On 31 August, at the 75th European Society of Cardiology (ESC) conference, during a late-breaking clinical science session on the topic of “Risk Factors and Prevention”, Nils Kruger, MD, presented findings on semaglutide and tirzepatide in patients with heart failure with preserved ejection fraction (HFpEF). Kruger focused on Novo Nordisk’s semaglutide and Lilly’s tirzepatide to highlight the progress made in glucagon-like peptide-1 receptor agonists (GLP-1RAs) for the management of HFpEF.
The findings presented at ESC highlighted that patients initiating semaglutide or tirzepatide had more than 40 % lower risk of hospitalisation for heart failure (HF) or all-cause mortality compared to sitagliptin. Head-to-head comparison showed tirzepatide provided no statistically significant advantage over semaglutide (HR = 0.86, 95% CI 0.70-1.06). Kruger also emphasised these findings exemplify how real-world evidence can meaningfully complement randomised clinical trials through structured and rigorous analyses rooted in benchmarks.
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The study included 58,333 patients in the semaglutide cohort and 11,257 patients in the tirzepatide cohort, with robust safety profiles and no significant increase in adverse events. This real-world evidence supports expanding GLP-1 agonist use beyond traditional diabetes and obesity indications to cardiometabolic HFpEF, addressing a significant unmet medical need where conventional heart failure therapies have shown limited efficacy.
Both semaglutide and tirzepatide have demonstrated transformative clinical efficacy in patients with heart failure HFpEF and obesity, establishing GLP-1 receptor agonists as a paradigm-shifting therapeutic class. In the STEP-HFpEF program, semaglutide significantly improved Kansas City Cardiomyopathy Questionnaire scores, reduced body weight by 7.8%-13.3%, enhanced exercise capacity as measured by 6-minute walk distance, and decreased inflammatory markers like C-reactive protein by over 40%. Tirzepatide demonstrated even more robust outcomes in the SUMMIT trial, reducing the composite risk of cardiovascular death or worsening heart failure events by 38% (HR 0.62), with particularly striking reductions in heart failure hospitalisations by 46% (HR 0.54). This positions them as adjunctive therapy alongside foundational therapies like SGLT2 inhibitors.
While GLP-1RAs demonstrate significant promise in HFpEF, penetration in HFrEF remains limited due to neutral or adverse effects, including a four-fold arrhythmia risk. A key opinion leader interviewed by GlobalData states: “I think that probably GLP-1RAs are more effective in interfering with the mechanisms, which are responsible for heart failure, and I would see GLP-1 receptor more effective, maybe in patients with preserved ejection fraction, because this kind of drug probably is more able to interfere with that kind of patient.”
While therapies such as GLP-1RAs address unmet needs in HF, they come with high price tags, and gaining market access against the cheaper, generic drugs continues to be a major barrier.
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