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A. Basics
B. Imaging
C. Arrhythmias and Device Therapy
D. Heart Failure
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01. History of Cardiology
02. Clinical Skills
03. Imaging
04. Arrhythmias, General
05. Atrial Fibrillation
06. Supraventricular Tachycardia (non-AF)
07. Syncope and Bradycardia
08. Ventricular Arrhythmias and Sudden Cardiac Death (SCD)
09. Device Therapy
10. Chronic Heart Failure
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20. Congenital Heart Disease and Pediatric Cardiology
21. Pulmonary Circulation, Pulmonary Embolism, Right Heart Failure
22. Aortic Disease
23. Peripheral Vascular and Cerebrovascular Disease
24. Stroke
25. Interventional Cardiology
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28. Risk Factors and Prevention
29. Rehabilitation and Sports Cardiology
30. Cardiovascular Disease in Special Populations
31. Pharmacology and Pharmacotherapy
32. Cardiovascular Nursing
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Role of Urocortin-2 in Heart Failure with Preserved Ejection Fraction
Session:
Prémio Jovem Investigador
Speaker:
Rui Adão
Congress:
CPC 2020
Topic:
O. Basic Science
Theme:
36. Basic Science
Subtheme:
36.3 Basic Science - Cardiac Diseases
Session Type:
Prémios
FP Number:
---
Authors:
Rui Adão; Glória Conceição; Daniela Miranda-Silva; Sónia Miranda; Luís D. Pimentel; Pedro Vaz-Salvador; Carolina Maia-Rocha; Pedro Mendes-Ferreira; André Lourenço; Inês Falcão-Pires; Adelino Leite-Moreira; Carmen Brás Silva
Abstract
<p>Introduction: Heart failure with preserved ejection fraction (HFpEF) is frequently accompanied by the metabolic syndrome and kidney disease. Because current treatment options of HFpEF are limited, evaluation of therapies in experimental models of HFpEF with the metabolic syndrome is needed. Urocortin 2 (Ucn2) is a cardioprotective peptide belonging to the corticotrophin-releasing hormone (CRH) family. In animal models and humans with HF with reduced ejection fraction, Ucn2 has been shown to exert favorable effects on left ventricle (LV) function, as well as on neurohumoral and renal parameters.</p> <p>Aims: In this work we studied the role of the Ucn2/CRHR2 system in the pathophysiology of HFpEF, and we evaluated the efficacy of Ucn2 as a novel therapeutic strategy in this disease.</p> <p>Methods: Ucn2 (15 microg/Kg/day, subcutaneous) or vehicle was administered to lean and obese ZSF1 rats aged 18 to 30 weeks (6-7 animals/group). Animals were then used for oxygen consumption under maximum effort (VO2max) evaluation, oral glucose tolerance test, insulin resistance test and sample collection after 12 weeks of treatment. Temporal evolution of cardiac (dys)function was assessed by echocardiography.</p> <p>Results: mRNA expression of Ucn2 and CRHR2 is decreased in LV from ZSF1 obese rats compared to ZSF1 lean, and it is correlated to left atrium area and diastolic function (E/E´). Although Ucn-2 chronic treatment did not attenuate the body weight gain and the impaired exercise capacity in experimental HFpEF, Ucn-2 treatment improved glucose tolerance in ZSF1 obese rats. By echocardiography, we demonstrated that there is no differences in ejection fraction between groups and that Ucn-2 therapy attenuated LV mass in ZSF1-Obese animals compared to non-treated group. No differences were observed in E/E´ parameter.</p> <p>Conclusion: This study suggests that chronic administration of Ucn2 could be beneficial in patients with HFpEF, attenuating LV remodelling and improving glucose tolerance.</p>
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