Why the study?
Conflicting evidence and apparent contradictions exist in the HFpEF metabolism literature regarding cardiac fatty acid and glucose oxidation.
This systematic review clarifies that in HFpEF, fatty acid oxidation is maintained or increased while glucose oxidation is impaired, suggesting therapeutic strategies should focus on restoring metabolic flexibility.
Supports targeting metabolic flexibility in HFpEF trials; extends evidence via direct over indirect phenotyping.
Direct measurements reveal fatty acid oxidation remains active or increased in HFpEF hearts, whereas glucose oxidation becomes impaired, challenging previous assumptions. Apparent contradictions in HFpEF metabolism literature arise from methodological differences-studies using isolated mitochondria versus intact hearts. Evidence demonstrates fatty acid oxidation is maintained in HFpEF, with defects primarily in glucose oxidation. Successful therapeutic strategies should prioritize restoring metabolic flexibility rather than simply modulating fatty acid oxidation pathways.
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Shehadeh et al. (2025) studied this question.
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