols w/w (HCD + GTE). Hepatic steatosis, oxidative, and inflammatory markers and bile acid synthesis pathways were measured. HCD supplementation resulted in hepatic steatosis and liver damage. In animals supplemented with the HCD + GTE an exacerbated hepatic steatosis, oxidative stress, and inflammatory response were observed compared to HCD supplemented animals. HCD + GTE supplementation elevated blood levels of liver enzymes and serum bile acids compared HCD-treated animals. HCD + GTE supplementation altered bile acid synthesis in the cholesterol clearance pathway, inducing a shift from the classically regulated CYP7A1 pathway to the alternative acidic pathway. CONCLUSION: Prolonged GTE supplementation dramatically increased hepatic oxidative stress, inflammation and liver injury, and altered the bile acid synthesis pathway in mice fed a HCD.

[The pedicled groin flap for defect closure of the hand]. / Der gestielte Leistenlappen zur Defektdeckung an der Hand.

OBJECTIVE: Soft-tissue defect closure of the volar and dorsal aspect of the hand and lower arm with a maximum defect size of 10 × 25 cm. INDICATIONS: Soft-tissue defects of the entire palm and dorsum of the hand and lower arm with a maximum defect size of 10 × 25 cm. CONTRAINDICATIONS: Polytraumatized patients presenting with concomitant life-threatening injuries. In these cases one should perform the definite defect closure secondary after cardiovascular stabilization. Scars and vascular injury at the donor site. Lack of vascularity and necrosis of implantation site. Poorly vascularized recipient site (e.g. after radiation) Infection and necrosis at the donor and/or recipient site. Prior operations of the groin with impairment of the vasculature. Noncompliant patient. SURGICAL TECHNIQUE: Landmarks are the femoral artery, inguinal ligament, anterior superior iliac spine, and sartorius muscle. The superior and inferior border of the flap should be orientated parallel to the inguinal ligament. The longitudinal axis of the flap is parallel to the superficial circumflex iliac artery, which is partially located superior to the inguinal ligament. One third of the flap is located superior, and two thirds inferior, to the inguinal ligament. Flap dissection starts at the lateral border without including the fascia. Identification of the lateral border of the sartorius muscle, incision of its fascia and inclusion of the fascia into flap dissection in order to preserve the vessel. If a long flap pedicle is favored, flap dissection is continued to the source of the superficial circumflex iliac artery. Primary closure of the donor site and, finally, inset of the flap. A tubed pedicle protects the vessels and simplifies the ischemic preconditioning during the postoperative phase. According to the flap size, the donor site closure is either primary or split-thickness skin grafting is necessary at the lateral aspect of the donor site. The mean duration of the procedure is 120 min in a teaching hospital (own data). POSTOPERATIVE MANAGEMENT: The patient should be mobilized as early as possible. Dressings and flap monitoring should be performed daily. Ischemic preconditioning by applying a tourniquet starts after 10-14 days. The ischemic period is increased continuously from 3 × 5 min/d in the beginning to 3 × 1 h/d before flap dissection. Flap dissection of the pedicle is performed after 3 weeks. The residual donor site is closed, while the distal pedicle is left untrimmed and closed secondarily a few days later to allow for sufficient venous drainage. Finally, defect closure can be completed after demarcation of the pedicle. RESULTS: In a 3-year period, defect closure with a pedicled groin flap was performed in 14 patients. Indications for this procedure were the following: thumb reconstruction for lengthening and defect closure after amputation and burn injury, soft-tissue reconstruction of the dorsum of the hand after decollement and infection, soft-tissue reconstruction of the distal part of the lower arm, wrist and palm after complex and combined trauma, and plastic reconstructive preservation of multiple fingers with subsequent phalangealization and syndactyly release, respectively. In all patients, complete soft-tissue coverage and flap survival could be achieved. The functional and aesthetic result was satisfactory in all cases.

Ischemic preconditioning mediates cyclooxygenase-2 expression via nuclear factor-kappa B activation in mixed cortical neuronal cultures.

Nuclear factor-kappaB (NF-κB) activation occurs following ischemic preconditioning (IPC) in brain. However, the upstream signaling messengers and down-stream targets of NF-κB required for induction of IPC remain undefined. In a previous study, we demonstrated that epsilon protein kinase c (εPKC) was a key mediator of IPC in brain. Activation of εPKC induced cyclooygenase-2 (COX-2) expression and conferred ischemic tolerance in the neuronal and hippocampal slice models. Here, we hypothesized that IPC-mediated COX-2 expression was mediated by NF-κB. We tested this hypothesis in mixed cortical neuron/astrocyte cell cultures. To simulate IPC or ischemia, cell cultures were exposed to 1 or 4 h of oxygen-glucose deprivation, respectively. Our results demonstrated translocation of p65 and p50 subunits of NF-κB into nucleus following IPC or εPKC activation. NF-κB inhibition with pyrrolidine dithiocarbamate (10 µM) abolished IPC or εPKC activator-mediated neuroprotection indicating that NF-κB activation was involved in ischemic tolerance. In parallel studies, inhibition of either εPKC or the extracellular signal-regulated kinase (ERK 1/2) pathway reduced IPC-induced NF-κB activation. Finally, inhibition of NF-κB blocked IPC-induced COX-2 expression. In conclusion, we demonstrated that IPC-signaling cascade comprises εPKC activation→ERK1/2 activation→NF-κB translocation to nucleus→COX-2 expression resulting in neuroprotection in mixed neuronal culture.