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

AIM: This study 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. METHODS: We studied 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. Levels 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. RESULTS: The early 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. Regarding cytokines, patients showed significantly elevated TNF-a (P=.005), sTNFRII (P<.001), and IL-6 (P<.001) levels compared to controls. IL-6 and sTNFRII were found to correlate with the WR (r=0.468, P=.028 and r=0.455, P=.034, respectively). CONCLUSION: Patients 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.

Effects of Nebivolol on left ventricular function and exercise capacity in patients with non-ischaemic dilated cardiomyopathy. A randomised placebo-controlled study.

INTRODUCTION: This study assessed the effects of Nebivolol on left ventricular (LV) function and exercise capacity in patients with non-ischaemic dilated cardiomyopathy (NIDC). METHODS: After enrolment in this double-blind trial, 60 patients, aged 55 +/- 9.5 years, with angiographically proven NIDC, LV ejection fraction (EF) < 45%, NYHA class II-III, were randomised to either Nebivolol (target dose 5 mg) or placebo and were evaluated using echocardiography and exercise tests over 3 months. RESULTS: There were no baseline differences between the 2 groups regarding NYHA class, heart rate (HR), blood pressure (BP), LVEF or other echocardiographic variables. During follow-up, 4 patients in the Nebivolol and 5 in the placebo group discontinued treatment. After 3-months' treatment a significant decrease in NYHA class (p = 0.001), resting HR (p = 0.03), systolic and diastolic BP (both p < 0.001), left atrial diameter (p = 0.01) and LV end-systolic volume (p = 0.046), and an increase in LVEF (p = 0.01) were observed in the Nebivolol group compared to placebo. The atrial contribution to total LV filling (p = 0.007) and the pulmonary venous (PV) systolic wave velocity (p = 0.007) increased, whereas the atrial PV component decreased (p < 0.001) in the Nebivolol patients compared to placebo. Exercise duration decreased at 3 months (p = 0.01) compared to placebo, probably as a result of reduced maximal exercise HR (p < 0.001). CONCLUSIONS: Nebivolol is a safe and well-tolerated drug that improves NYHA class, systolic and diastolic LV function in NIDC patients, although it is associated with a lower maximal exercise duration at 3 months.