Endovascular shedding markers in patients with heart failure with reduced ejection fraction

Nijst, Petra; Cops, Jirka; Martens, Pieter; Swennen, Quirine; Dupont, Matthias; Tang, W.H. Wilson; Mullens, Wilfried

doi:10.1111/micc.12432

Cited by 9 publications

(6 citation statements)

References 45 publications

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“…Elevated haematocrit, a risk factor for stroke and myocardial infarction, could induce a reduction in GCX thickness [ 27 ]. Patients with heart failure with reduced ejection fraction have increased levels of the GCX shedding marker median hyaluronic acid [ 28 ]. Lacunar stroke patients with white matter lesions show compromised GCX barrier properties [ 29 ].…”

Section: Ed Associated To Aging and Chronic Diseasementioning

confidence: 99%

Shared Features of Endothelial Dysfunction between Sepsis and Its Preceding Risk Factors (Aging and Chronic Disease)

Bermejo-Martín

Martín-Fernández

López-Mestanza

et al. 2018

JCM

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Acute vascular endothelial dysfunction is a central event in the pathogenesis of sepsis, increasing vascular permeability, promoting activation of the coagulation cascade, tissue edema and compromising perfusion of vital organs. Aging and chronic diseases (hypertension, dyslipidaemia, diabetes mellitus, chronic kidney disease, cardiovascular disease, cerebrovascular disease, chronic pulmonary disease, liver disease, or cancer) are recognized risk factors for sepsis. In this article we review the features of endothelial dysfunction shared by sepsis, aging and the chronic conditions preceding this disease. Clinical studies and review articles on endothelial dysfunction in sepsis, aging and chronic diseases available in PubMed were considered. The main features of endothelial dysfunction shared by sepsis, aging and chronic diseases were: (1) increased oxidative stress and systemic inflammation, (2) glycocalyx degradation and shedding, (3) disassembly of intercellular junctions, endothelial cell death, blood-tissue barrier disruption, (4) enhanced leukocyte adhesion and extravasation, (5) induction of a pro-coagulant and anti-fibrinolytic state. In addition, chronic diseases impair the mechanisms of endothelial reparation. In conclusion, sepsis, aging and chronic diseases induce similar features of endothelial dysfunction. The potential contribution of pre-existent endothelial dysfunction to sepsis pathogenesis deserves to be further investigated.

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Section: Ed Associated To Aging and Chronic Diseasementioning

confidence: 99%

Shared Features of Endothelial Dysfunction between Sepsis and Its Preceding Risk Factors (Aging and Chronic Disease)

Bermejo-Martín

Martín-Fernández

López-Mestanza

et al. 2018

JCM

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“…However, contrary to our results, Nijst et al . did not find any difference in syndecan‐1 levels between stable or decompensated HFrEF and healthy controls, which they speculated may be due to a wide distribution of syndecan‐1 in their healthy subjects 42 . We have recently found in another study that increased levels of syndecan‐1 in HF patients normalized towards the healthy controls' levels after heart transplantation 43 .…”

Section: Discussionmentioning

confidence: 93%

Plasma proteoglycan prolargin in diagnosis and differentiation of pulmonary arterial hypertension

