alexa Plasma sFlt-1 Fluctuations in Response to Pulmonary Arterial Hypertension Treatment
ISSN: 2329-6607

Cardiovascular Pharmacology: Open Access
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Research Article

Plasma sFlt-1 Fluctuations in Response to Pulmonary Arterial Hypertension Treatment

Bouzina H1,2*, Nielsen S3,4, Scheele C3-5 and Rådegran G1,2

1Department of Clinical Sciences Lund, Cardiology, Lund University, Lund, Sweden

2The Hemodynamic Lab, The Section for Heart Failure and Valvular Disease, VO Heart and Lung Medicine, Skåne University Hospital, Lund, Sweden

3The Centre for Inflammation and Metabolism, University of Copenhagen and Rigshospitalet, Copenhagen, Denmark

4Centre for Physical Activity Research, University of Copenhagen and Rigshospitalet, Copenhagen, Denmark

5The Novo Nordisk Foundation Center for Basic Metabolic Research, University of Copenhagen, Denmark

*Corresponding Author:
Habib Bouzina
The Hemodynamic Lab
The Section for Heart Failure and Valvular Disease
VO Heart and Lung Medicine
Skåne University Hospital, Lund, Sweden
Tel: +46 73 74 72 914
E-mail: [email protected]

Received Date: March 18, 2017; Accepted Date: April 10, 2017; Published Date: April 17, 2017

Citation: Bouzina H, Nielsen S, Scheele C, Rådegran G (2017) Plasma sFlt- 1 Fluctuations in Response to Pulmonary Arterial Hypertension Treatment. Cardiovasc Pharm Open Access 6:207. doi: 10.4172/2329-6607.1000207

Copyright: © 2017 Bouzina H, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

 

Abstract

Background: Pulmonary Arterial Hypertension (PAH) is characterized by vasoconstriction and remodeling of distal pulmonary arteries, which result in increased Pulmonary Vascular Resistance (PVR) and right ventricular overload. In the present study, we measured plasma fluctuations of nine proteins, involved in inflammation or tyrosine kinase signaling, in PAH patients, to assess their value as biomarkers of treatment response.

Methods: Plasma vascular endothelial growth factor A and D, soluble fms-like tyrosine kinase-1 (sFlt-1), placenta growth factor, fibroblast growth factor 2, angiopoietin-1 receptor, interleukin (IL)-6 and -8 and tumor necrosis factor α were determined by multiplex immunoassays in 21 treatment-naïve PAH patients at baseline and at first and second clinical checkups.

Results: From baseline to first checkup, sFlt-1 (p<0.02) and IL-6 (p<0.005) decreased in PAH patients. sFlt-1 remained decreased (p<0.003) at the second checkup, compared to baseline. No significant changes were observed in the other measured biomarkers. Patients receiving initial combination therapy showed a more marked initial decrease (p<0.02) in plasma sFlt-1, compared to initial monotherapy. Plasma sFlt-1 changes correlated positively with changes in PVR and negatively with changes in left ventricular stroke work index (LVSWI).

Conclusion: Plasma sFlt-1 is significantly reduced after the initiation of PAH-specific treatment and its fluctuations are correlated to changes in PVR and LVSWI. Thus, plasma sFlt-1 is a new potential biomarker for evaluating treatment response in PAH

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