Abstract
AimsHypoglycaemia 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.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 (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.ResultsSalbutamol administration caused QT c and TpTend prolongation and a decrease in Tamp and Tsym. Hypoglycaemia caused increased plasma catecholamines, hypokalaemia, QT c and TpTend prolongation, and a decrease in Tamp and Tsym. 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), 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.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.
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