Catheter Balloon Adjustment of the Pulmonary Artery Band: Feasibility and Safety

The study aimed to assess the feasibility and safety of increasing pulmonary artery band (PAB) diameter by catheter-based PAB balloon dilation (PABBD). Eight dilations were performed between October 2006 and December 2008. Hemoclips were used to fix PABs surgically in a procedure designed to permit progressive clip dislodgment in a controlled manner. The PABBD resulted in gradual band loosening until the desired physiologic state was achieved. At time of PABBD, the patients had a mean age of 6 months (range 3–14 months) and a mean weight of 5 kg (range 2.6–7.3 kg). The median time from PAB placement until PABBD was 4.5 months (range 1–9 months). The single-balloon technique was used in seven cases (serial dilations in 5 cases) and the double-balloon technique in one case. The PABBDs were successful for all the patients, who experienced a mean saturation increase of 75–89% (P = 0.01) (mean increase of 20%), a mean PAB gradient decrease from 69 to 36 mmHg (P = 0.002) (mean decrease of 49%), and a mean band site diameter increase from 4.1 to 6.1 mm (P = 0.01) (mean increase of 45%). The only complication was transient pulmonary edema in one patient. The PABBD procedure is a feasible and safe method for increasing pulmonary blood flow in a staged manner and may eliminate the need for surgical band removal in some cases

Cardiovascular magnetic resonance of pulmonary artery growth and ventricular function after Norwood procedure with Sano modification

For hypoplastic left heart syndrome (HLHS), there have been concerns regarding pulmonary artery growth and ventricular dysfunction after first stage surgery consisting of the Norwood procedure modified with a right ventricle-to-pulmonary artery conduit. We report our experience using cardiovascular magnetic resonance (CMR) to determine and follow pulmonary arterial growth and ventricular function in this cohort

Creatine Protects against Excitoxicity in an In Vitro Model of Neurodegeneration

Creatine has been shown to be neuroprotective in aging, neurodegenerative conditions and brain injury. As a common molecular background, oxidative stress and disturbed cellular energy homeostasis are key aspects in these conditions. Moreover, in a recent report we could demonstrate a life-enhancing and health-promoting potential of creatine in rodents, mainly due to its neuroprotective action. In order to investigate the underlying pharmacology mediating these mainly neuroprotective properties of creatine, cultured primary embryonal hippocampal and cortical cells were challenged with glutamate or H2O2. In good agreement with our in vivo data, creatine mediated a direct effect on the bioenergetic balance, leading to an enhanced cellular energy charge, thereby acting as a neuroprotectant. Moreover, creatine effectively antagonized the H2O2-induced ATP depletion and the excitotoxic response towards glutamate, while not directly acting as an antioxidant. Additionally, creatine mediated a direct inhibitory action on the NMDA receptor-mediated calcium response, which initiates the excitotoxic cascade. Even excessive concentrations of creatine had no neurotoxic effects, so that high-dose creatine supplementation as a health-promoting agent in specific pathological situations or as a primary prophylactic compound in risk populations seems feasible. In conclusion, we were able to demonstrate that the protective potential of creatine was primarily mediated by its impact on cellular energy metabolism and NMDA receptor function, along with reduced glutamate spillover, oxidative stress and subsequent excitotoxicity