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Endovascular shedding markers in patients with heart failure with reduced ejection fraction
Author(s) -
Nijst Petra,
Cops Jirka,
Martens Pieter,
Swennen Quirine,
Dupont Matthias,
Tang Wai Hong W.,
Mullens Wilfried
Publication year - 2018
Publication title -
microcirculation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.793
H-Index - 83
eISSN - 1549-8719
pISSN - 1073-9688
DOI - 10.1111/micc.12432
Subject(s) - glycocalyx , pathophysiology , medicine , ejection fraction , heart failure , cardiology , syndecan 1 , aldosterone , inflammation , gastroenterology , immunology , biology , cell , genetics
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 HF r EF 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 HF r EF patients compared to healthy subjects, but only 31% of HF r EF patients had HA ‐levels above the cutoff of normal. There was no significant difference among HF r EF patients and healthy subjects regarding syndecan‐1 levels. HF r EF 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 ‐pro BNP ), myocardial injury ( HS ‐trop), inflammation ( CRP ), or other baseline characteristics. Conclusions The glycocalyx shedding marker HA is significantly elevated in a subgroup of HF r EF 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.