Peter M van Brussel1, Daan W Eeftinck Schattenkerk2, Linn C Dobrowolski3, Robbert J de Winter4, Jim A Reekers5, Hein J Verberne6, Liffert Vogt3, Bert-Jan H van den Born2. 1. Department of Cardiology of the Academic Medical Center, University of Amsterdam, The Netherlands. Electronic address: p.m.vanbrussel@amc.uva.nl. 2. Department of Vascular Medicine of the Academic Medical Center, University of Amsterdam, The Netherlands. 3. Department of Nephrology of the Academic Medical Center, University of Amsterdam, The Netherlands. 4. Department of Cardiology of the Academic Medical Center, University of Amsterdam, The Netherlands. 5. Department of Radiology of the Academic Medical Center, University of Amsterdam, The Netherlands. 6. Department of Nuclear Medicine of the Academic Medical Center, University of Amsterdam, The Netherlands.
Abstract
BACKGROUND: Renal sympathetic denervation (RSD) is currently being investigated in multiple studies of sympathetically driven cardiovascular diseases such as heart failure and arrhythmias. Our aim was to assess systemic and cardiac sympatholytic effects of RSD by the measurement of cardiac sympathetic activity and cardiovascular parameters. METHODS: A total of 21 consecutive patients with refractory hypertension (daytime ambulatory blood pressure (BP)≥150/100 mmHg despite the use of 3 or more antihypertensive drugs), no evidence for secondary hypertension and normal renovascular anatomy were included. RSD was performed with the Medtronic Symplicity renal denervation catheter with an average of 4.2 (range 3-6) ablations per renal artery. To assess cardiac sympathetic activity, 123I-mIBG cardiac scintigraphy was performed before and 6 weeks after. In addition, the effect of RSD on peripheral BP and cardiac hemodynamics were assessed non-invasively. RESULTS: 123I-mIBG uptake before and after RSD was 1.7±0.4% vs. 1.7±0.5% at 15 min. and 1.4±0.4% vs. 1.5±0.5% after 4 h. As a consequence, washout rate was similar before (33.7±11.7%) and after RSD (30.1±12.6%, p=0.27). In line with earlier RSD studies, a significant drop in systolic office BP (-12.2 mmHg, p=0.04) was detected, whereas the decrease in ambulatory BP was not significant. No changes were seen in heart rate, stroke volume or left ventricular contractility, both in supine position and after standing. CONCLUSION: In concert with previous reports, RSD leads to a significant drop in office BP. However, a reduction in sympathetic activity could not be demonstrated on a cardiac level.
BACKGROUND: Renal sympathetic denervation (RSD) is currently being investigated in multiple studies of sympathetically driven cardiovascular diseases such as heart failure and arrhythmias. Our aim was to assess systemic and cardiac sympatholytic effects of RSD by the measurement of cardiac sympathetic activity and cardiovascular parameters. METHODS: A total of 21 consecutive patients with refractory hypertension (daytime ambulatory blood pressure (BP)≥150/100 mmHg despite the use of 3 or more antihypertensive drugs), no evidence for secondary hypertension and normal renovascular anatomy were included. RSD was performed with the Medtronic Symplicity renal denervation catheter with an average of 4.2 (range 3-6) ablations per renal artery. To assess cardiac sympathetic activity, 123I-mIBG cardiac scintigraphy was performed before and 6 weeks after. In addition, the effect of RSD on peripheral BP and cardiac hemodynamics were assessed non-invasively. RESULTS:123I-mIBG uptake before and after RSD was 1.7±0.4% vs. 1.7±0.5% at 15 min. and 1.4±0.4% vs. 1.5±0.5% after 4 h. As a consequence, washout rate was similar before (33.7±11.7%) and after RSD (30.1±12.6%, p=0.27). In line with earlier RSD studies, a significant drop in systolic office BP (-12.2 mmHg, p=0.04) was detected, whereas the decrease in ambulatory BP was not significant. No changes were seen in heart rate, stroke volume or left ventricular contractility, both in supine position and after standing. CONCLUSION: In concert with previous reports, RSD leads to a significant drop in office BP. However, a reduction in sympathetic activity could not be demonstrated on a cardiac level.
Authors: Marat Fudim; Asher A Sobotka; Yue-Hui Yin; Joanne W Wang; Howard Levin; Murray Esler; Jie Wang; Paul A Sobotka Journal: Curr Hypertens Rep Date: 2018-05-01 Impact factor: 5.369
Authors: Karl Fengler; Diana Heinemann; Thomas Okon; Karoline Röhnert; Thomas Stiermaier; Maximilian von Röder; Christian Besler; Ulrike Müller; Robert Höllriegel; Gerhard Schuler; Steffen Desch; Philipp Lurz Journal: Clin Res Cardiol Date: 2016-01-04 Impact factor: 5.460
Authors: Linn C Dobrowolski; Daan W Eeftinck Schattenkerk; C T Paul Krediet; Peter M Van Brussel; Liffert Vogt; Frederike J Bemelman; Jim A Reekers; Bert-Jan H Van Den Born; Hein J Verberne Journal: EJNMMI Res Date: 2018-01-26 Impact factor: 3.138