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AIMS: Fasting periods represent a significant challenge for glycaemic control in hospitalised patients. The study aims to evaluate the efficacy and safety of basal-bolus insulin therapy in managing glycaemia during fasting periods in hospitalised patients with type 2 diabetes. MATERIALS AND METHODS: We performed a post-hoc analysis of two prospective, uncontrolled interventional trials that applied electronic decision support system guided basal-bolus (meal-related and correction) insulin therapy. We searched for fasting periods (invasive or diagnostic procedures, medical condition) during inpatient stays. In a mixed-model analysis, patients' glucose levels and insulin doses on days with regular food intake were compared to days with fasting periods. RESULTS: Out of 249 patients, 115 patients (33.9% female, age 68.3±10.3 years, diabetes duration 15.1±10.9 years, BMI 30.1±5.4 kg/m2 , HbA1c 69±20 mmol/mol) had 194 days with fasting periods. Mean daily blood glucose was lower (Modelled difference (ModDiff): -0.5±0.2 mmol/L, p=0.006), and the proportion of glucose values within the target range (3.9-10.0 mmol/L) increased on days with fasting periods compared to days with regular food intake (ModDiff: +0.06±0.02, p=0.005). Glycaemic control on fasting days was driven by a reduction in daily bolus insulin doses (ModDiff: -11.0±0.9 IU, p

A healthy woman with acute onset of pulmonary oedema and severely depressed left ventricular function underwent endomyocardial biopsy under the clinical suspicion of fulminant myocarditis. While awaiting the results of biopsy, the situation deteriorated to Interagency Registry for Mechanically Assisted Circulatory Support (INTERMACS) and extracorporeal membrane oxygenation was implanted. Finally, immunohistochemistry in biopsy specimen corresponded to fulminant lymphocytic myocarditis, although active myocarditis was excluded. Furthermore, gene expression profiling identified giant cell myocarditis although multinuclear cells were absent. This prompted the start of immunosuppression with cortisone and cyclosporine. The patient fully recovered.

Background: Metoprolol is a beta1-selective beta-adrenergic antagonist while carvedilol is a non-selective beta-blocker with additional blockades of alpha1-adrenoceptors. Administration of metoprolol has been shown to cause up-regulation of beta-adrenoceptor density and to decrease nocturnal melatonin release, whereas carvedilol lacks these typical effects of beta-blocking drugs. Aims: To compare beta-blocking effects of metoprolol and carvedilol when applied orally in healthy subjects. Methods: We investigated the effects of single oral doses of clinically recommended amounts of metoprolol (50, 100 and 200 mg) and carvedilol (25, 50 and 100 mg) to those of a placebo in a randomised, double-blind, cross-over study in 12 healthy male volunteers. Two hours after oral administration of the drugs heart rate and blood pressure were measured at rest, after 10 min of exercise, and after 15 min of recovery. Results: Metoprolol tended to decrease heart rate during exercise (−21%, −25% and −24%) to a greater extent than carvedilol (−16%, −16% and −18%). At rest, increasing doses of metoprolol caused decreasing heart rates (62, 60 and 58 beats/min) whereas increasing doses of carvedilol caused increasing heart rates (62, 66 and 69 beats/min), 50 and 100 mg carvedilol failed to differ significantly from the placebo (71 beats/min). Conclusions: We conclude that clinically recommended doses of carvedilol cause a clinically relevant beta-blockade in humans predominantly during exercise where it appears to be slightly (although not significantly) less effective than metoprolol. On the other hand, the effects of carvedilol on heart rate at rest appear rather weak, particularly in subjects with a low sympathetic tone. This might be caused by a reflex increase on sympathetic drive secondary to peripheral vasodilation resulting from the alpha-blocking effects of the drug. These results might be helpful in explaining why carvedilol, in contrast to metoprolol, may fail to cause up-regulation of beta-adrenoceptor density and does not decrease nocturnal melatonin release. This, in turn, may be a reason for the weak side-effects of carvedilol resulting from the beta-blockade. In addition, our data might be of interest in the interpretation of the forthcoming results of the COMET trial, although it has to be emphasised that they were derived from healthy subjects and, therefore, cannot be directly extrapolated to patients with heart failure.