et al. 2021

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Aims Right ventricular dysfunction may arise because of pulmonary arterial hypertension (PAH). Development of new diagnostic methods able to identify PAH and allow for earlier treatment initiation, before the development of vascular remodelling and manifest right heart failure (HF), could potentially improve prognosis. Proteoglycans and inflammatory proteins are involved in vascular remodelling. We aimed to investigate their potential as biomarkers to differentiate PAH in a dyspnoeic population. Methods and results Plasma from 152 patients with PAH (n = 48), chronic thrombo-embolic pulmonary hypertension (n = 20), pulmonary hypertension due to HF with reduced (n = 36) or preserved (n = 33) ejection fraction, and HF without pulmonary hypertension (n = 15) and 20 healthy controls were analysed with proximity extension assays. Haemodynamics were assessed in the patients with right heart catheterization. Plasma prolargin levels in PAH were lower compared with all the other studied disease groups (P < 0.001) but higher than the controls' levels (P = 0.003). Receiver operating characteristic curve of prolargin as a PAH-differentiating marker in a pooled population, encompassing all the other studied disease groups, had a sensitivity of 74% and a specificity of 83.3% (area under the curve = 0.84, P < 0.001). Prolargin correlated with the mean right atrial pressure (r s = 0.65, P < 0.001), N-terminal pro-brain natriuretic peptide (r s = 0.64, P < 0.001), cardiac index (r s = À0.31, P = 0.029), stroke volume index (r s = À0.41, P = 0.004), right ventricular stroke work index (r s = À0.31, P = 0.032), six-minute walking distance (r s = À0.41, P = 0.005), and mixed venous blood oxygen saturation (r s = À0.42, P = 0.003). Conclusions Plasma prolargin levels differentiate PAH patients from controls and the other investigated dyspnoea groups including HF. Its potential in PAH differentiation may be enhanced by inclusion in a multi-marker panel. Larger studies are needed to evaluate its discriminative ability of PAH in relation to other dyspnoea aetiologies and its potential role in PAH risk stratification and pathobiology.

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“…HA was significantly elevated in HFrEF patients and an independent predictor for worse clinical outcome, whereas SDC1 elevation was not significant. 152 …”

Section: Part B: the Role Of The Glycocalyx In Vascular Related Diseamentioning

confidence: 99%

The Glycocalyx and Its Role in Vascular Physiology and Vascular Related Diseases

Weinbaum

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et al. 2020

Cardiovasc Eng Tech

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Purpose In 2007 the two senior authors wrote a review on the structure and function of the endothelial glycocalyx layer (Weinbaum in Annu Rev Biomed Eng 9:121–167, 2007). Since then there has been an explosion of interest in this hydrated gel-like structure that coats the luminal surface of endothelial cells that line our vasculature due to its important functions in (A) basic vascular physiology and (B) vascular related diseases. This review will highlight the major advances that have occurred since our 2007 paper. Methods A literature search mainly focusing on the role of the glycocalyx in the two major areas described above was performed using electronic databases. Results In part (A) of this review, the new formulation of the century old Starling principle, now referred to as the Michel–Weinbaum glycoclayx model or revised Starling hypothesis, is described including new subtleties and physiological ramifications. New insights into mechanotransduction and release of nitric oxide due to fluid shear stress sensed by the glycocalyx are elaborated. Major advances in understanding the organization and function of glycocalyx components, and new techniques for measuring both its thickness and spatio-chemical organization based on super resolution, stochastic optical reconstruction microscopy (STORM) are presented. As discussed in part (B) of this review, it is now recognized that artery wall stiffness associated with hypertension and aging induces glycocalyx degradation, endothelial dysfunction and vascular disease. In addition to atherosclerosis and cardiovascular diseases, the glycocalyx plays an important role in lifestyle related diseases (e.g., diabetes) and cancer. Infectious diseases including sepsis, Dengue, Zika and Corona viruses, and malaria also involve the glycocalyx. Because of increasing recognition of the role of the glycocalyx in a wide range of diseases, there has been a vigorous search for methods to protect the glycocalyx from degradation or to enhance its synthesis in disease environments. Conclusion As we have seen in this review, many important developments in our basic understanding of GCX structure, function and role in diseases have been described since the 2007 paper. The future is wide open for continued GCX research.

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Endovascular shedding markers in patients with heart failure with reduced ejection fraction

Abstract: 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.

Cited by 9 publications

References 45 publications

Shared Features of Endothelial Dysfunction between Sepsis and Its Preceding Risk Factors (Aging and Chronic Disease)

Shared Features of Endothelial Dysfunction between Sepsis and Its Preceding Risk Factors (Aging and Chronic Disease)

Plasma proteoglycan prolargin in diagnosis and differentiation of pulmonary arterial hypertension

The Glycocalyx and Its Role in Vascular Physiology and Vascular Related Diseases

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