Evidence Supporting the Existence of a Distinct Obese Phenotype of Heart Failure With Preserved Ejection Fraction
Open accessAbstract
Background: Heart failure (HF) with preserved ejection fraction (HFpEF) is a heterogeneous syndrome. Phenotyping patients into pathophysiologically homogeneous groups may enable better targeting of treatment. Obesity is common in HFpEF and has many cardiovascular effects, suggesting that it may be a viable candidate for phenotyping. We compared cardiovascular structure, function, and reserve capacity in subjects with obese HFpEF, those with nonobese HFpEF, and control subjects. Methods: Subjects with obese HFpEF (body mass index ≥35 kg/m 2 ; n=99), nonobese HFpEF (body mass index <30 kg/m 2 ; n=96), and nonobese control subjects free of HF (n=71) underwent detailed clinical assessment, echocardiography, and invasive hemodynamic exercise testing. Results: Compared with both subjects with nonobese HFpEF and control subjects, subjects with obese HFpEF displayed increased plasma volume (3907 mL [3563–4333 mL] versus 2772 mL [2555–3133 mL], and 2680 mL [2380–3006 mL]; P <0.0001), more concentric left ventricular remodeling, greater right ventricular dilatation (base, 34±7 versus 31±6 and 30±6 mm, P =0.0005; length, 66±7 versus 61±7 and 61±7 mm, P <0.0001), more right ventricular dysfunction, increased epicardial fat thickness (10±2 versus 7±2 and 6±2 mm; P <0.0001), and greater total epicardial heart volume (945 mL [831–1105 mL] versus 797 mL [643–979 mL] and 632 mL [517–768 mL]; P <0.0001), despite lower N-terminal pro-B-type natriuretic peptide levels. Pulmonary capillary wedge pressure was correlated with body mass and plasma volume in obese HFpEF ( r =0.22 and 0.27, both P <0.05) but not in nonobese HFpEF ( P ≥0.3). The increase in heart volumes in obese HFpEF was associated with greater pericardial restraint and heightened ventricular interdependence, reflected by increased ratio of right- to left-sided heart filling pressures (0.64±0.17 versus 0.56±0.19 and 0.53±0.20; P =0.0004), higher pulmonary venous pressure relative to left ventricular transmural pressure, and greater left ventricular eccentricity index (1.10±0.19 versus 0.99±0.06 and 0.97±0.12; P <0.0001). Interdependence was enhanced as pulmonary artery pressure load increased ( P for interaction <0.05). Compared with those with nonobese HFpEF and control subjects, obese patients with HFpEF displayed worse exercise capacity (peak oxygen consumption, 7.7±2.3 versus 10.0±3.4 and12.9±4.0 mL/min·kg; P <0.0001), higher biventricular filling pressures with exercise, and depressed pulmonary artery vasodilator reserve. Conclusions: Obesity-related HFpEF is a genuine form of cardiac failure and a clinically relevant phenotype that may require specific treatments.
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Patients with heart failure with preserved ejection fraction and obesity have more adverse hemodynamic and clinical features, greater symptom burden, worse functional capacity, and more severely impaired quality of life than those with heart failure with preserved ejection fraction but no obesity.
“Patients with this condition and obesity have more adverse hemodynamic and clinical features and a greater symptom burden, worse functional capacity, and more severely impaired quality of life than those with heart failure with preserved ejection fraction but no obesity. 9-12”
From Semaglutide in Patients with Heart Failure with Preserved Ejection Fraction and Obesity (2023) · cites this paper as [9]
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredAmong patients with established heart failure with preserved ejection fraction, those with the obesity phenotype have distinct clinical and hemodynamic features, including expanded plasma and stressed blood volume, reduced venous capacitance, elevations in exercise pulmonary wedge pressures, adverse hemodynamic response to diuresis, higher inflammatory markers, more pronounced hypertension, and m
“Among patients with established heart failure with preserved ejection fraction, those with the obesity phenotype have distinct clinical and hemodynamic features, including expanded plasma and stressed blood volume, reduced venous capacitance, elevations in exercise pulmonary wedge pressures, adverse hemodynamic response to diuresis, higher inflammatory markers, and more pronounced”
From Semaglutide in Patients with Heart Failure with Preserved Ejection Fraction and Obesity (2023) · cites this paper as [9]
The Results and Discussion report greater estimated plasma volume and higher exercise filling pressures, including pulmonary capillary wedge pressure, in obese than non-obese HFpEF. They do not establish expanded stressed blood volume, reduced venous capacitance, an adverse response to diuresis, or higher inflammatory markers. The Results report higher exercise blood pressure than controls, but not more pronounced hypertension than non-obese HFpEF. (LLM, conf=0.90)
Experimental — accuracy not yet measuredObesity causes increased epicardial and chest wall adiposity, amplifying ventricular interdependence, which is further exacerbated by plasma and blood volume expansion and excessive vasoconstriction, resulting in further worsening of HFpEF.
