title: Beneficial effects of renal sympathetic denervation on cardiovascular inflammation and remodeling in essential hypertension.
abstract: BACKGROUND
  Renal sympathetic denervation (RSD) represents a potential treatment option for certain patients with resistant arterial hypertension (HT). HT is associated with chronic vascular inflammation and remodeling, contributing to progressive vascular damage, and atherosclerosis. The present study aimed to evaluate the influence of RSD on cardiovascular inflammation and remodeling by determining serum levels of interleukin-6 (IL-6), high-sensitive C-reactive protein (hsCRP), matrix metalloproteinases (MMP), and tissue inhibitor of metalloproteinases (TIMP).
  
  
  METHODS
  A total of 60 consecutive patients (age 67.9 ± 9.6 years) undergoing RSD were included. A therapeutic response was defined as an office systolic blood pressure (SBP) reduction of >10 mmHg 6 months after RSD. Venous serum samples for measurement of hsCRP, IL-6, MMP-2, MMP-9, and TIMP-1 were collected prior to and 6 months after RSD.
  
  
  RESULTS
  A significant reduction in office SBP of 26.4 mmHg [SBPbaseline 169.3 mmHg (SD 11.3), p < 0.001] was documented 6 months after RSD. The serum levels of hsCRP (p < 0.001) and the pro-inflammatory cytokine IL-6 (p < 0.001) were significantly decreased compared to baseline values. The levels of MMP-9 (p = 0.024) and MMP-2 (p < 0.01) were significantly increased compared to baseline values.
  
  
  CONCLUSIONS
  In addition to the effective blood pressure reduction in response to RSD, this study demonstrates a positive effect of RSD on biomarkers reflecting vascular inflammation and remodeling. These results suggest a possible prognostic benefit of RSD in high-risk patients for endothelial dysfunction and cardiovascular remodeling as well as end-organ damage.
authors.affiliation: Department of Cardiology, University of Giessen, Klinikstr. 33, 35392, Giessen, Germany, oliver.doerr@innere.med.uni-giessen.de.
authors.forename: Oliver
authors.initials: O
authors.lastname: Dörr
authors.forename: Christoph
authors.initials: C
authors.lastname: Liebetrau
authors.forename: Helge
authors.initials: H
authors.lastname: Möllmann
authors.forename: Felix
authors.initials: F
authors.lastname: Mahfoud
authors.forename: Sebastian
authors.initials: S
authors.lastname: Ewen
authors.forename: Luise
authors.initials: L
authors.lastname: Gaede
authors.forename: Christian
authors.initials: C
authors.lastname: Troidl
authors.forename: Jedrzej
authors.initials: J
authors.lastname: Hoffmann
authors.forename: Nikolai
authors.initials: N
authors.lastname: Busch
authors.forename: Gerald
authors.initials: G
authors.lastname: Laux
authors.forename: Jens
authors.initials: J
authors.lastname: Wiebe
authors.forename: Timm
authors.initials: T
authors.lastname: Bauer
authors.forename: Christian
authors.initials: C
authors.lastname: Hamm
authors.forename: Holger
authors.initials: H
authors.lastname: Nef
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood; D016207:Cytokines / Q000097:blood; D000075222:Essential Hypertension; D005260:Female; D006801:Humans; D006973:Hypertension / Q000150:complications* / Q000175:diagnosis / Q000628:therapy*; D007668:Kidney / Q000294:innervation* / Q000601:surgery; D008137:Longitudinal Studies; D008297:Male; D009205:Myocarditis / Q000175:diagnosis / Q000209:etiology* / Q000517:prevention & control*; D013562:Sympathectomy / Q000379:methods*; D016896:Treatment Outcome; D020257:Ventricular Remodeling
chemical_list: D015415:Biomarkers; D016207:Cytokines