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

Figures

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  Fig. 1. Selection of proteins corresponding to the reversal of heart failure and related pulmonary hypertension. RTK receptor tyrosine kinases, HF heart failure, PH pulmonary hypertension. Proteins’ abbreviations as in Table 2. False discovery rate (FDR) was used to accommodate for mass significance, (criterion I–III, FDR < 0.01); (correlation analysis, FDR < 0.1)

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  Fig. 2. Plasma VEGF-D and correlations with haemodynamic changes following heart transplantation. Outliers calculated with Tukey’s fence. HT heart transplantation, AU arbitrary units, rs Spearman’s correlation coefficient; ***p < 0.0001. Haemodynamic abbreviations as in Table 2. a VEGF-D levels in controls and heart failure patients before and 1-year after HT. The decrease (∆) of VEGF-D post-HT correlated with b ∆mPAP, c ∆PAWP, d ∆PAC and e PVR

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  Fig. 3. Plasma HER4 and correlations with haemodynamic changes following heart transplantation. Outliers calculated with Tukey’s fence. HT heart transplantation, AU arbitrary units, rs Spearman’s correlation coefficient; **p < 0.001; ***p < 0.0001. Haemodynamic abbreviations as in Table 2. a HER4 levels in controls and heart failure patients before and 1-year after HT. The decrease (∆) of HER4 post-HT correlated with b ∆NT-proBNP, c ∆MRAP and d improved CI

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  Fig. 4. Illustration of vascular endothelial growth factor-D physiological roles and hypotheses. a Based on previous reports, the effects of VEGF-D mediated signalling through binding to its receptors. b Hypothetical roles and the possible clinical applicability of elevated plasma VEGF-D in heart failure (HF) and related pulmonary hypertension (PH). PAC pulmonary arterial compliance, PVR pulmonary vascular resistance