{"title":"Pathophysiology of heart failure with preserved ejection fraction in overweight and obesity - Clinical and treatment implications.","authors":"Mariana M Rodrigues, L Menezes Falcão","doi":"10.1016/j.ijcard.2025.133182","DOIUrl":null,"url":null,"abstract":"<p><p>Heart failure with preserved ejection fraction (HFpEF) is a heterogeneous syndrome with vast prevalence worldwide. Despite recent advances in understanding its pathophysiology, HFpEF remains under-diagnosed in clinical practice. Obesity-related HFpEF is a distinct and frequent phenotype with an additionally challenging diagnosis. We address the importance of overweight and obesity in HFpEF, focusing on the influence of adipose tissue in inflammation and neurohormonal activity. We also discuss atrial and ventricular remodelling in obesity-related HFpEF and potential clinical implications. Obesity is an independent risk factor for HFpEF. Adipose tissue synthesizes aldosterone, causing lower levels of natriuretic peptide. Adipocytes dysfunction promotes a pro-inflammatory state and leads to extracellular matrix remodelling and consequently stiffening of the heart and vessels. Thus, the quantity, distribution and quality of the excess fat influences cardiovascular risk. Visceral and epicardial adipose tissue are often associated with an increased likelihood of developing HFpEF. Obesity-related HFpEF presents higher risk of left ventricular concentric remodelling and inadequate accommodation of the expanded volume due to the obesity, resulting in higher left ventricular filling pressure. Nevertheless, microvascular endothelium inflammation modifies cardiomyocyte elasticity and increases collagen deposition, which enhances myocardial fibrosis and results in HFpEF. Furthermore, neurohormonal activation may also contribute to cardiac remodelling by inducing plasma volume expansion. In turn, leptin also stimulates aldosterone synthesis and enhances renin-angiotensin-aldosterone system. Obesity-related HFpEF presents worse overall prognosis, with increased risk of heart failure hospitalization and all-cause mortality. Intentional weight loss through caloric restriction, physical activity, pharmacological intervention and/or bariatric surgery are promising strategies.</p>","PeriodicalId":13710,"journal":{"name":"International journal of cardiology","volume":" ","pages":"133182"},"PeriodicalIF":3.2000,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"International journal of cardiology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1016/j.ijcard.2025.133182","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"CARDIAC & CARDIOVASCULAR SYSTEMS","Score":null,"Total":0}
引用次数: 0
Abstract
Heart failure with preserved ejection fraction (HFpEF) is a heterogeneous syndrome with vast prevalence worldwide. Despite recent advances in understanding its pathophysiology, HFpEF remains under-diagnosed in clinical practice. Obesity-related HFpEF is a distinct and frequent phenotype with an additionally challenging diagnosis. We address the importance of overweight and obesity in HFpEF, focusing on the influence of adipose tissue in inflammation and neurohormonal activity. We also discuss atrial and ventricular remodelling in obesity-related HFpEF and potential clinical implications. Obesity is an independent risk factor for HFpEF. Adipose tissue synthesizes aldosterone, causing lower levels of natriuretic peptide. Adipocytes dysfunction promotes a pro-inflammatory state and leads to extracellular matrix remodelling and consequently stiffening of the heart and vessels. Thus, the quantity, distribution and quality of the excess fat influences cardiovascular risk. Visceral and epicardial adipose tissue are often associated with an increased likelihood of developing HFpEF. Obesity-related HFpEF presents higher risk of left ventricular concentric remodelling and inadequate accommodation of the expanded volume due to the obesity, resulting in higher left ventricular filling pressure. Nevertheless, microvascular endothelium inflammation modifies cardiomyocyte elasticity and increases collagen deposition, which enhances myocardial fibrosis and results in HFpEF. Furthermore, neurohormonal activation may also contribute to cardiac remodelling by inducing plasma volume expansion. In turn, leptin also stimulates aldosterone synthesis and enhances renin-angiotensin-aldosterone system. Obesity-related HFpEF presents worse overall prognosis, with increased risk of heart failure hospitalization and all-cause mortality. Intentional weight loss through caloric restriction, physical activity, pharmacological intervention and/or bariatric surgery are promising strategies.
期刊介绍:
The International Journal of Cardiology is devoted to cardiology in the broadest sense. Both basic research and clinical papers can be submitted. The journal serves the interest of both practicing clinicians and researchers.
In addition to original papers, we are launching a range of new manuscript types, including Consensus and Position Papers, Systematic Reviews, Meta-analyses, and Short communications. Case reports are no longer acceptable. Controversial techniques, issues on health policy and social medicine are discussed and serve as useful tools for encouraging debate.