Alexandre Persu1,2, Daniel Gordin3,4, Lotte Jacobs5, Lutgarde Thijs5, Michiel L Bots6, Wilko Spiering7, Atena Miroslawska8,9, Jonas Spaak10, Ján Rosa11,12, Mark R de Jong13, Elena Berra1,14, Fadl Elmula M Fadl Elmula15, Gregoire Wuerzner16, Alison H M Taylor17, Agnieszka Olszanecka18, Danuta Czarnecka18, Patrick B Mark17, Michel Burnier16, Jean Renkin1,2, Sverre E Kjeldsen15, Jiří Widimský11, Arif Elvan13, Thomas Kahan10, Terje K Steigen8, Peter J Blankestijn19, Ilkka Tikkanen3,20, Jan A Staessen5,21. 1. Pole of Cardiovascular Research, Institut de Recherche Expérimentale et Clinique, Université Catholique de Louvain. 2. Cliniques Universitaires Saint-Luc, Université Catholique de Louvain, Brussels, Belgium. 3. Abdominal Center Nephrology, University of Helsinki and Helsinki University Central Hospital. 4. Folkhälsan Institute of Genetics, Folkhälsan Research Center, Helsinki, Finland. 5. Studies Coordinating Centre, Research Unit Hypertension and Cardiovascular Epidemiology, KU Leuven Department of Cardiovascular Sciences, University of Leuven, Leuven, Belgium. 6. Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht. 7. Department of Vascular Medicine, University Medical Center Utrecht, Utrecht, The Netherlands. 8. Department of Cardiology, University Hospital of North Norway, Tromsø. 9. Cardiovascular Diseases Research Group, UiT The Arctic University of Norway, Norway. 10. Karolinska Institute, Department of Clinical Sciences, Danderyd Hospital, Division of Cardiovascular Medicine, Stockholm, Sweden. 11. Third Department of Internal Medicine, General University Hospital and First Faculty of Medicine, Charles University, Prague. 12. Cardiocentre University Hospital Královské Vinohrady and Third Faculty of Medicine, Charles University, Prague, Czech Republic. 13. Department of Cardiology, Isala Klinieken, Zwolle, The Netherlands. 14. Department of Medical Sciences, Internal Medicine and Hypertension Division, AOU Città della Salute e della Scienza, Turin, Italy. 15. Department of Cardiology and Department of Acute Medicine, Oslo University Hospital, University of Oslo, Oslo, Norway. 16. Service of Nephrology, Lausanne University Hospital, Lausanne, Switzerland. 17. BHF Glasgow Cardiovascular Research Centre, University of Glasgow, Glasgow, UK. 18. 1st Department of Cardiology, Interventional Electrocardiology and Hypertension, Jagiellonian University Medical College, Krakow, Poland. 19. Department of Nephrology, University Medical Center Utrecht, Utrecht, The Netherlands. 20. Minerva Institute for Medical Research, Helsinki, Finland. 21. R&D Group VitaK, Maastricht University, Maastricht, The Netherlands.
Abstract
BACKGROUND: Sympathetic tone is one of the main determinants of blood pressure (BP) variability and treatment-resistant hypertension. The aim of our study was to assess changes in BP variability after renal denervation (RDN). In addition, on an exploratory basis, we investigated whether baseline BP variability predicted the BP changes after RDN. METHODS: We analyzed 24-h BP recordings obtained at baseline and 6 months after RDN in 167 treatment-resistant hypertension patients (40% women; age, 56.7 years; mean 24-h BP, 152/90 mmHg) recruited at 11 expert centers. BP variability was assessed by weighted SD [SD over time weighted for the time interval between consecutive readings (SDiw)], average real variability (ARV), coefficient of variation, and variability independent of the mean (VIM). RESULTS: Mean office and 24-h BP fell by 15.4/6.6 and 5.5/3.7 mmHg, respectively (P < 0.001). In multivariable-adjusted analyses, systolic/diastolic SDiw and VIM for 24-h SBP/DBP decreased by 1.18/0.63 mmHg (P ≤ 0.01) and 0.86/0.42 mmHg (P ≤ 0.05), respectively, whereas no significant changes in ARV or coefficient of variation occurred. Furthermore, baseline SDiw (P = 0.0006), ARV (P = 0.01), and VIM (P = 0.04) predicted the decrease in 24-h DBP but not 24-h SBP after RDN. CONCLUSION: RDN was associated with a decrease in BP variability independent of the BP level, suggesting that responders may derive benefits from the reduction in BP variability as well. Furthermore, baseline DBP variability estimates significantly correlated with mean DBP decrease after RDN. If confirmed in younger patients with less arterial damage, in the absence of the confounding effect of drugs and drug adherence, baseline BP variability may prove a good predictor of BP response to RDN.
