Key result
Metabolic inflammation drives HFpEF pathophysiology and influences its treatment and prevention.
Why the study?
HFpEF is a highly prevalent condition lacking effective therapies, where the complex interplay between metabolic disturbance and inflammatory burden contributes importantly to pathogenesis.
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.
May guide HFpEF prevention strategies; extends pathogenesis understanding but leaves open clinical validation.
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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Schiattarella et al. (2020) studied this question. Metabolic inflammation plays a central role in the pathophysiology of heart failure with preserved ejection fraction (HFpEF), influencing its treatment and prevention.
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