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Refining the link between obesity and heart failure: insights from GLP-1 receptor agonist trials and studies adopting
Nicola Riccardo Pugliese1, Francesco Paneni2,3, Domenico Tricò1
1Department of Clinical and Experimental Medicine, University of Pisa, Via Roma 67, 56126, Pisa, Italy.
Insights
Intentional weight loss improves heart failure (HF) outcomes in overweight patients, challenging the "obesity paradox." Research highlights epicardial adipose tissue (EAT) as a key factor for targeted therapies.
Area of Science:
- Cardiology
- Metabolic Diseases
- Obesity Research
Background:
- Overweight and obesity are significant risk factors for heart failure (HF), impacting cardiac function through various physiological pathways.
- The relationship between adiposity and HF outcomes is complex, with the "obesity paradox" suggesting better survival in some obese HF patients.
- Recent trials with GLP-1 receptor agonists (GLP-1 RAs) indicate that weight loss interventions can positively affect outcomes in overweight/obese HF patients.
Purpose of the Study:
- To review the impact of weight loss on HF outcomes, particularly in light of recent GLP-1 RA trial findings.
- To explore the role of epicardial adipose tissue (EAT) as a potential marker for identifying HF patients who may benefit from anti-obesity treatments.
- To emphasize the need for further research into the mechanisms linking visceral fat accumulation to HF and to guide personalized therapeutic strategies.
Main Methods:
- Narrative review of current scientific literature.
- Analysis of recent clinical trial data, focusing on GLP-1 RA studies in HF patients.
- Examination of epidemiological and molecular data related to adiposity, EAT, and HF pathophysiology.
Main Results:
- Evidence suggests intentional weight loss, as achieved with GLP-1 RAs, can improve outcomes in overweight and obese patients with HF.
- Epicardial adipose tissue (EAT) is identified as a critical factor in HF pathophysiology, influencing cardiac structure and function.
- EAT may serve as a novel biomarker for stratifying patients for weight-loss therapies.
Conclusions:
- Weight loss interventions, including those using GLP-1 RAs, offer a promising therapeutic avenue for overweight/obese patients with HF.
- Characterizing adiposity phenotypes, particularly focusing on EAT, is crucial for optimizing patient selection for pharmacological weight-loss treatments.
- Future research should elucidate causal pathways between visceral fat measures and HF outcomes to enable personalized and effective treatment strategies.
Abstract:
Overweight and obesity are major risk factors for heart failure (HF), contributing to its development through metabolic, neurohormonal, haemodynamic, and inflammatory alterations. While overweight/obesity increases the risk of developing HF, its impact on patient outcomes remains complex. The "obesity paradox" suggests that a higher BMI may be associated with improved survival in patients with established HF. However, recent GLP-1 receptor agonist (GLP-1 RA) trials suggest that intentional weight loss positively influences outcomes in overweight/obese patients with HF. This seemingly contradictory evidence highlights the need for a deeper understanding of the mechanisms linking adiposity to HF outcomes. A more precise characterization of adiposity phenotypes using alternative and accurate measures of pathological fat accumulation is crucial in identifying individuals who may benefit most from anti-obesity treatments. In this context, recent research underscores the role of epicardial adipose tissue (EAT) in HF pathophysiology, as it directly influences cardiac function and structure through inflammatory, metabolic, and mechanical effects. This narrative review summarises current evidence on the impact of weight loss on HF outcomes, focusing on recent GLP-1 RA trial results. Additionally, it highlights epidemiological and molecular data supporting EAT as a novel adiposity measure that might allow refining patient selection for pharmacological weight-loss treatments. Finally, it emphasizes the need for future research to identify causal pathways linking alternative measures of visceral fat accumulation to HF outcomes. These efforts will be essential in optimizing the benefits of novel weight-loss treatments, ensuring effective and individualized therapeutic strategies for overweight or obese patients with HF.
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