BACKGROUND: Sympathetic tone is one of the main determinants of blood pressure (BP) variability and treatment-resistant hypertension. The aim of our study was to assess changes in BP variability after renal denervation (RDN). In addition, on an exploratory basis, we investigated whether baseline BP variability predicted the BP changes after RDN. METHODS: We analyzed 24-h BP recordings obtained at baseline and 6 months after RDN in 167 treatment-resistant hypertensionpatients (40% women; age, 56.7 years; mean 24-h BP, 152/90 mmHg) recruited at 11 expert centers. BP variability was assessed by weighted SD [SD over time weighted for the time interval between consecutive readings (SDiw)], average real variability (ARV), coefficient of variation, and variability independent of the mean (VIM). RESULTS: Mean office and 24-h BP fell by 15.4/6.6 and 5.5/3.7 mmHg, respectively (P < 0.001). In multivariable-adjusted analyses, systolic/diastolic SDiw and VIM for 24-h SBP/DBP decreased by 1.18/0.63 mmHg (P ≤ 0.01) and 0.86/0.42 mmHg (P ≤ 0.05), respectively, whereas no significant changes in ARV or coefficient of variation occurred. Furthermore, baseline SDiw (P = 0.0006), ARV (P = 0.01), and VIM (P = 0.04) predicted the decrease in 24-h DBP but not 24-h SBP after RDN. CONCLUSION: RDN was associated with a decrease in BP variability independent of the BP level, suggesting that responders may derive benefits from the reduction in BP variability as well. Furthermore, baseline DBP variability estimates significantly correlated with mean DBP decrease after RDN. If confirmed in younger patients with less arterial damage, in the absence of the confounding effect of drugs and drug adherence, baseline BP variability may prove a good predictor of BP response to RDN.
Authors: Christopher T Banek; Madeline M Gauthier; Daniel C Baumann; Dusty Van Helden; Ninitha Asirvatham-Jeyaraj; Angela Panoskaltsis-Mortari; Gregory D Fink; John W Osborn Journal: Am J Physiol Regul Integr Comp Physiol Date: 2018-03-07 Impact factor: 3.619
Authors: Christopher T Banek; Madeline M Gauthier; Dusty A Van Helden; Gregory D Fink; John W Osborn Journal: Hypertension Date: 2019-05 Impact factor: 10.190
Authors: David E Kandzari; Felix Mahfoud; Michael A Weber; Raymond Townsend; Gianfranco Parati; Naomi D L Fisher; Melvin D Lobo; Michael Bloch; Michael Böhm; Andrew S P Sharp; Roland E Schmieder; Michel Azizi; Markus P Schlaich; Vasilios Papademetriou; Ajay J Kirtane; Joost Daemen; Atul Pathak; Christian Ukena; Philipp Lurz; Guido Grassi; Martin Myers; Aloke V Finn; Marie-Claude Morice; Roxana Mehran; Peter Jüni; Gregg W Stone; Mitchell W Krucoff; Paul K Whelton; Konstantinos Tsioufis; Donald E Cutlip; Ernest Spitzer Journal: Circulation Date: 2022-03-14 Impact factor: 29.690
Authors: Yann Vuignier; Eric Grouzmann; Olivier Muller; Nima Vakilzadeh; Mohamed Faouzi; Marc P Maillard; Salah D Qanadli; Michel Burnier; Grégoire Wuerzner Journal: Front Cardiovasc Med Date: 2018-05-23