Andersen Andreas, Jørgensen Peter G, Knop Filip K, Vilsbøll Tina
Steno Diabetes Center Copenhagen, Gentofte Hospital, Hellerup, Denmark.
Department of Cardiology, Herlev and Gentofte Hospital, University of Copenhagen, Hellerup, Denmark.
Ther Adv Endocrinol Metab. 2020 May 19;11:2042018820911803. doi: 10.1177/2042018820911803. eCollection 2020.
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,并且与多种不良后果相关。低血糖是糖尿病患者致命性心律失常的原因,还是仅仅是易感性的一个标志,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诱发1型糖尿病患者的心律失常,即所谓的“睡梦中死亡综合征”。随后,在糖尿病控制心血管风险行动(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以及严重低血糖增加三倍的情况支持了这一怀疑。已有研究探讨了低血糖诱发心律失常之间的关联。在大鼠模型中,严重低血糖会导致特定模式的心律失常,包括QT间期延长、室性心动过速、二度和三度房室传导阻滞,最终导致心肺骤停。在实验性诱发低血糖的临床研究中,QTc间期延长(室性心律失常的一个危险因素)几乎是一个一致的发现。QT间期延长的程度似乎受到几个因素的影响,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,低血糖期间心电图改变模式存在昼夜差异,白天QTc间期延长幅度更大,而夜间心律失常的风险可能增加。白天低血糖发作的特点是持续时间较短、意识增强和儿茶酚胺大幅增加。夜间低血糖发作期间,对抗调节反应减弱,导致低血糖持续时间延长且出现多个最低点。血浆葡萄糖最低点时最初的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。在此,我们概述了现有文献,探讨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。