Obesity is a major risk factor for heart failure (HF), particularly heart failure with preserved ejection fraction (HFpEF).
Up to 80% of individuals with HFpEF are overweight or obese, making it a critical treatment focus.
The "obesity paradox" suggested that mild overweight might protect against HF-related morbidity and mortality.
Observational studies supporting the paradox failed to distinguish between intentional and unintentional weight loss.
Recent trials, STEP-HFpEF and STEP-HFpEF DM have disproved the obesity paradox.
Semaglutide, a GLP-1 receptor agonist (GLP-1 RA), showed significant benefits in HFpEF patients.
These benefits included improved HF symptoms, physical limitations, and weight loss.
Semaglutide was effective in patients with and without type 2 diabetes (T2D).
The trials demonstrated reductions in inflammatory markers and improved cardiac remodeling.
The findings highlight that weight loss is an essential but not the sole mechanism of benefit.
Combination therapies, such as GLP-1 RAs with SGLT2 inhibitors, are highly effective.
In severe cases, bariatric surgery remains a critical option for rapid and sustained weight loss.
Emerging therapies like tirzepatide are showing promise for both HF and obesity management.
Future research is needed to explore long-term outcomes and equitable access to these treatments.
These advancements represent a paradigm shift in HF care and obesity management.
Take-Home Points:
- Obesity is a critical factor in the management of HFpEF.
- The "obesity paradox" has been disproven by recent clinical trials.
- Semaglutide improves HF symptoms, weight loss, and underlying pathology.
- Bariatric surgery offers rapid and effective weight loss for severe cases.
- Combination therapies like GLP-1 RAs and SGLT2 inhibitors are transformative.
- Emerging drugs such as tirzepatide hold great promise in HF care.
- Further research is crucial for understanding long-term benefits and access.
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