Key result
Obese patients with HFpEF exhibit a distinct clinical phenotype characterized by worse hemodynamics, increased biventricular remodeling, and poorer functional capacity compared to non-obese patients.
Why the study?
Obesity is a predominant comorbid condition in the rising incidence of HFpEF, making it crucial to clearly characterize the obesity phenotype and compare it to HFpEF without obesity.
Obesity drives a distinct and severe phenotype in HFpEF, emphasizing the importance of targeted weight management and specific pharmacotherapies like SGLT2 inhibitors and GLP-1 receptor agonists.
Obese HFpEF identifies a high-risk phenotype; extends observational data but leaves open whether weight-focused therapies improve outcomes.
The incidence of heart failure with preserved ejection fraction (HFpEF) continues to rise, and obesity continues to be a predominant comorbid condition affecting patients with HFpEF. Recent research sheds light on the important pathophysiologic role that obesity plays in the development of HFpEF, with many areas of opportunity existing for future developments in understanding the etiology and management of the disease. Crucial in these pathophysiologic developments are studies that clearly characterize the obesity phenotype in HFpEF and compare it to presentations of HFpEF in patients without obesity. This paper reviews the existing literature on the obesity phenotype within HFpEF and discusses some of the prevailing ideas behind the pathophysiologic interplay between the conditions, as well as the existing treatments demonstrating improved outcomes in HFpEF.
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Michelle et al. (2024) conducted a review in Heart Failure with Preserved Ejection Fraction (HFpEF) and Obesity. Obesity vs. Non-obese patients with HFpEF was evaluated. Obese patients with HFpEF exhibit a distinct clinical phenotype characterized by worse hemodynamics, increased biventricular remodeling, and poorer functional capacity compared to non-obese patients.
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