Langer A, Freeman M R, Josse R G, Armstrong P W
Department of Medicine, St. Michael's Hospital, University of Toronto, Ontario, Canada.
J Am Coll Cardiol. 1995 Mar 1;25(3):610-8. doi: 10.1016/0735-1097(94)00459-4.
This study in patients with diabetes mellitus was undertaken 1) to evaluate cardiac sympathetic innervation in diabetic patients using metaiodobenzylguanidine (MIBG) imaging; 2) to study the relation between autonomic function assessed by clinical maneuvers and abnormalities in MIBG uptake; and 3) to examine the basis for our previous observation of an association between abnormalities in autonomic nervous system dysfunction and silent myocardial ischemia.
The clinical detection of autonomic dysfunction in diabetes mellitus has been linked to both abnormal perception of pain, including angina, and poor prognosis.
Uptake of MIBG was measured by dual-isotope imaging in 23 normal subjects and 65 asymptomatic diabetic patients. Silent myocardial ischemia was defined as the presence of a reversible perfusion defect in patients with ST segment depression.
The MIBG uptake in the diabetic patients was significantly lower than that in normal subjects in the apex (67 +/- 17% vs. 82 +/- 7%, p = 0.0001), distal third (77 +/- 11% vs. 85 +/- 3%, p = 0.0001), proximal third (77 +/- 9% vs. 84 +/- 3%, p = 0.0001) and base (71 +/- 9% vs. 80 +/- 4%, p = 0.0001) of the left ventricle. Similarly, MIBG uptake was variable across different vascular territories. When MIBG uptake was corrected for perfusion abnormalities, diabetic patients had a greater MIBG uptake defect than normal subjects on visual score assessment (16 +/- 13 vs. 8 +/- 7%, p = 0.0002) and on quantitative MIBG mismatch assessment (13 +/- 15% vs. 2 +/- 2%, p = 0.0001). Diabetic patients with versus without autonomic dysfunction had more extensive MIBG uptake mismatch (17 +/- 17% vs. 4 +/- 6%, p = 0.0001). There was a greater diffuse abnormality in diabetic patients with versus without silent myocardial ischemia detected by sestamibi/MIBG uptake ratio (68 +/- 35% vs. 19 +/- 33%, p = 0.001).
Sympathetic cardiac innervation in normal subjects is inhomogeneous. In contrast to normal subjects, diabetic patients have evidence of a significant reduction in MIBG uptake, most likely on the basis of autonomic dysfunction. Furthermore, diabetic patients with silent myocardial ischemia have evidence of a diffuse abnormality in MIBG uptake, suggesting that abnormalities in pain perception may be linked to sympathetic denervation.
本研究针对糖尿病患者开展，旨在：1）使用间碘苄胍（MIBG）显像评估糖尿病患者的心脏交感神经支配情况；2）研究通过临床操作评估的自主神经功能与MIBG摄取异常之间的关系；3）探究我们之前观察到的自主神经系统功能障碍异常与无症状心肌缺血之间关联的依据。
糖尿病自主神经功能障碍的临床检测与包括心绞痛在内的疼痛感知异常及不良预后均有关联。
通过双同位素显像测量23名正常受试者和65名无症状糖尿病患者的MIBG摄取情况。无症状心肌缺血定义为ST段压低患者存在可逆性灌注缺损。
糖尿病患者左心室心尖部（67±17%对82±7%，p = 0.0001）、下三分之一处（77±11%对85±3%，p = 0.0001）、上三分之一处（77±9%对84±3%，p = 0.0001）及心底（71±9%对80±4%，p = 0.0001）的MIBG摄取显著低于正常受试者。同样，不同血管区域的MIBG摄取也存在差异。当对灌注异常进行校正后，在视觉评分评估（16±13对8±7%，p = 0.0002）和定量MIBG不匹配评估（13±15%对2±2%，p = 0.0001）中，糖尿病患者的MIBG摄取缺损均大于正常受试者。有自主神经功能障碍的糖尿病患者与无自主神经功能障碍的糖尿病患者相比，MIBG摄取不匹配情况更广泛（17±17%对4±6%，p = 0.0001）。通过 sestamibi/MIBG摄取比值检测，有无症状心肌缺血的糖尿病患者与无无症状心肌缺血的糖尿病患者相比，弥漫性异常更明显（68±35%对19±33%，p = 0.001）。
正常受试者的心脏交感神经支配不均匀。与正常受试者不同，糖尿病患者有证据表明MIBG摄取显著降低，很可能是基于自主神经功能障碍。此外，有无症状心肌缺血的糖尿病患者有MIBG摄取弥漫性异常的证据，提示疼痛感知异常可能与交感神经去神经支配有关。
