Salbutamol‐induced electrophysiological changes show no correlation with electrophysiological changes during hyperinsulinaemic–hypoglycaemic clamp in young people with Type 1 diabetes |
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| Authors: | P. Novodvorsky A. Bernjak E. J. Robinson A. Iqbal I. A. Macdonald R. M. Jacques J. L. B. Marques P. J. Sheridan S. R. Heller |
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| Affiliation: | 1. Department of Oncology and MetabolismUniversity of Sheffield;2. Sheffield Teaching Hospitals NHS Foundation Trust;3. INSIGNEO Institute for in silico Medicine;4. Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield, Sheffield;5. School of Life Sciences, University of Nottingham, Nottingham;6. School of Health and Related Research, University of Sheffield, Sheffield, UK |
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| Abstract: | Aims Hypoglycaemia causes QT‐interval prolongation and appears pro‐arrhythmogenic. Salbutamol, a β2‐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. Methods Eighteen 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 (QTc), T‐wave amplitude (Tamp), T‐peak to T‐end interval duration (TpTend) and T‐wave area symmetry (Tsym). The maximum changes vs. baseline in both experiments were assessed for their linear dependence. Results Salbutamol administration caused QTc and TpTend prolongation and a decrease in Tamp and Tsym. Hypoglycaemia caused increased plasma catecholamines, hypokalaemia, QTc and TpTend prolongation, and a decrease in Tamp and Tsym. No significant correlations were found between maximum changes in QTc [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), Tsym (r = 0.355, 95% CI ?0.132 to 0.706; P = 0.149) or Tamp (r = 0.148, 95% CI ?0.347 to 0.572; P = 0.558) in either experiment. Conclusions Both 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. |
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