Hypoglycaemia remains an inevitable risk in insulin-treated type 1 diabetes and type 2 diabetes and has been associated with multiple adverse outcomes. Whether hypoglycaemia is a cause of fatal cardiac arrhythmias in diabetes, or merely a marker of vulnerability, is still unknown. Since a pivotal report in 1991, hypoglycaemia has been suspected to induce cardiac arrhythmias in patients with type 1 diabetes, the so-called ‘dead-in-bed syndrome’. This suspicion has subsequently been supported by the coexistence of an increased mortality and a three-fold increase in severe hypoglycaemia in patients with type 2 diabetes receiving intensive glucose-lowering treatment in the Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial. Studies have investigated the association between hypoglycaemia-induced cardiac arrhythmias. In a rat-model, severe hypoglycaemia resulted in a specific pattern of cardiac arrhythmias including QT-prolongation, ventricular tachycardia, second- and third-degree AV block and ultimately cardiorespiratory arrest. In clinical studies of experimentally induced hypoglycaemia, QTc-prolongation, a risk factor of ventricular arrhythmias, is an almost consistent finding. The extent of QT-prolongation seems to be modified by several factors, including antecedent hypoglycaemia, diabetes duration and cardiac autonomic neuropathy. Observational studies indicate diurnal differences in the pattern of electrocardiographic alterations during hypoglycaemia with larger QTc-prolongations during daytime, whereas the risk of bradyarrhythmias may be increased during sleep. Daytime periods of hypoglycaemia are characterized by shorter duration, increased awareness and a larger increase in catecholamines. The counterregulatory response is reduced during nightly episodes of hypoglycaemia, resulting in prolonged periods of hypoglycaemia with multiple nadirs. An initial sympathetic activity at plasma glucose nadir is replaced by increased vagal activity, which results in bradycardia. Here, we provide an overview of the existing literature exploring potential mechanisms for hypoglycaemia-induced cardiac arrhythmias and studies linking hypoglycaemia to cardiac arrhythmias in patients with diabetes.

低血糖仍然是胰岛素治疗的 1 型糖尿病和 2 型糖尿病不可避免的风险，并与多种不良后果相关。低血糖是否是糖尿病患者致命性心律失常的一个原因，或者仅仅是脆弱性的标志，目前仍不清楚。自 1991 年的一份关键报告以来，低血糖一直被怀疑会导致 1 型糖尿病患者出现心律失常，即所谓的“卧床不起综合症”。在控制糖尿病心血管风险行动 (ACCORD) 试验中，接受强化降糖治疗的 2 型糖尿病患者死亡率增加，严重低血糖增加三倍，这一结果证实了这一怀疑。研究调查了低血糖引起的心律失常之间的关联。在大鼠模型中，严重低血糖导致特定模式的心律失常，包括 QT 延长、室性心动过速、二度和三度房室传导阻滞以及最终的心肺骤停。在实验性低血糖的临床研究中，QTc 延长（室性心律失常的危险因素）几乎是一致的发现。 QT 延长的程度似乎会受到多种因素的影响，包括既往低血糖、糖尿病病程和心脏自主神经病变。观察性研究表明，低血糖期间心电图变化模式存在昼夜差异，白天 QTc 延长较大，而睡眠期间发生缓慢性心律失常的风险可能会增加。白天低血糖的特点是持续时间较短、意识增强以及儿茶酚胺增加较多。 在夜间低血糖发作期间，反调节反应会减弱，导致低血糖持续时间延长并出现多个最低点。血浆葡萄糖最低点的初始交感神经活动被迷走神经活动增加所取代，从而导致心动过缓。在这里，我们概述了现有文献，探索低血糖诱发心律失常的潜在机制，以及将低血糖与糖尿病患者心律失常联系起来的研究。