Key result
Obesity significantly contributes to the development of HFpEF.
Why the study?
A paucity of effective therapies in HFpEF underscores the need to understand the distinct pathophysiological mechanisms of obese HFpEF to develop novel therapies.
This review highlights the distinct pathophysiological mechanisms of the obese HFpEF phenotype and underscores the need for novel targeted therapies.
May support obesity assessment in HFpEF; leaves open targeted therapy validation in trials.
Obesity and heart failure with preserved ejection fraction (HFpEF) represent two intermingling epidemics driving perhaps the greatest unmet health problem in cardiovascular medicine in the 21st century. Many patients with HFpEF are either overweight or obese, and recent data have shown that increased body fat and its attendant metabolic sequelae have widespread, protean effects systemically and on the cardiovascular system leading to symptomatic HFpEF. The paucity of effective therapies in HFpEF underscores the importance of understanding the distinct pathophysiological mechanisms of obese HFpEF to develop novel therapies. In this review, we summarize the current understanding of the cardiovascular and non-cardiovascular features of the obese phenotype of HFpEF, how increased adiposity might pathophysiologically contribute to the phenotype, and how these processes might be targeted therapeutically.
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Borlaug et al. (2022) studied this question. Obesity significantly contributes to the development of heart failure with preserved ejection fraction, highlighting the need for targeted therapies.
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