Oliver Dörr 1 , Christoph Liebetrau 2 , Helge Möllmann 2 , Luise Gaede 2 , Christian Troidl 2 , Kareen Morczeck 3 , Jens Wiebe 3 , Jedrzej Hoffmann 2 , Sandra Voss 2 , Timm Bauer 3 , Christian Hamm 4 , Holger Nef 3 . Show Affiliations »
Abstract
BACKGROUND: Renal sympathetic denervation (RSD) represents an effective treatment option for patients with resistant arterial hypertension (HT). Extracellular matrix (ECM) turnover and deposition are essential processes in HT-related cardiovascular remodeling, fibrosis, and cardiac hypertrophy and contribute to hypertensive heart disease. OBJECTIVES: The primary aim of the present study was to examine the effect of RSD on increased collagen turnover as reflected by serum levels of amino-terminal pro-peptides (PINP, PIIINP) and a carboxyl-terminal pro-peptide (PICP), specific biomarkers for cardiac ECM turnover and cardiovascular fibrosis. METHODS: A total of 100 consecutive patients (mean age: 65.9±10.1 years) undergoing RSD were included in this study. A therapeutic response was defined as an office systolic blood pressure (SBP) reduction of >10mm Hg 6 months after RSD. Venous serum samples for measurement of PICP, PINP, and PIIINP were collected prior to and 6 months after RSD. RESULTS: A significant reduction in the office SBP of 24.3 mm Hg (SBP baseline: 166.9±14.3 mm Hg (P < 0.001) was documented 6 months after RSD. At this time point, the serum levels of PICP, PINP, and PIIINP (P < 0.01) were significantly decreased compared to baseline values in patients with an increased collagen turnover, showing significant differences comparing BP responders and nonresponders. CONCLUSION: In addition to the effective blood pressure reduction in response to RSD, this study demonstrates a positive effect of RSD on biomarkers reflecting cardiovascular ECM turnover and deposition. These results suggest a beneficial effect of RSD on cardiovascular fibrosis, hypertensive heart disease, and end-organ damage in high-risk patients. © American Journal of Hypertension, Ltd 2015. All rights reserved. For Permissions, please email: journals.permissions@oup.com.
BACKGROUND: Renal sympathetic denervation (RSD ) represents an effective treatment option for patients with resistant arterial hypertension (HT ). Extracellular matrix (ECM) turnover and deposition are essential processes in HT -related cardiovascular remodeling , fibrosis , and cardiac hypertrophy and contribute to hypertensive heart disease . OBJECTIVES: The primary aim of the present study was to examine the effect of RSD on increased collagen turnover as reflected by serum levels of amino-terminal pro-peptides (PINP, PIIINP) and a carboxyl-terminal pro-peptide (PICP), specific biomarkers for cardiac ECM turnover and cardiovascular fibrosis . METHODS: A total of 100 consecutive patients (mean age: 65.9±10.1 years) undergoing RSD were included in this study. A therapeutic response was defined as an office systolic blood pressure (SBP) reduction of >10mm Hg 6 months after RSD . Venous serum samples for measurement of PICP, PINP, and PIIINP were collected prior to and 6 months after RSD . RESULTS: A significant reduction in the office SBP of 24.3 mm Hg (SBP baseline: 166.9±14.3 mm Hg (P < 0.001) was documented 6 months after RSD . At this time point, the serum levels of PICP, PINP, and PIIINP (P < 0.01) were significantly decreased compared to baseline values in patients with an increased collagen turnover, showing significant differences comparing BP responders and nonresponders. CONCLUSION: In addition to the effective blood pressure reduction in response to RSD , this study demonstrates a positive effect of RSD on biomarkers reflecting cardiovascular ECM turnover and deposition. These results suggest a beneficial effect of RSD on cardiovascular fibrosis , hypertensive heart disease , and end-organ damage in high-risk patients . © American Journal of Hypertension , Ltd 2015. All rights reserved. For Permissions, please email: journals.permissions@oup.com.
Entities: Chemical
Disease
Species
Keywords:
blood pressure; essential hypertension; fibrosis; hypertension; renal denervation.
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Year: 2015
PMID: 25767136 DOI: 10.1093/ajh/hpv020
Source DB: PubMed Journal: Am J Hypertens ISSN: 0895-7061 Impact factor: 2.689