Sympathetic dysfunction in type 1 diabetes
Association with impaired myocardial blood flow reserve and diastolic dysfunction
Rodica Pop-Busui, MD*, ,
Ian Kirkwood, MBBS*,
Helena Schmid, MD*,
Victor Marinescu, BS*,
Justin Schroeder, BS*,
Dennis Larkin, BS*,
Elina Yamada, MD ,
David M. Raffel, PhD and
Martin J. Stevens, MD*,*
* Endocrinology and Metabolism
Cardiology
Nuclear Medicine, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan
Division of Endocrinology and Metabolism, Department of Internal Medicine, Medical College of Ohio, Toledo, Ohio

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Figure 1 (A) Extent of left ventricular (LV) [11C]meta-hydroxyephedrine ([11C]HED) retention deficits in different subject groups. Normalized [11C]HED retention data are displayed as polar coordinate maps of relative tracer activity ([11C]/[13N]). The "extent" of the heterogeneity is expressed as the percentage of sectors in the polar map that are abnormal, i.e., zi >2.5. p < 0.01 early microangiopathy (DMA+) versus diabetic control subjects (DC). Horizontal bars = mean value. (B) Left ventricular [11C]HED retention is globally decreased in a DMA+ subject. Quantitative assessment of LV [11C]HED retention (expressed as a retention index [RI]) demonstrated reduced retention in all LV sectors in a DMA+ subject (open plot) compared with the values obtained in nondiabetic control subjects (shaded plot).
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Figure 2 Change in global myocardial blood flow reserve (MBFR) in response to adenosine infusion. [13N]ammonia positron emission tomography was used to explore MBF regulation in response to adenosine. p < 0.05 diabetic control subjects (DC) versus controls (C). p < 0.05 early microangiopathy (DMA+) versus C and DC. Horizontal bars = mean value.
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