Key result
Salbutamol-induced maximum changes in QTc showed no significant correlation with changes during hypoglycaemia in young people with Type 1 diabetes (r=0.15; 95% CI -0.341 to 0.576; P=0.553).
Why the study?
Does the magnitude of electrophysiological changes induced by salbutamol correlate with those induced by hypoglycaemia in individuals with Type 1 diabetes?
Does the magnitude of electrophysiological changes induced by salbutamol correlate with those induced by hypoglycaemia in individuals with Type 1 diabetes?
Effect estimate: r = 0.15 (95% CI -0.341 to 0.576)
p-value: p=0.553
Salbutamol cannot be used as a non-invasive screening tool to predict an individual's pro-arrhythmogenic electrophysiological response to hypoglycaemia.
Does not support salbutamol as QTc screening tool in T1D; leaves open alternative arrhythmia risk markers.
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.
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Novodvorský et al. (2018) studied Type 1 diabetes (n=18). Nebulized salbutamol and hyperinsulinaemic-hypoglycaemic clamp was evaluated on Linear dependence of maximum changes vs. baseline in QTc between salbutamol and hypoglycaemia (r = 0.15, 95% CI -0.341 to 0.576, p=0.553). Salbutamol-induced maximum changes in QTc showed no significant correlation with changes during hypoglycaemia in young people with Type 1 diabetes (r=0.15; 95% CI -0.341 to 0.576; P=0.553).
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