Salbutamol-Induced Electrophysiological Changes Show No Correlation With Electrophysiological Changes During Hyperinsulinaemic-Hypoglycaemic Clamp In Young People With Type 1 Diabetes

AimsHypoglycaemia causes QT-interval prolongation and appears pro-arrhythmogenic. Salbutamol, a (2)-adrenoreceptor agonist also causes QT-interval prolongation. We hypothesized that the magnitude of electrophysiological changes induced by salbutamol and hypoglycaemia might relate to each other and that salbutamol could be used as a non-invasive screening tool for predicting an individual's electrophysiological response to hypoglycaemia.MethodsEighteen individuals with Type 1 diabetes were administered 2.5 mg of nebulized salbutamol. Participants then underwent a hyperinsulinaemic-hypoglycaemic clamp (2.5 mmol/l for 1 h). During both experiments, heart rate and serum potassium (and catecholamines during the clamp) were measured and a high-resolution electrocardiogram (ECG) was recorded at pre-set time points. Cardiac repolarization was measured by QT-interval duration adjusted for heart rate (QT(c)), T-wave amplitude (T-amp), T-peak to T-end interval duration (TpTend) and T-wave area symmetry (T-sym). The maximum changes vs. baseline in both experiments were assessed for their linear dependence.ResultsSalbutamol administration caused QT(c) and TpTend prolongation and a decrease in T-amp and T-sym. Hypoglycaemia caused increased plasma catecholamines, hypokalaemia, QT(c) and TpTend prolongation, and a decrease in T-amp and T-sym. No significant correlations were found between maximum changes in QT(c) [r = 0.15, 95% confidence interval (95% CI) -0.341 to 0.576; P = 0.553), TpTend (r = 0.075, 95% CI -0.406 to 0.524; P = 0.767), T-sym (r = 0.355, 95% CI -0.132 to 0.706; P = 0.149) or T-amp (r = 0.148, 95% CI -0.347 to 0.572; P = 0.558) in either experiment.ConclusionsBoth hypoglycaemia and salbutamol caused pro-arrhythmogenic electrophysiological changes in people with Type 1 diabetes but were not related in any given individual. Salbutamol does not appear useful in assessing an individual's electrophysiological response to hypoglycaemia.