Do obesity and visceral adiposity promote heart failure with reduced ejection fraction?

Published Sep 2, 2025European heart journal

Do Obesity and Belly Fat Increase the Risk of Heart Failure with Reduced Pumping Strength?

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Abstract

Central obesity is more strongly associated with adverse heart failure outcomes in than in .

Obesity or excess visceral fat is important in heart failure with preserved ejection fraction (HFpEF) but not clearly linked to heart failure with reduced ejection fraction (HFrEF).
Epicardial adipose tissue is expanded in HFpEF, while it is diminished in HFrEF, with decreased levels associated with worse prognosis.
In the general population, obesity predicts the occurrence of HFpEF but not HFrEF.
Elevated levels of high-sensitivity C-reactive protein (hsCRP) predict HFpEF development, suggesting a role of systemic inflammation in its progression.
Weight loss from incretin-based drugs reduces systolic blood pressure and lowers the risk of worsening heart failure events in HFpEF, but not in HFrEF.

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Obesity or excess visceral adiposity plays a fundamental role in the pathogenesis of heart failure with preserved ejection fraction (), but it is not clear that an expanded adipose tissue mass contributes importantly to the evolution and progression of heart failure with reduced ejection fraction (). Whereas central adiposity characterizes most patients with HFpEF, obesity was not a remarkable feature of HFrEF in the large-scale trials carried out in the 1980s and 1990s, and studies typically characterized obesity as a protective factor against adverse outcomes. In the general community without apparent heart disease, the finding of obesity or central adiposity precedes and predicts the subsequent occurrence of HFpEF, but not HFrEF. The mass of epicardial adipose tissue-an important source of cardioactive molecules-is expanded in HFpEF, but it is diminished in HFrEF, and the decrease has adverse prognostic significance. An increased waist-to-height ratio (a marker of excess abdominal adiposity) is more strongly associated with adverse heart failure outcomes in HFpEF than in HFrEF. Systemic inflammation [as reflected by elevations of high-sensitivity C-reactive protein (hsCRP)] in the general community presages the development of HFpEF, but not HFrEF, presumably because excess adiposity augments hsCRP in HFpEF, whereas increases in hsCRP in HFrEF may be related to coexisting atherosclerosis or clinical congestion. Whereas obesity is the principal determinant of serum levels of leptin and adiponectin in HFpEF, cardiac and neurohormonal signalling may drive circulating levels of these adipokines in HFrEF. Central obesity identifies patients more likely to respond to mineralocorticoid receptor antagonists in both HFpEF and in HFrEF, but this feature also identifies patients more likely to respond neprilysin inhibition or sodium-glucose cotransporter 2 inhibitors if they have HFpEF, but not HFrEF. Weight loss by incretin-based drugs lowers systolic blood pressure in patients with HFpEF, but potentially not with HFrEF, and such weight loss is accompanied by a reduced risk of worsening heart failure events in patients with HFpEF, but without a similar benefit in HFrEF. Taken collectively, these observations raise important questions about the potential role of obesity and visceral adiposity as contributing factors in the evolution and progression of HFrEF.

Key numbers

60%–70%

Obesity Prevalence in

Percentage of patients with body mass index ≥ 30 kg/m.

27%

Obesity Prevalence in

Percentage of patients with body mass index ≥ 30 kg/m.

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Do obesity and visceral adiposity promote heart failure with reduced ejection fraction?

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