Glycaemic rises after waking up in response to an alarm clock in type 1-diabetic patients analysed with continuous glucose monitoring (GlucoDay® S).

AIMS: Waking up in response to an alarm-clock may evoke a stress reaction that leads to rising glucose concentrations. METHOD: 30 type 1-diabetic patients participated in 3 overnight conditions: (a) with an alarm-clock set at 2 h intervals for glucose self monitoring, (b) with a nurse performing blood glucose determinations, and (c) with the patients left undisturbed. Continuous glucose monitoring (CGM) was performed with a GlucoDay® S device. RESULTS: After waking up in response to an alarm-clock, CGM-determined glucose concentrations rose by 18±6 mg/dl at 4 a.m. (p=0.0003), whereas negligible increments were seen with nurse assistance (e. g., 0±4 mg/dl at 4 a.m.). CONCLUSIONS: Waking up in response to an alarm-clock leads to an arousal reaction that causes significant elevations in glucose concentrations. Continuous glucose monitoring is a suitable method to detect such short-lived increments in glucose concentrations. But at the moment the CGMS is not able to substitute for inpatient glucose profiles.

Continuous glucose monitoring reveals associations of glucose levels with QT interval length.

BACKGROUND: QTc interval lengthening during hypoglycemia is discussed as a mechanism linked to sudden death in diabetes patients and the so-called "dead in bed syndrome." Previous research reported a high interindividual variability in the glucose-QTc association. The present study aimed at deriving parameters for direction and strength of the glucose-QTc association on the patient level using combined Holter electrocardiogram (ECG) and continuous glucose monitoring. METHODS: Twenty type 1 diabetes patients were studied: mean (SD, range) age, 43.6 (10.8, 22-65) years; gender male (n [%]), 10 (50.0%); mean (SD) hemoglobin A1C, 8.5% (1.0%); and impaired hypoglycemia awareness (n [%]), six (30.0%). Continuous interstitial glucose monitoring and Holter ECG monitoring were performed for 48 h. Hierarchical (mixed) regression modeling was used to account for the structure of the data. RESULTS: Glucose levels during nighttime were negatively associated with QTc interval length if the data structure was accounted for (b [SE] = -0.76 [0.17], P = 0.000). Exploratory regression analysis revealed hypoglycemia awareness as the only predictor of the individual strength of the glucose-QTc association, with the impaired awareness group showing less evidence for an association of low glucose with QTc lengthening. CONCLUSIONS: Mixed regression allows for deriving parameters for the glucose-QTc association on the patient level. Consistent with previous studies, we found a large interindividual variability in the glucose-QTc association. The finding on impaired hypoglycemia awareness patients has to be interpreted with caution but provides some support for the role of sympathetic activation for the QTc-glucose link.