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Therapeutic effect of Urocortin-2 in Heart Failure with Preserved Ejection Fraction
Session:
Comunicações Orais (Sessão 17) - Ciência Básica e Saúde Digital
Speaker:
Inês Vasconcelos
Congress:
CPC 2022
Topic:
O. Basic Science
Theme:
36. Basic Science
Subtheme:
36.3 Basic Science - Cardiac Diseases
Session Type:
Comunicações Orais
FP Number:
---
Authors:
Inês Vasconcelos; Rui Adão; Pedro Vaz-Salvador; Glória Conceição; Daniela Miranda-Silva; Joana Santos-Gomes; Beatriz Rego; Carolina Maia-Rocha; Inês Gandra; Pedro Mendes-Ferreira; Adelino Leite-Moreira; Ana Patrícia Fontes-Sousa; Carmen Brás-Silva
Abstract
<p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:Arial,sans-serif"><strong><span style="font-size:11.0pt">Introduction: </span></strong><span style="font-size:11.0pt">Although initially believed to be less severe than heart failure with reduced ejection fraction (HFrEF), heart failure with preserved ejection fraction (HFpEF) prevalence has increased and accounts for as much as 50% of heart failure cases. Treatment options remain limited and aim primarily for symptom relief and improvement of patients’ quality of life. Urocortin-2 (Ucn-2) belongs to the corticotrophin-releasing hormone family and has been found to have significant beneficial hemodynamic, hormonal and renoprotective effects in both animal models and humans with HFrEF.</span></span></span></p> <p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:Arial,sans-serif"><strong><span style="font-size:11.0pt">Objectives: </span></strong><span style="font-size:11.0pt">In this work we studied the role of the Ucn-2/CRHR2 system in the pathophysiology of HFpEF and evaluated the efficacy of Ucn-2 as a novel therapeutic strategy in this clinical syndrome.</span></span></span></p> <p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:Arial,sans-serif"><strong><span style="font-size:11.0pt">Methods: </span></strong><span style="font-size:11.0pt">18-week-old male ZSF1-Lean (n=26) and ZSF1-Obese (n=28) rats randomly received either Ucn-2 (15 μg/kg/day, subcutaneously) or vehicle (0.9% NaCl), for 12 weeks. During the treatment period evolution of cardiac (dys)function was assessed by echocardiography. After treatment, invasive hemodynamic analysis was performed, with subsequent sample collection.</span> <span style="font-size:11.0pt">Histological analysis of the left ventricle (LV) was performed as well as quantitative RT-PCR analysis for relevant molecular markers.</span></span></span></p> <p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:Arial,sans-serif"><strong><span style="font-size:11.0pt">Results: </span></strong><span style="font-size:11.0pt">mRNA expression of Ucn-2 and CRHR2 was decreased in the LV of ZSF1-Obese rats compared to ZSF1-Lean and correlated with LV structure and diastolic function. In both morphometric and echocardiographic analysis we found that ZSF1-Obese rats presented significantly higher cardiac and LV weight, compared to Lean counterparts. Cardiomyocyte cross-sectional area and fibrosis were found to be increased in Obese rats, corroborating morphometric and echocardiographic measurements. Chronic Ucn-2 treatment showed beneficial effects in both cardiac hypertrophy and fibrosis. Furthermore, </span><span style="font-size:11.0pt">ZSF1-Obese rats displayed increased BNP and TNF-</span><span style="font-size:11.0pt">α LV </span><span style="font-size:11.0pt">mRNA expression, both of which were decreased with chronic treatment. Interestingly, Col3A1 LV mRNA expression was found to be decreased in ZSF1-Obese rats compared to ZSF1-Lean, and Ucn-2 chronic treatment resulted in a faint further decrease of Col3A1 expression, compared to non-treated animals. </span></span></span></p> <p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:Arial,sans-serif"><strong><span style="font-size:11.0pt">Conclusion:</span></strong><span style="font-size:11.0pt"> This work suggests that Ucn-2/CRHR2 system is altered in experimental HFpEF and that chronic administration of Ucn-2 attenuates LV remodeling, in particular the hypertrophic changes of the cardiac muscle, a beneficial effect for patients with HFpEF.</span></span></span></p>
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