“Obesity also causes increased epicardial and chest wall adiposity, amplifying ventricular interdependence, 9 which is further exacerbated by plasma and blood volume expansion and excessive vasoconstriction, resulting in further worsening of HFpEF. 10,11,12”
From Semaglutide versus placebo in people with obesity-related heart failure with preserved ejection fraction: a pooled analysis of the STEP-HFpEF and STEP-HFpEF DM randomised trials (2024) · cites this paper as [9]
The Results section, “Myocardial, Pericardial and Ventricular Interactions” (page unavailable), reports greater epicardial fat and ventricular interaction in obese HFpEF. The Discussion links volume overload to hemodynamic abnormalities and reports inadequate pulmonary vasodilation during exercise. It does not establish a role for chest-wall adiposity or demonstrate excessive vasoconstriction as the claimed cause. (LLM, conf=0.87)
Experimental — accuracy not yet measuredAdditional evidence confirms that obesity is a contributing factor for type 2 diabetes, hypertension, and thrombotic episodes, as well as conditions linked to inflammation such as heart failure with preserved ejection fraction.
“Additional evi dence confirms that obesity is a contributing factor for type 2 diabetes, hypertension, and thrombotic ep isodes, as well as conditions linked to inflammation such as heart failure with preserved ejection frac tion. 2-7”
From Comprehensive Long-Term Changes in Cardiovascular Risk Biomarkers With Tirzepatide (2026) · cites this paper as [7]
The Discussion sections “Obesity and HFpEF” and “Clinical Implications” link obesity to HFpEF and describe inflammatory mechanisms. The cited paper does not establish the sentence’s additional claims that obesity contributes to type 2 diabetes, hypertension, or thrombotic episodes. Page numbers were not provided in our copy. (LLM, conf=0.88)
Experimental — accuracy not yet measuredThe favorable effects of tirzepatide on HF may be related to an amelioration of blood volume expansion that characterizes obesity-related HF, and the decrease in adipocyte mass would be expected to minimize the antinatriuretic effects of secreted adipocytokines (particularly leptin and aldosterone).
“The favorable effects of tirzepatide on HF may be related to an amelioration of the blood volume expansion that characterizes obesity-related HF,41 and the decrease in adipocyte mass would be expected to minimize the antinatriuretic effects of secreted adipocytokines (particularly leptin and aldosterone).42–44”
From Effects of Tirzepatide on the Clinical Trajectory of Patients With Heart Failure, Preserved Ejection Fraction, and Obesity (2025) · cites this paper as [41]
EAT mass may drive an abnormal ventricular distensibility determining a constrictive pattern responsible of pressure equalization across ventricles in different physiologic states, particularly during exercise and in patients with obesity and with or without diabetes.
“Occupying a fixed pericardial space, the EAT mass may drive an abnormal ventricular distensibility determining a constrictive pattern responsible of pressure equalization across ventricles in different physiologic states, particularly during exercise and in patients with obesity and with or without diabetes [85,86].”
From Dysregulated epicardial adipose tissue as a risk factor and potential therapeutic target of heart failure with preserved ejection fraction in diabetes (2022) · cites this paper as [85]
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Comprehensive Long-Term Changes in Cardiovascular Risk Biomarkers With Tirzepatide
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- Authors
- Obokata, M., Reddy, Y. N. V., Pislaru, S. V., Melenovsky, V., & Borlaug, B. A.
- Affiliations
- Mayo Clinic (US)
- From Department of Cardiovascular Medicine, Mayo Clinic, Rochester, MN (M.O., Y.N.V.R., S.V.P., V.M., B.A.B.); and Institute for Clinical and Experimental Medicine–IKEM, Prague, Czech Republic (V.M.).
- Venue
- Circulation
- Published
- 2017-07-04
- Volume
- 136
- Issue
- 1
- Pages
- 6-19
- ISSN
- 0009-7322 (ISSN-L)
- 1524-4539
- PMC
- PMC5501170
- OpenAlex
- W2604584410
- Cited by
- 1,179
- References
- 60
- Citations by year
- 2026: 147 · 2025: 190 · 2024: 149 · 2023: 121 · 2022: 138 · 2021: 124 · 2020: 120 · 2019: 82 · 2018: 82 · 2017: 23 · 2016: 1
- FWCI
- 64.98
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Circulation (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Heart, Lung, and Blood Institute (R01HL128526, U10HL110262, T32HL007111)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Heart Failure Treatment and Management
- Health Sciences › Medicine › Complementary and alternative medicine › Cardiovascular and exercise physiology
- Keywords
- heart failure with preserved ejection fraction, obesity, phenotyping, plasma volume, left ventricular remodeling, right ventricular dilatation, right ventricular dysfunction, epicardial adipose tissue, pulmonary capillary wedge pressure, N-terminal pro-brain natriuretic peptide, cardiac reserve, body mass index, echocardiography, cardiovascular structure and function
- MeSH terms
- Aged, Aged, 80 and over, Exercise Test, Female, Heart Failure, Hemodynamics, Humans, Male, Middle Aged, Obesity, Phenotype, Retrospective Studies, Stroke Volume, Cohort Studies, Ventricular Remodeling
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