ESPE Abstracts (2019) 92 P1-29

What Hypoglycemia Does to the Heart: Impact of Nocturnal Hypoglycemia on Cardiac Repolarization in Diabetic Children

Sara Bachmann1, Anne Auderset2, Urs Zumsteg1, Gabor Szinnai1, Birgit Donner3 1University Children's Hospital Basel, Pediatric Endocrinology/Diabetology, Basel, Switzerland. 2University of Basel, Basel, Switzerland. 3University Children's Hospital Basel, Pediatric Cardiology, Basel, Switzerland

Background: Hypoglycemia is the most common and most feared complication of insulin treated diabetes. Though mostly asymptomatic, nocturnal hypoglycemia can be fatal in rare cases: sudden nocturnal death is more frequent in diabetic patients than in others. It is postulated that hypoglycemia related QTc prolongation contributes to cardiac arrhythmia and can lead to dead in bed.

Objective: To evaluate influence of nocturnal hypoglycemia on QTc in children with type 1 diabetes.

Patients and Methods: In 25 (11f, 14m) children with type 1 diabetes (mean age 13.5 y, range 8.1–17.5) continuous glucose monitoring (iProTM, Medtronic Minimed) was performed for 5 days, and simultaneously, holter ECG (Schiller) was recorded during each night. All subjects had normal cardiac findings in clinical examination/echocardiography and normal values for potassium, calcium and magnesium. No patient was under medication knowing to affect cardiac function or repolarization. Nocturnal hypoglycemia was defined as every period with a sensor glucose measurement below 3.7 mmol/l for at least 15minutes during documented nighttime. ECG was transferred to labchart and mean QTc was calculated by the Bazett formula for every episode of nocturnal hypoglycemia and compared to a period of the same duration preceding hypoglycemia.

Results: 41 episodes of nocturnal hypoglycemia were observed, 33 with ECG recording. Mean duration of hypoglycemia was 96min (range 15-365min). Nadir was below 3 mmol/l in 16 events and 3.0–3.7 mmol/l in 17 cases. No relevant cardiac arrhythmia was documented. However, mean QTc during hypoglycemia was significantly longer compared to normoglycemia (411+/–15 vs 405+/–18 ms, P=0.005).

These changes were not dependent on age, HbA1c, diabetes duration, duration or nadir of hypoglycemia. The increase in QTc though was more pronounced in subjects with lower magnesium levels (P=0.04).

Conclusion: This study evaluated changes in cardiac repolarization during nocturnal hypoglycemia. We could document a QTc lengthening and thereby potentially arrhythmogenic effect of nocturnal hypoglycemia in otherwise healthy children with diabetes. This is of special relevance in predisposed subjects or in the face of comedications. In such risk patients, nocturnal hypoglycemia has to be avoided even more aggressively. Based on these findings, it may be reasonable to perform a resting ECG in diabetic children. As higher magnesium values could have a protective effect, testing of these levels should also be considered.

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