Cargando…

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(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 an...

Descripción completa

Detalles Bibliográficos
Autores principales: Novodvorsky, P., Bernjak, A., Robinson, E. J., Iqbal, A., Macdonald, I. A., Jacques, R. M., Marques, J. L. B., Sheridan, P. J., Heller, S. R.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6099209/
https://www.ncbi.nlm.nih.gov/pubmed/29682793
http://dx.doi.org/10.1111/dme.13650
Descripción
Sumario:AIMS: Hypoglycaemia causes QT‐interval prolongation and appears pro‐arrhythmogenic. Salbutamol, a β(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. 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 (c)), T‐wave amplitude (T(amp)), T‐peak to T‐end interval duration (T(p)T(end)) and T‐wave area symmetry (T(sym)). The maximum changes vs. baseline in both experiments were assessed for their linear dependence. RESULTS: Salbutamol administration caused QT (c) and T(p)T(end) prolongation and a decrease in T(amp) and T(sym). Hypoglycaemia caused increased plasma catecholamines, hypokalaemia, QT (c) and T(p)T(end) 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), T(p)T(end) (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. 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.