Angiopoietins, vascular endothelial growth factors and secretory phospholipase A in heart failure patients with preserved ejection fraction.

Eur J Intern Med

Department of Advanced Biomedical Sciences, University of Naples Federico II, 80131, Naples, Italy; Gèrontopole de Toulouse, Institut du Vieillissement, CHU de Toulouse, 31000, Toulouse, France.

Published: December 2022

AI Article Synopsis

  • - Heart failure (HF) is a significant health issue, with a rise in cases of HF with preserved ejection fraction (HFpEF), currently making up about 50% of all HF patients, which is increasing in prevalence.
  • - A study analyzed levels of various angiogenic and lymphangiogenic factors, finding reduced ANGPT1 in HFrEF patients and increased ANGPT2 in both HFrEF and HFpEF compared to healthy individuals, suggesting different inflammatory profiles between these types of HF.
  • - The findings indicate that specific proinflammatory regulators are altered differently in HFpEF and HFrEF, which may have clinical implications; however, more research with larger patient groups is needed to confirm these results.

Article Abstract

Background: Heart failure (HF) is a growing public health burden, with high prevalence and mortality rates. A proportion of patients with HF have a normal ventricular ejection fraction (EF), referred to as HF with preserved EF (HFpEF), as opposed to patients with HF with reduced ejection fraction (HFrEF). HFpEF currently accounts for about 50% of all HF patients, and its prevalence is rising. Angiopoietins (ANGPTs), vascular endothelial growth factors (VEGFs) and secretory phospholipases A (sPLAs) are proinflammatory mediators and key regulators of endothelial cells.

Methods: The aim of this study was to analyze the plasma concentrations of angiogenic (ANGPT1, ANGPT2, VEGF-A) and lymphangiogenic (VEGF-C, VEGF-D) factors and the plasma activity of sPLA in patients with HFpEF and HFrEF compared to healthy controls.

Results: The concentration of ANGPT1 was reduced in HFrEF compared to HFpEF patients and healthy controls. ANGPT2 levels were increased in both HFrEF and HFpEF subjects compared to controls. The ANGPT2/ANGPT1 ratio was increased in HFrEF patients compared to controls. The concentrations of both VEGF-A and VEGF-C did not differ among the three groups examined. VEGF-D was increased in both HFrEF and HFpEF patients compared to controls. Plasma activity of sPLA was increased in HFrEF but not in HFpEF patients compared to controls.

Conclusions: Our results indicate that three different classes of proinflammatory regulators of vascular permeability and smoldering inflammation are selectively altered in HFrEF or HFpEF patients. Studies involving larger cohorts of these patients will be necessary to demonstrate the clinical implications of our findings.

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Source
http://dx.doi.org/10.1016/j.ejim.2022.10.014DOI Listing

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