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Please use this identifier to cite or link to this item: http://hdl.handle.net/1942/26293

Title: Endovascular shedding markers in patients with heart failure with reduced ejection fraction: Results from a single-center exploratory study
Authors: Nijst, Petra
Cops, Jirka
Martens, Pieter
Swennen, Quirine
Dupont, Matthias
Tang, Wai Hong W.
Mullens, Wilfried
Issue Date: 2018
Citation: MICROCIRCULATION, 25(2) (Art N° e12432)
Abstract: Background: Endothelial glycocalyx degradation has been associated with multiple pathophysiological processes in cardiovascular disease. Aims: To explore the role of glycocalyx shedding markers in pathophysiology of HFrEF. Methods: In 123 HFrEF patients, the concentration, prognostic value, and association of glycocalyx shedding markers with other disease processes were investigated. Results: Median HA levels and syndecan-1 levels in HFrEF patients were, respectively, 29.4 (10.7;61.6) ng/mL and 48.5 (33.6;80.8) ng/mL. Overall, HA-levels were significantly higher in HFrEF patients compared to healthy subjects, but only 31% of HFrEF patients had HA-levels above the cutoff of normal. There was no significant difference among HFrEF patients and healthy subjects regarding syndecan-1 levels. HFrEF patients with elevated HA-levels had a significantly worse outcome (log rank = 0.01) which remained significant after correction for established risk factors (HR 2.53 (1.13-5.69); P = .024). There was no significant relation between levels of shedding markers and neurohumoral activation (PRA, serum aldosterone, NT-proBNP), myocardial injury (HS-trop), inflammation (CRP), or other baseline characteristics. Conclusions: The glycocalyx shedding marker HA is significantly elevated in a subgroup of HFrEF patients and an independent predictor for worse clinical outcome. Glycocalyx shedding might be an additional factor in the pathophysiology of HF which warrants further investigation.
Notes: Nijst, P (reprint author), Ziekenhuis Oost Limburg, Dept Cardiol, Genk, Belgium. nijst.petra@gmail.com
URI: http://hdl.handle.net/1942/26293
DOI: 10.1111/micc.12432
ISI #: 000424813900006
ISSN: 1073-9688
Category: A1
Type: Journal Contribution
Appears in Collections: Research publications

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