Salbutamol-induced electrophysiological changes show no correlation with electrophysiological changes during hyperinsulinaemic-hypoglycaemic clamp in young people with Type 1 diabetes.

AIMS

Hypoglycaemia causes QT-interval prolongation and appears pro-arrhythmogenic. Salbutamol, a β -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 (QT ), T-wave amplitude (T ), T-peak to T-end interval duration (T T ) and T-wave area symmetry (T ). The maximum changes vs. baseline in both experiments were assessed for their linear dependence.

RESULTS

Salbutamol administration caused QT and T T prolongation and a decrease in T and T . Hypoglycaemia caused increased plasma catecholamines, hypokalaemia, QT and T T prolongation, and a decrease in T and T . No significant correlations were found between maximum changes in QT [r = 0.15, 95% confidence interval (95% CI) -0.341 to 0.576; P = 0.553), T T (r = 0.075, 95% CI -0.406 to 0.524; P = 0.767), T (r = 0.355, 95% CI -0.132 to 0.706; P = 0.149) or T (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.