Non-contact radiofrequency-induced reduction of subcutaneous abdominal fat correlates with initial cardiovascular autonomic balance and fat tissue hormones: safety analysis [v1; ref status: indexed, http://f1000r.es/4pj]

Background and objective: The non-invasive reduction of subcutaneous abdominal fat became popular in the last decade. Radiofrequency (RF), non-contact, selective-field device Vanquish® has been developed to selectively induce deep fat tissue heating to reduce waist circumference. Our analysis evaluates immediate and sustained effects of this treatment on cardiovascular autonomic function and on selected metabolic parameters. Study design/patients and methods: A retrospective proof-of-concept analysis of RF treatment effects was conducted in 20 individuals with metabolic syndrome, to reduce the subcutaneous abdominal fat. Four 30-minutes treatment sessions (manufacturer´s standard protocol) were performed in 1-week intervals. Vital signs, ECG, lab screening, body composition, subcutaneous fat thickness and spectral analysis of heart rate variability (HRV) have been examined before, after the 1st and 4th treatment, and at follow-up visits 1 month and 3 months after the treatment. Results: The RF treatment led to a significant reduction of abdominal circumference after the 4th session (p0.59, p<0.04). Conclusions: Our analysis shows that the selective-field RF treatment is safe and efficient for reduction of subcutaneous abdominal fat. While the treatment increases the immediate sympathetic response of the body to deep tissue heating, no sustained change in autonomic function could be recorded at 1 month follow-up. The observed correlation between initial VLF spectral power and waist circumference reduction at follow-up, as well as the association of initial adiponectin values and immediate autonomic response to the treatment might be instrumental for decisions on body contouring strategies

Neuro-vascular coupling and heart rate variability in patients with type II diabetes at different stages of diabetic retinopathy

Aims/Hypothesis: There is evidence that diabetes is accompanied by a break-down of functional hyperemia, an intrinsic mechanism of neural tissues to adapt blood flow to changing metabolic demands. However, to what extent functional hyperemia is altered in different stages of diabetic retinopathy (DR) in patients with type II diabetes is largely unknown. The current study set out to investigate flicker-induced retinal blood flow changes in patients with type II diabetes at different stages of DR. Materials and methods: A total of 76 subjects were included in the present parallel-group study, of which 56 had diabetes with either no DR or different stages of non-proliferative DR (n = 29 no DR, 12 mild DR, 15 moderate to severe DR). In addition, 20 healthy subjects were included as controls. Retinal blood flow was assessed before and during visual stimulation using a combined measurement of retinal vessel calibers and blood velocity by the means of Doppler optical coherence tomography (OCT). To measure systemic autonomic nervous system function, heart rate variability (HRV) was assessed using a short-term orthostatic challenge test. Results: In healthy controls, retinal blood flow increased by 40.4 ± 27.2% during flicker stimulation. Flicker responses in patients with DR were significantly decreased depending on the stage of the disease (no DR 37.7 ± 26.0%, mild DR 26.2 ± 28.2%, moderate to severe DR 22.3 ± 13.9%; p = 0.035, ANOVA). When assessing systemic autonomous neural function using HRV, normalized low frequency (LF) spectral power showed a significantly different response to the orthostatic maneuver in diabetic patients compared to healthy controls (p < 0.001). Conclusion/Interpretation: Our study indicates that flicker induced hyperemia is reduced in patients with DR compared to healthy subjects. Further, this impairment is more pronounced with increasing severity of DR. Further studies are needed to elucidate mechanisms behind the reduced hyperemic response in patients with type II diabetes. Clinical trial registration: [https://clinicaltrials.gov/], identifier [NCT03 552562].Published versionFinancial support from the Austrian Science Foundation FWF Projects Grant numbers: KLI529 and KLI721 are gratefully acknowledged

Retinal oxygen extraction in individuals with type 1 diabetes with no or mild diabetic retinopathy

Aims/hypothesis The aim of this study was to compare retinal oxygen extraction in individuals with diabetes with no or mild non-proliferative diabetic retinopathy and healthy age- and sex-matched volunteers. Methods A total of 24 participants with type 1 diabetes and 24 healthy age- and sex-matched volunteers were included in this cross-sectional study. Retinal oxygen extraction was measured by combining total retinal blood flow measurements using a custom-built bi-directional Doppler optical coherence tomography system with measurements of oxygen saturation using spectroscopic reflectometry. Based on previously published mathematical modelling, the oxygen content in retinal vessels and total retinal oxygen extraction were calculated. Results Total retinal blood flow was higher in diabetic participants (46.4 7.4 l/min) than in healthy volunteers (40.4 5.3 l/min, p = 0.002 between groups). Oxygen content in retinal arteries was comparable between the two groups, but oxygen content in retinal veins was higher in participants with diabetes (0.15 0.02 ml O2/ml) compared with healthy control participants (0.13 0.02 ml O2/ml, p < 0.001). As such, the arteriovenous oxygen difference and total retinal oxygen extraction were reduced in participants with diabetes compared with healthy volunteers (total retinal oxygen extraction 1.40 0.44 vs 1.70 0.47 l O2/min, respectively, p = 0.03). Conclusions/interpretation Our data indicate early retinal hypoxia in individuals with type 1 diabetes with no or mild diabetic retinopathy as compared with healthy control individuals. Further studies are required to fully understand the potential of the technique in risk stratification and treatment monitoring. Trial registration: ClinicalTrials.gov NCT01843114.(VLID)355032