Ziegler D, Weise F, Langen K J, Piolot R, Boy C, Hübinger A, Müller-Gärtner H W, Gries F A
Diabetes Research Institute at the Heinrich Heine University, Düsseldorf, Germany.
Diabetologia. 1998 Apr;41(4):443-51. doi: 10.1007/s001250050928.
Diabetic cardiovascular autonomic neuropathy (CAN) has been directly characterized by reduced or absent myocardial [123I]metaiodobenzylguanidine (MIBG) uptake, but there is no information available on the relationship between the myocardial adrenergic innervation defects and long-term glycaemic control. In a prospective study over a mean of 4 years we examined myocardial sympathetic innervation in 12 Type 1 (insulin-dependent) diabetic patients using MIBG scintigraphy (absolute and relative global MIBG uptake at 2 h p.i.) in conjunction with cardiovascular autonomic function tests, QTc interval, and QT dispersion. Six healthy non-diabetic subjects served as controls for the MIBG scintigraphy at baseline. HbA1c was measured twice a year. One patient, in whom MIBG accumulation was reduced maximally, died during follow up. Among the remaining patients 5 had good or borderline glycaemic control (mean HbA1c < 7.6%; Group 1), whereas 6 patients were poorly controlled (mean HbA1c > or = 7.6%; Group 2). Absolute global MIBG uptake increased from baseline to follow-up by 260 (-190-540) [median (range)] cpm/g in Group 1 and decreased by -150 (-450-224) cpm/g in Group 2 (p < 0.05 vs Group 1). Relative global MIBG uptake decreased by -1.7 (-3.4-9.4) % in Group 1 and by -4.7 (-17.4-1.3) % in Group 2 (p < 0.05 vs Group 1). No differences between the groups were noted for the changes in the automatic function tests, QTc interval, and QT dispersion. In conclusion, long-term poor glycaemic control constitutes an essential determinant in the progression of left ventricular adrenergic dysinnervation which may be prevented by near-normoglycaemia. Evaluation of susceptibility to metabolic intervention may be superior when CAN is characterized directly by MIBG scintigraphy rather than by indirect autonomic function testing.
糖尿病性心血管自主神经病变（CAN）的直接特征是心肌[123I]间碘苄胍（MIBG）摄取减少或缺失，但关于心肌肾上腺素能神经支配缺陷与长期血糖控制之间的关系尚无可用信息。在一项平均为期4年的前瞻性研究中，我们使用MIBG闪烁显像（静脉注射后2小时的绝对和相对整体MIBG摄取），结合心血管自主功能测试、QTc间期和QT离散度，对12例1型（胰岛素依赖型）糖尿病患者的心肌交感神经支配进行了检查。6名健康非糖尿病受试者作为基线时MIBG闪烁显像的对照。每年测量两次糖化血红蛋白（HbA1c）。1例MIBG摄取最大程度降低的患者在随访期间死亡。在其余患者中，5例血糖控制良好或临界（平均HbA1c<7.6%；第1组），而6例患者控制不佳（平均HbA1c≥7.6%；第2组）。第1组的绝对整体MIBG摄取从基线到随访增加了260（-190-540）[中位数（范围）]cpm/g，第2组减少了-150（-450-224）cpm/g（与第1组相比，p<0.05）。第1组的相对整体MIBG摄取降低了-1.7（-3.4-9.4）%，第2组降低了-4.7（-17.4-1.3）%（与第1组相比，p<0.05）。两组在自主功能测试、QTc间期和QT离散度的变化方面未发现差异。总之，长期血糖控制不佳是左心室肾上腺素能神经支配异常进展的重要决定因素，接近正常血糖水平可能预防这种情况。当通过MIBG闪烁显像直接而非间接自主功能测试来表征CAN时，对代谢干预易感性的评估可能更优。
