Robinson R T C E, Harris N D, Ireland R H, Macdonald I A, Heller S R
University of Sheffield, UK.
Diabetologia. 2004 Feb;47(2):312-5. doi: 10.1007/s00125-003-1292-4. Epub 2004 Jan 8.
AIMS/HYPOTHESIS: Experimental hypoglycaemia leads to abnormal cardiac repolarization manifest by a lengthened QT interval and caused by adrenergic stimulation. However it is less clear whether spontaneous clinical episodes lead to similar changes. We have therefore measured cardiac ventricular repolarization and counterregulatory responses in patients with Type 1 diabetes during hypoglycaemic and euglycaemic nights.
We studied 22 patients with Type 1 diabetes (mean age 40.4+/-17.2 years, duration of diabetes 17.2+/-9.3 years, HbA1c 8.2+/-1.2% overnight). Measurements were taken hourly of blood glucose, plasma potassium, catecholamines and high resolution electrocardiograms.
Hypoglycaemia (blood glucose level <2.5 mmol/l) occurred on 7 of the 22 nights. During overnight hypoglycaemia, QTc interval increased by 27 ms (+/-15) above baseline, compared with 9 ms (+/-19) during nights with no nocturnal hypoglycaemia (p=0.034, 95%CI 2, 35). Adrenaline increased by 0.33 nmol/l (+/-0.21) above baseline during hypoglycaemia, compared with -0.05 nmol/l (+/-0.08) during euglycaemia (p=0.001, 95%CI 0.19, 0.56 nmol/l). There was no significant difference between potassium, and noradrenaline concentrations between the two groups.
CONCLUSION/INTERPRETATION: QTc interval lengthens significantly during spontaneous nocturnal hypoglycaemia. Increases are generally less than those observed during experimental hypoglycaemia and could reflect attenuated sympathoadrenal responses during clinical episodes. The clinical relevance of these changes is uncertain but is consistent with the hypothesis that clinical hypoglycaemia can cause abnormal cardiac repolarization and an attendant risk of cardiac arrhythmia.
目的/假设：实验性低血糖会导致心脏复极异常，表现为QT间期延长，且由肾上腺素能刺激引起。然而，尚不清楚自发性临床发作是否会导致类似变化。因此，我们测量了1型糖尿病患者在低血糖和血糖正常夜间的心室复极及对抗调节反应。
我们研究了22例1型糖尿病患者（平均年龄40.4±17.2岁，糖尿病病程17.2±9.3年，夜间糖化血红蛋白8.2±1.2%）。每小时测量血糖、血钾、儿茶酚胺及高分辨率心电图。
22个夜间中有7个出现低血糖（血糖水平<2.5 mmol/L）。夜间低血糖期间，QTc间期较基线增加27 ms（±15），而无夜间低血糖的夜间增加9 ms（±19）（p = 0.034，95%CI 2，35）。低血糖期间肾上腺素较基线增加0.33 nmol/L（±0.21），而血糖正常期间为-0.05 nmol/L（±0.08）（p = 0.001，95%CI 0.19，0.56 nmol/L）。两组间血钾和去甲肾上腺素浓度无显著差异。
结论/解读：自发性夜间低血糖期间QTc间期显著延长。延长幅度通常小于实验性低血糖期间观察到的幅度，这可能反映了临床发作期间交感肾上腺反应减弱。这些变化的临床相关性尚不确定，但与临床低血糖可导致心脏复极异常及随之而来的心律失常风险这一假设一致。
