Myocardial sympathetic innervation in patients with impaired glucose tolerance: relationship to subclinical inflammation

Aim tudy was designed to assess cardiac adrenergic nerve activity, using iodine (I)-123-labeled metaiodobenzylguanidine (MIBG), in patients with impaired glucose tolerance (IGT) and to investigate its relation to circulating levels of proinflammatory cytokines. s died 22 patients with IGT (aged 34–68 years) and 18 age-matched healthy controls, using I-123 MIBG cardiac imaging. The early (10 min) and late (4 h) heart to mediastinum MIBG uptake (H/M) ratio and washout were calculated. of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-a), and its soluble receptor [soluble TNF receptor II (sTNFRII)] were measured by immunoassay of blood samples from patients and controls. s rly and late MIBG uptake was lower (both P<.001) and the WR was higher (P<.001) in patients than in controls. The analysis showed innervation defects in 20 of the 22 patients. Nearly half (45.4%) showed severe adrenergic innervation defects in both the inferior wall and the apex. ing cytokines, patients showed significantly elevated TNF-a (P=.005), sTNFRII (P<.001), and IL-6 (P<.001) levels compared to controls. nd sTNFRII were found to correlate with the WR (r=0.468, P=.028 and r=0.455, P=.034, respectively). sion ts with IGT show reduced MIBG cardiac uptake with a segmental pattern. The reduced cardiac sympathetic innervation was related to the elevated proinflammatory cytokine levels and could be considered an index of early atherosclerotic process in these patients.