Myocardial Metabolism in Heart Failure with Preserved Ejection Fraction

Henry, John Aaron; Couch, Liam S.; Rider, Oliver J.

doi:10.3390/jcm13051195

Cited by 3 publications

References 116 publications

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Lifestyle interventions in cardiometabolic HFpEF: dietary and exercise modalities

Vacca,

Wang,

Nambiar

et al. 2024

Heart Fail Rev

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Heart failure with preserved ejection fraction (HFpEF) is rapidly growing as the most common form of heart failure. Among HFpEF phenotypes, the cardiometabolic/obese HFpEF — HFpEF driven by cardiometabolic alterations — emerges as one of the most prevalent forms of this syndrome and the one on which recent therapeutic success have been made. Indeed, pharmacological approaches with sodium-glucose cotransporter type 2 inhibitors (SGLT2i) and glucagon-like peptide-1 receptor agonists (GLP-1RA) have proved to be effective due to metabolic protective effects. Similarly, lifestyle changes, including diet and exercise are crucial in HFpEF management. Increasing evidence supports the important role of diet and physical activity in the pathogenesis, prognosis, and potential reversal of HFpEF. Metabolic derangements and systemic inflammation are key features of HFpEF and represent the main targets of lifestyle interventions. However, the underlying mechanisms of the beneficial effects of these interventions in HFpEF are incompletely understood. Hence, there is an unmet need of tailored lifestyle intervention modalities for patients with HFpEF. Here we present the current available evidence on lifestyle interventions in HFpEF management and therapeutics, discussing their modalities and potential mechanisms.

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Lifestyle interventions in cardiometabolic HFpEF: dietary and exercise modalities

Vacca,

Wang,

Nambiar

et al. 2024

Heart Fail Rev

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The fate of pyruvate dictates cell growth by modulating cellular redox potential

Toshniwal,

Lam,

Bott

et al. 2024

Preprint

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Pyruvate occupies a central node in carbohydrate metabolism such that how it is produced and consumed can optimize a cell for energy production or biosynthetic capacity. This has been primarily studied in proliferating cells, but observations from the post-mitotic Drosophila fat body led us to hypothesize that pyruvate fate might dictate the rapid cell growth observed in this organ during development. Indeed, we demonstrate that augmented mitochondrial pyruvate import prevented cell growth in fat body cells in vivo as well as in cultured mammalian hepatocytes and human hepatocyte-derived cells in vitro. This effect on cell size was caused by an increase in the NADH/NAD+ ratio, which rewired metabolism toward gluconeogenesis and suppressed the biomass-supporting glycolytic pathway. Amino acid synthesis was decreased, and the resulting loss of protein synthesis prevented cell growth. Surprisingly, this all occurred in the face of activated pro-growth signaling pathways, including mTORC1, Myc, and PI3K/Akt. These observations highlight the evolutionarily conserved role of pyruvate metabolism in setting the balance between energy extraction and biomass production in specialized post-mitotic cells.

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Efficacy of Sacubitril/Valsartan in a Patient With Heart Failure and Impaired Secretion of Atrial Natriuretic Peptide Due to Long-Standing Persistent Atrial Fibrillation

Kurisu,

Fujiwara

2024

Cureus

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Atrial natriuretic peptide (ANP) is a circulating hormone released from the atria in response to wall stretch and volume overload in the setting of heart failure. When atrial fibrillation (AF) becomes long-standing persistent, ANP secretion in response to volume overload is impaired due to degenerative changes of the atria. Here, we report a case of heart failure with preserved ejection fraction and impaired ANP secretion due to long-standing AF. N-terminal pro-brain natriuretic peptide (NT-proBNP) level was elevated (269 pg/mL), whereas the increase in ANP level was marginal (46.1 pg/mL), suggesting impaired ANP secretion due to long-standing AF. Valsartan (80 mg/day) was replaced with sacubitril/valsartan (100 mg/day) without changing other medications. Administration of sacubitril/valsartan was effective in improving the patient’s symptoms, such as dyspnea and edema, and reducing NT-proBNP level by increasing endogenous ANP level from 46.1 pg/mL to 117 pg/mL in the first four weeks. This case highlights the possibility of impaired ANP secretion in response to volume overload as a predictor of the diuretic effect of sacubitril/valsartan in heart failure. This may lead to individualized treatment for each patient with heart failure based on natriuretic peptide profiles.

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Myocardial Metabolism in Heart Failure with Preserved Ejection Fraction

Cited by 3 publications

References 116 publications

Lifestyle interventions in cardiometabolic HFpEF: dietary and exercise modalities

Lifestyle interventions in cardiometabolic HFpEF: dietary and exercise modalities

The fate of pyruvate dictates cell growth by modulating cellular redox potential

Efficacy of Sacubitril/Valsartan in a Patient With Heart Failure and Impaired Secretion of Atrial Natriuretic Peptide Due to Long-Standing Persistent Atrial Fibrillation

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