Regression and progression of cardiac sympathetic dysinnervation complicating diabetes: an assessment by C-11 hydroxyephedrine and positron emission tomography.
Regression and progression of cardiac sympathetic dysinnervation complicating diabetes: an assessment by C-11 hydroxyephedrine and positron emission tomography.
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DOI：
10.1016/s0026-0495(99)90016-1
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发表时间：
1999
期刊：
影响因子：
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通讯作者：
M. Stevens;M. Stevens;D. Raffel;D. Raffel;K. Allman;K. Allman;M. Schwaiger;M. Schwaiger;D. Wieland;D. Wieland
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文献类型：
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作者：
M. Stevens;M. Stevens;D. Raffel;D. Raffel;K. Allman;K. Allman;M. Schwaiger;M. Schwaiger;D. Wieland;D. Wieland
心血管失神经支配并发糖尿病可能通过改变心肌电稳定性和损害心肌血流而与心源性猝死有关。在无症状的糖尿病患者中，心脏交感神经完整性的星形图评估经常显示出左心室远端交感神经支配的缺陷，而心血管反射试验没有异常。然而，这些小的局部缺陷的临床意义和随后的命运是未知的。本研究报告了一项前瞻性观察研究的结果，该研究使用正电子发射断层扫描（PET）和(-)-[11C]-间羟麻黄碱（[11C]- hed）来评估血糖控制对11名胰岛素依赖性糖尿病患者小区域LV [11C]- hed保留缺陷进展的影响，研究时间为3年。根据受试者在此期间的血糖控制情况分为两组：A组有6例血糖控制良好（个体平均HbA1c < 8%）， B组有5例血糖控制不良（个体平均HbA1c≥8%）。比较10名年龄匹配的健康非糖尿病受试者区域[11C]-HED潴留的参考值变化。基线时，A组和B组[11C]-HED保留异常分别影响7.3%±1.4%和9.9%±6.6%的左室，最大的左室[11C]-HED保留缺陷累及远端心肌节段。在A组的最终评估中，[11C]-HED保留缺陷的程度下降到仅涉及1.7%±0.7%的左室（P < 0.05 v基线扫描），[11C]-HED保留在远端和近端心肌节段均显著增加。相比之下，在血糖控制较差的B组中，[11C]-HED缺陷的程度增加到左室的34%±3.5%（基线P < 0.01 v），远端节段[11C]-HED保留指数显著降低（基线和最终评估时[11C]-HED保留指数分别为0.066±0.003 v 0.057±0.002,P < 0.05）。血糖控制不良与LV [11C]-HED潴留的异质性增加有关，因为5名B组受试者中有3名在近端心肌节段出现了异常的[11C]-HED潴留。综上所述，糖尿病患者血糖控制良好或较差时，左室交感神经缺损可退行或进展。在早期心血管失神经的糖尿病患者中，良好的血糖控制可以预防心肌交感神经障碍的发生和心脏风险的增加。
Cardiovascular denervation complicating diabetes has been implicated in sudden cardiac death potentially by altering myocardial electrical stability and impairing myocardial blood flow. Scintigraphic evaluation of cardiac sympathetic integrity has frequently demonstrated deficits in distal left ventricular (LV) sympathetic innervation in asymptomatic diabetic subjects without abnormalities on cardiovascular reflex testing. However, the clinical significance and subsequent fate of these small regional defects is unknown. This study reports the results of a prospective observational study in which positron emission tomography (PET) with (—)-[11C]-meta-hydroxyephedrine ([11C]-HED) was used to evaluate the effects of glycemic control on the progression of small regional LV [11C]-HED retention deficits in 11 insulin-dependent diabetic subjects over a period of 3 years. The subjects were divided into two groups based on attained glycemic control during this period: group A contained six subjects with good glycemic control (individual mean HbA1c < 8%), and group B contained five subjects with poor glycemic control (individual mean HbA1c ≥ 8%). Changes in regional [11C]-HED retention were compared with reference values obtained from 10 healthy aged-matched nondiabetic subjects. At baseline, abnormalities of [11C]-HED retention affected 7.3% ± 1.4% and 9.9% ± 6.6% of the LV in group A and B subjects, respectively, with maximal deficits of LV [11C]-HED retention involving the distal myocardial segments. At the final assessment in group A, the extent of the deficits in [11C]-HED retention decreased to involve only 1.7% ± 0.7% of LV (P < .05v baseline scan), with significant increases in [11C]-HED retention occurring in both the distal and proximal myocardial segments. In contrast, in group B with poor glycemic control, the extent of [11C]-HED deficits increased to involve 34% ± 3.5% of the LV (P < .01 v baseline), with retention of [11C]-HED significantly decreasing in the distal segments ([11C]-HED retention index, 0.066 ± 0.003 v 0.057 ± 0.002, P < .05, at baseline and final assessment, respectively). Poor glycemic control was associated with increased heterogeneity of LV [11C]-HED retention, since three of five group B subjects developed abnormally increased [11C]-HED retention in the proximal myocardial segments. In conclusion, defects in LV sympathetic innervation can regress or progress in diabetic subjects achieving good or poor glycemic control, respectively. In diabetic subjects with early cardiovascular denervation, institution of good glycemic control may prevent the development of myocardial sympathetic dysinnervation and enhanced cardiac risk.