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Elevated plasma endocan and BOC in heart failure patients decrease after heart transplantation in association with improved hemodynamics

Ahmed, Salaheldin LU orcid ; Ahmed, Abdulla LU orcid ; Bouzina, Habib LU ; Lundgren, Jakob LU and Rådegran, Göran LU (2020) In Heart and Vessels 35(11). p.1614-1628
Abstract

Background: The prevalence of heart failure (HF) is rising with ageing population and constitutes a major health problem globally. A common complication of HF is pulmonary hypertension (PH) which negatively impacts survival. A pathophysiological association between HF and PH with tumorigenic processes has been suggested. We aimed to identify the plasma levels of, and the association between tumour-related proteins and hemodynamic improvements in patients with HF and PH due to left heart disease (LHD) before and 1-year after heart transplantation (HT). Methods: Forty-eight tumour-related proteins were measured with proximity extension assay in plasma from 20 controls and 26 HF patients before and 1-year after HT. Patients’ hemodynamics... (More)

Background: The prevalence of heart failure (HF) is rising with ageing population and constitutes a major health problem globally. A common complication of HF is pulmonary hypertension (PH) which negatively impacts survival. A pathophysiological association between HF and PH with tumorigenic processes has been suggested. We aimed to identify the plasma levels of, and the association between tumour-related proteins and hemodynamic improvements in patients with HF and PH due to left heart disease (LHD) before and 1-year after heart transplantation (HT). Methods: Forty-eight tumour-related proteins were measured with proximity extension assay in plasma from 20 controls and 26 HF patients before and 1-year after HT. Patients’ hemodynamics were measured with right heart catheterization. Results: Out of 48 proteins, specifically, plasma levels of endocan and brother of CDO (BOC) were elevated in end-stage HF patients compared to controls (p < 0.001), but decreased after HT (p < 0.01), towards controls’ levels. The decrease of endocan levels after HT correlated with improved mean pulmonary arterial pressure (rs = 0.80, p < 0.0001), pulmonary arterial wedge pressure (rs = 0.63, p = 0.0012), and pulmonary vascular resistance (rs = 0.70, p < 0.001). The decrease and normalization of BOC after HT correlated with decreased mean right atrial pressure (rs = 0.61 p = 0.0015) and NT-proBNP (rs = 0.57, p = 0.0022), as well as increased cardiac index (rs = − 0.51, p = 0.0086) and left-ventricular stroke work index (rs = − 0.57, p = 0.0039). Conclusion: Our results suggest that (i) plasma endocan in HF may reflect the state of pulmonary vascular congestion and PH-LHD, whereas (ii) plasma BOC may reflect the cardiac function and the hemodynamic overload in HF. The exact role of these proteins and their clinical applicability as biomarkers in HF and PH-LHD ought to be investigated in larger cohorts.

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author
; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Biomarkers, Heart failure, Heart transplantation, Hemodynamics, Pulmonary hypertension
in
Heart and Vessels
volume
35
issue
11
pages
15 pages
publisher
Springer
external identifiers
  • pmid:32651845
  • scopus:85087721014
ISSN
0910-8327
DOI
10.1007/s00380-020-01656-3
language
English
LU publication?
yes
id
f4691afd-a843-43d8-9920-5a07ca611677
date added to LUP
2020-07-23 09:43:27
date last changed
2024-07-24 22:42:55
@article{f4691afd-a843-43d8-9920-5a07ca611677,
  abstract     = {{<p>Background: The prevalence of heart failure (HF) is rising with ageing population and constitutes a major health problem globally. A common complication of HF is pulmonary hypertension (PH) which negatively impacts survival. A pathophysiological association between HF and PH with tumorigenic processes has been suggested. We aimed to identify the plasma levels of, and the association between tumour-related proteins and hemodynamic improvements in patients with HF and PH due to left heart disease (LHD) before and 1-year after heart transplantation (HT). Methods: Forty-eight tumour-related proteins were measured with proximity extension assay in plasma from 20 controls and 26 HF patients before and 1-year after HT. Patients’ hemodynamics were measured with right heart catheterization. Results: Out of 48 proteins, specifically, plasma levels of endocan and brother of CDO (BOC) were elevated in end-stage HF patients compared to controls (p &lt; 0.001), but decreased after HT (p &lt; 0.01), towards controls’ levels. The decrease of endocan levels after HT correlated with improved mean pulmonary arterial pressure (r<sub>s</sub> = 0.80, p &lt; 0.0001), pulmonary arterial wedge pressure (r<sub>s</sub> = 0.63, p = 0.0012), and pulmonary vascular resistance (r<sub>s</sub> = 0.70, p &lt; 0.001). The decrease and normalization of BOC after HT correlated with decreased mean right atrial pressure (r<sub>s</sub> = 0.61 p = 0.0015) and NT-proBNP (r<sub>s</sub> = 0.57, p = 0.0022), as well as increased cardiac index (r<sub>s</sub> = − 0.51, p = 0.0086) and left-ventricular stroke work index (r<sub>s</sub> = − 0.57, p = 0.0039). Conclusion: Our results suggest that (i) plasma endocan in HF may reflect the state of pulmonary vascular congestion and PH-LHD, whereas (ii) plasma BOC may reflect the cardiac function and the hemodynamic overload in HF. The exact role of these proteins and their clinical applicability as biomarkers in HF and PH-LHD ought to be investigated in larger cohorts.</p>}},
  author       = {{Ahmed, Salaheldin and Ahmed, Abdulla and Bouzina, Habib and Lundgren, Jakob and Rådegran, Göran}},
  issn         = {{0910-8327}},
  keywords     = {{Biomarkers; Heart failure; Heart transplantation; Hemodynamics; Pulmonary hypertension}},
  language     = {{eng}},
  number       = {{11}},
  pages        = {{1614--1628}},
  publisher    = {{Springer}},
  series       = {{Heart and Vessels}},
  title        = {{Elevated plasma endocan and BOC in heart failure patients decrease after heart transplantation in association with improved hemodynamics}},
  url          = {{http://dx.doi.org/10.1007/s00380-020-01656-3}},
  doi          = {{10.1007/s00380-020-01656-3}},
  volume       = {{35}},
  year         = {{2020}},
}