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Endovascular shedding markers in patients with heart failure with reduced ejection fraction: Results from a
Petra Nijst1,2, Jirka Cops3, Pieter Martens1,2
1Department of Cardiology, Ziekenhuis Oost-Limburg, Genk, Belgium.
Insights
Hyaluronic acid (HA) is elevated in some heart failure patients and predicts worse outcomes. Glycocalyx shedding may contribute to heart failure pathophysiology, warranting further study.
Area of Science:
- Cardiovascular Research
- Biomarker Discovery
- Pathophysiology
Background:
- Endothelial glycocalyx degradation is linked to cardiovascular disease.
- The role of glycocalyx shedding markers in heart failure with reduced ejection fraction (HFrEF) requires exploration.
Purpose of the Study:
- To investigate the concentration, prognostic value, and associations of glycocalyx shedding markers in HFrEF patients.
Main Methods:
- Assessed glycocalyx shedding markers (hyaluronic acid [HA] and syndecan-1) in 123 HFrEF patients.
- Compared marker levels to healthy subjects and correlated them with clinical outcomes and other disease processes.
Main Results:
- Median HA levels were higher in HFrEF patients, but only 31% exceeded the normal cutoff.
- Elevated HA levels predicted significantly worse clinical outcomes, independent of other risk factors.
- No significant differences in syndecan-1 levels were found between HFrEF patients and controls, nor were shedding markers associated with neurohumoral activation, myocardial injury, or inflammation.
Conclusions:
- Hyaluronic acid (HA), a glycocalyx shedding marker, is elevated in a subgroup of HFrEF patients.
- Elevated HA is an independent predictor of worse clinical outcomes in HFrEF.
- Glycocalyx shedding may be an additional contributing factor to heart failure pathophysiology.
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.
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