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A. Basics
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01. History of Cardiology
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04. Arrhythmias, General
05. Atrial Fibrillation
06. Supraventricular Tachycardia (non-AF)
07. Syncope and Bradycardia
08. Ventricular Arrhythmias and Sudden Cardiac Death (SCD)
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21. Pulmonary Circulation, Pulmonary Embolism, Right Heart Failure
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30. Cardiovascular Disease in Special Populations
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CLEAR FILTERS
Ketones strike back on the failing right ventricle
Session:
Sessão de Comunicações Orais 02 – Perspectivas translacionais na Insuficiência Cardíaca: dos modelos experimentais ao prognóstico clínico
Speaker:
Alexandre Gonçalves
Congress:
CPC 2026
Topic:
D. Heart Failure
Theme:
36. Basic Science
Subtheme:
36.3 Basic Science - Cardiac Diseases
Session Type:
Comunicações Orais
FP Number:
---
Authors:
Alexandre Gonçalves; Inês N Alves; Cláudia Mendes; Daniela Miranda-Silva; Diana Martins; Panagiotis Peppas; Carolina Silva; Isabel Miranda; Henrique Girao; Adelino Leite-Moreira; Vasco Sequeira; Inês Falcão-Pires
Abstract
<p><strong>Introduction</strong></p> <p>Pulmonary hypertension (PH) is a progressive condition characterized by elevated pulmonary arterial pressure, which increases the workload on the right ventricle (RV), often leading to RV hypertrophy, right heart failure, and ultimately decreased survival. This study examines the effects of a ketogenic diet (KD) on cardiac remodelling and function in a monocrotaline (MCT)-induced rat model of PH.</p> <p><strong>Methods</strong></p> <p>One week after MCT injection, Wistar Han rats were assigned to either a standard diet or KD, with dietary fat gradually increased following a one-week adaptation period (<strong>Figure 1A</strong>). During the weeks leading to the terminal procedures, the groups were subjected to echocardiography, metabolic, VO2max and endurance tests and blood collection. At the terminal procedures, tissue samples were collected for biochemical work and histology. Hearts were perfused in order to isolate left ventricular cardiomyocytes for intact studies.</p> <p><strong>Results</strong></p> <p>KD markedly improved RV remodelling and function, demonstrated by decreased RV area and eccentricity index paired with increased cardiac output (VTI) and reduced pulmonary arterial pressure (PAT) (<strong>Figure 1B</strong>). This improved remodelling was confirmed by a reduction in Fulton’s index, RV hypertrophy, lung congestion, pulmonary artery thickness and RV fibrosis (<strong>Figure 1C</strong>). These effects were associated with normalised levels of Rho family GTPase 1 (RND1) and latent transforming growth factor beta-binding protein 2 (LTBP2) (<strong>Figure 1D</strong>). Together, these effects contributed towards a significant delay in mortality and improved maximum exercise capacity, the main outcomes of this study (<strong>Figure 1E</strong>). However, improvements in cardiac function did not extend to single-cell studies, where KD failed to reverse MCT-induced defects in excitation-contraction coupling. Restoration of RV PPARGC1A levels in MCT-KD rats suggests enhanced mitochondrial function, despite persistent bioenergetic deficits.</p> <p><strong>Conclusion</strong></p> <p>Overall, these findings indicate that KD may offer a promising adjuvant therapeutic strategy in PH by improving RV function, reducing adverse remodelling, and favourably modulating cardiac metabolism.</p>
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