Rl (mL blood/minute/mL tissue)
Fig. 1. HED-PET images demonstrating advanced cardiac sympathetic dysinnervation. (A) Top panels show the blood flow images, which are normal. However in the lower panels, the [11C]HED retention deficits are extensive with only the proximal cardiac segments demonstrating retained tracer retention, consistent with "islands" of innervation. (B) Retention of LV [11C]HED is globally decreased in a subject with microangiopathy. Retention of LV [11C]HED (expressed as a Retention Index [RI]) is globally reduced in a subject early background retinopathy and normal autonomic reflex tests (open plot), compared with the values obtained in a healthy nondiabetic control population (shaded plot).
abnormalities of autonomic reflex testing (23,27,29). Retention of [123I]-MIBG in the heart can be abnormal in metabolically compromised newly diagnosed subjects with type 1 diabetes, which are partially correctable by intensive insulin therapy (32). These defects most likely reflect acute neuronal dysfunction. In contrast, there are significantly fewer reports utilizing [11C]HED, and these are mostly restricted to subjects with type 1 diabetes. In type 1 diabetes, deficits of [11C]HED retention effecting upto about 10% of the left ventricle have been reported in 40% of healthy subjects without deficits of autonomic reflex testing (29). These small deficits typically begin distally in the LV in the infero-lateral walls, and with progression of CAN spread proximally and circumfer-entially, and might in some subjects eventually result in islands of basal increased [11C]HED retention (29) (Fig. 1, Panel A). However, a different pattern of reduced [11C]HED retention has recently been reported in a subset of asymptomatic subjects with type 1 diabetes (4). In these subjects, extensive global deficits of LV [11C]HED retention were observed, despite good glycemic control indicating an etiology other than neuronal loss or acute hyperglycemia-induced neuronal dysfunction (Fig. 1, Panel B).
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