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Elevated plasma tyrosine kinases VEGF-D and HER4 in heart failure patients decrease after heart transplantation in association with improved haemodynamics.

ABSTRACT: Receptor tyrosine kinases (RTKs) are implicated in cardiovascular growth and remodelling. We aimed to identify the plasma levels of RTKs and related proteins and their association with haemodynamic alterations in heart failure (HF) and related pulmonary hypertension (PH) following heart transplantation (HT). Using proximity extension assay, 28 RTKs and related proteins were analysed in plasma from 20 healthy controls and 26 HF patients before and 1-year after HT. In end-stage HF, out of 28 RTKs, plasma vascular endothelial growth factor-D (VEGF-D) and human epidermal growth factor-4 (HER4) were elevated compared to controls (p?

SUBMITTER: Ahmed S

PROVIDER: S-EPMC7198637 | biostudies-literature | 2020 Jun

REPOSITORIES: biostudies-literature

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Elevated plasma tyrosine kinases VEGF-D and HER4 in heart failure patients decrease after heart transplantation in association with improved haemodynamics.

Ahmed Salaheldin S Ahmed Abdulla A Säleby Joanna J Bouzina Habib H Lundgren Jakob J Rådegran Göran G

Heart and vessels 20200120 6

Receptor tyrosine kinases (RTKs) are implicated in cardiovascular growth and remodelling. We aimed to identify the plasma levels of RTKs and related proteins and their association with haemodynamic alterations in heart failure (HF) and related pulmonary hypertension (PH) following heart transplantation (HT). Using proximity extension assay, 28 RTKs and related proteins were analysed in plasma from 20 healthy controls and 26 HF patients before and 1-year after HT. In end-stage HF, out of 28 RTKs, ...[more]

PMID: 31960146

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Elevated plasma sRAGE and IGFBP7 in heart failure decrease after heart transplantation in association with haemodynamics.

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| S-EPMC7524060 | biostudies-literature

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

Project description: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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Vascular endothelial growth factor D (VEGF-D) is a ligand for the tyrosine kinases VEGF receptor 2 (Flk1) and VEGF receptor 3 (Flt4).

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