Oliver Dörr1, Sebastian Ewen2, Christoph Liebetrau3,4, Helge Möllmann3,4, Luise Gaede3,4, Dominik Linz2, Mathias Hohl2, Christian Troidl3,4, Timm Bauer5, Michael Böhm2, Christian Hamm5,3, Felix Mahfoud2,6, Holger Nef5. 1. Department of Cardiology, University of Giessen, Giessen, Germany. oliver.doerr@innere.med.uni-giessen.de. 2. Department of Cardiology, Universitätsklinikum des Saarlandes, Homburg/Saar, Germany. 3. Department of Cardiology, Kerckhoff Heart and Thorax Center, Bad Nauheim, Germany. 4. DZHK (German Centre for Cardiovascular Research), partner site Rhein-Main, Bad Nauheim, Germany. 5. Department of Cardiology, University of Giessen, Giessen, Germany. 6. Institute of Medical Engineering and Science, Harvard-MIT Biomedical Engineering, E25-438, Cambridge, MA, 02139, USA.
Abstract
BACKGROUND: Renal sympathetic denervation (RSD) represents a safe and effective treatment option for certain patients with resistant hypertension and has been shown to decrease sympathetic activity. Neuropeptide Y (NPY) is a neurotransmitter that is co-released with norepinephrine and is up-regulated during increased sympathetic activity. The aim of the present study was to examine the effect of RSD on NPY and to analyze the association between changes in NPY levels and blood pressure reduction after RSD. METHODS: A total of 150 consecutive patients (age 64.9 ± 10.2 years) from three clinical centers undergoing RSD were included in this study. Response to RSD was defined as an office systolic blood pressure (SBP) reduction of >10 mmHg 6 months after RSD. Venous blood samples for measurement of NPY were collected prior to and 6 months after RSD. RESULTS: BP and NPY levels were significantly reduced by 23/9 mmHg (p = 0.001/0.001) and 0.24 mg/dL (p < 0.01) 6 months after RSD. There was a significant correlation between baseline SBP- and RSD-related systolic BP reduction (r = -0.43; p < 0.001) and between serum NPY baseline values and NPY level changes (r = -0.52; p < 0.001) at the 6-month follow-up. The BP response to RSD (>10 mmHg) was associated with a significantly greater reduction in NPY level when compared with BP non-responders (p = 0.001). CONCLUSION: This study demonstrates an effect of RSD on serum NPY levels, a specific marker for sympathetic activity. The association between RSD-related changes in SBP and NPY levels provides further evidence of the effect of RSD on the sympathetic nervous system.
BACKGROUND: Renal sympathetic denervation (RSD) represents a safe and effective treatment option for certain patients with resistant hypertension and has been shown to decrease sympathetic activity. Neuropeptide Y (NPY) is a neurotransmitter that is co-released with norepinephrine and is up-regulated during increased sympathetic activity. The aim of the present study was to examine the effect of RSD on NPY and to analyze the association between changes in NPY levels and blood pressure reduction after RSD. METHODS: A total of 150 consecutive patients (age 64.9 ± 10.2 years) from three clinical centers undergoing RSD were included in this study. Response to RSD was defined as an office systolic blood pressure (SBP) reduction of >10 mmHg 6 months after RSD. Venous blood samples for measurement of NPY were collected prior to and 6 months after RSD. RESULTS: BP and NPY levels were significantly reduced by 23/9 mmHg (p = 0.001/0.001) and 0.24 mg/dL (p < 0.01) 6 months after RSD. There was a significant correlation between baseline SBP- and RSD-related systolic BP reduction (r = -0.43; p < 0.001) and between serum NPY baseline values and NPY level changes (r = -0.52; p < 0.001) at the 6-month follow-up. The BP response to RSD (>10 mmHg) was associated with a significantly greater reduction in NPY level when compared with BP non-responders (p = 0.001). CONCLUSION: This study demonstrates an effect of RSD on serum NPY levels, a specific marker for sympathetic activity. The association between RSD-related changes in SBP and NPY levels provides further evidence of the effect of RSD on the sympathetic nervous system.
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