Key result
Systemic inflammation driven by obesity and aging underpins cardiometabolic HFpEF, requiring targeted immunometabolic interventions.
Why the study?
Broad anti-inflammatory therapy has not shown significant benefit in HFpEF outcomes, necessitating a better understanding of metabolic and age-related inflammation to guide targeted interventions.
Understanding the specific pathways of immunometabolic inflammation in cardiometabolic HFpEF is crucial for developing effective targeted therapies.
The most common form of heart failure is heart failure with preserved ejection fraction (HFpEF). While heterogeneous in origin, the most common form of HFpEF is the cardiometabolic manifestation. Obesity and aging promote systemic inflammation that appears integral to cardiometabolic HFpEF pathophysiology. Accumulation of immune cells within the heart, fueled by an altered metabolome, contribute to cardiac inflammation and fibrosis. In spite of this, broad anti-inflammatory therapy has not shown significant benefit in patient outcomes. Thus, understanding of the nuances to metabolic and age-related inflammation during HFpEF is paramount for more targeted interventions. Here, we review clinical evidence of inflammation in the context of HFpEF and summarize our mechanistic understanding of immunometabolic inflammation, highlighting pathways of therapeutic potential along the way.
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Thorp et al. (2024) conducted a review in Cardiometabolic Heart Failure with Preserved Ejection Fraction (HFpEF). Systemic inflammation driven by obesity and aging is integral to cardiometabolic HFpEF pathophysiology, highlighting the need for targeted immunometabolic interventions.
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