Metabolic inflammation plays a central role in the pathophysiology of heart failure with preserved ejection fraction (HFpEF), influencing its treatment and prevention.
Patients with heart failure with preserved ejection fraction (HFpEF)
This review highlights the central role of metabolic inflammation in the pathogenesis of HFpEF, suggesting it as a key framework for understanding syndrome progression and potential therapeutic targets.
Abstract One in 10 persons in the world aged 40 years and older will develop the syndrome of HFpEF (heart failure with preserved ejection fraction), the most common form of chronic cardiovascular disease for which no effective therapies are currently available. Metabolic disturbance and inflammatory burden contribute importantly to HFpEF pathogenesis. The interplay within these two biological processes is complex; indeed, it is now becoming clear that the notion of metabolic inflammation—metainflammation—must be considered central to HFpEF pathophysiology. Inflammation and metabolism interact over the course of syndrome progression, and likely impact HFpEF treatment and prevention. Here, we discuss evidence in support of a causal, mechanistic role of metainflammation in shaping HFpEF, proposing a framework in which metabolic comorbidities profoundly impact cardiac metabolism and inflammatory pathways in the syndrome.
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Gabriele G. Schiattarella
Daniele Rodolico
Joseph A. Hill
Cardiovascular Research
The University of Texas Southwestern Medical Center
Università Cattolica del Sacro Cuore
Federico II University Hospital
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Schiattarella et al. (Tue,) reported a other. Metabolic inflammation plays a central role in the pathophysiology of heart failure with preserved ejection fraction (HFpEF), influencing its treatment and prevention.
www.synapsesocial.com/papers/697240a8da50910f9664e742 — DOI: https://doi.org/10.1093/cvr/cvaa217