Influence of autonomic neuropathy on QTc interval lengthening during hypoglycemia in type 1 diabetes
Influence of autonomic neuropathy on QTc interval lengthening during hypoglycemia in type 1 diabetes
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DOI：
10.2337/diabetes.53.6.1535
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发表时间：
2004-06-01
期刊：
影响因子：
7.7
通讯作者：
Heller, SR
中科院分区：
文献类型：
--
作者：
Lee, SP;Yeoh, L;Heller, SR
低血压导致心电图QTc延长，是心律失常风险和猝死的预测因素。这是交感-肾上腺激活和血清钾降低的结果。有人认为，心脏自主神经病变（CAN）可能表明那些谁是在特定的风险。我们在28名1型糖尿病成人和8名非糖尿病对照受试者中验证了这一假设。在自主神经功能和压力反射敏感性（BRS）测量的标准测试之后，糖尿病参与者被分为三组：1）CAN-具有正常BRS（BRS+; n = 10），2）CAN-具有受损BRS（BRS-; n = 9），和3）CAN+（n = 9）。然后使用高胰岛素钳夹在控制性低血糖（2.5 mmol/l）期间测量QTc。在BRS+受试者中，平均（+/- E）QTc从377 +/- 9 ms（基线）延长至低血糖期间的最大值439 +/- 13 ms，在对照受试者中从378 +/- 5延长至439 +/- 10 ms。CAN+组（基线，383 +/- 6;最大值，408 +/- 10）和BRS-组（基线，380 +/- 8;最大值，421 +/- 11; F = 1.7，P = 0.18）的峰值QTc往往较低。肾上腺素峰浓度（nmol/l）为3.1 +/- 0.8（BRS+）、2.6 +/- 0.5（BRS-）、1.4 +/- 0.3（CAN+）和5.7 +/- 0.8（对照受试者）。这些数据并不表明CAN患者在低血糖期间心脏复极异常的风险特别高。事实上，他们认为这些患者可能相对受到保护，这可能是由于交感-肾上腺反应减弱的结果。
Hypoglycemia produces electrocardiographic QTc lengthening, a predictor of arrhythmia risk and sudden death. This results from both sympatho-adrenal activation and a lowered serum potassium. It has been suggested that cardiac autonomic neuropathy (CAN) might indicate those who are at particular risk. We tested this hypothesis in 28 adults with type 1 diabetes and 8 nondiabetic control subjects. After standard tests of autonomic function and baroreflex sensitivity (BRS) measurement, diabetic participants were divided into three groups: 1) CAN- with normal BRS (BRS+; n = 10), 2) CAN- with impaired BRS (BRS-; n = 9), and 3) CAN+ (n = 9). QTc was then measured during controlled hypoglycemia (2.5 mmol/l) using a hyperinsulinemic clamp. Mean ( +/- E) QTc lengthened from 377 +/- 9 ms (baseline) to a maximum during hypoglycemia of 439 +/- 13 ms in BRS+ subjects and from 378 +/- 5 to 439 +/- 10 ms in control subjects. Peak QTc tended to be lower in CAN+ (baseline, 383 +/- 6; maximum, 408 +/- 10) and BRS- groups (baseline, 380 +/- 8; maximum, 421 +/- 11; F = 1.7, P = 0.18). Peak epinephrine concentrations (nmol/l) were 3.1 +/- 0.8 (BRS+), 2.6 +/- 0.5 (BRS-), 1.4 +/- 0.3 (CAN+), and 5.7 +/- 0.8 (control subjects). These data do not indicate that those with CAN are at particular risk for abnormal cardiac repolarization during hypoglycemia. Indeed, they suggest that such patients may be relatively protected, perhaps as a result of attenuated sympatho-adrenal responses.