Photo Credit: EyeEm
The following is a summary of “Effect of Semaglutide on Cardiac Structure and Function in Patients With Obesity-Related Heart Failure,” published in the October 2024 issue of Cardiology by Solomon et al.
Obesity contributes to adverse cardiac remodeling and is a crucial factor in the development and progression of heart failure (HF). Patients with obesity-related heart failure with preserved ejection fraction (HFpEF) may benefit from once-weekly semaglutide (2.4 mg) treatment.
Researchers conducted a prospective study to evaluate the effects of semaglutide on cardiac structure and function in patients with obesity-related HFpEF.
They performed echocardiography at randomization and after 52 weeks in 491 of 1,145 participants (43%) from the STEP-HFpEF Program (Semaglutide Treatment Effect in People with Obesity and HFpEF) and STEP-HFpEF DM (Semaglutide Treatment Effect in People with Obesity, HFpEF, and Type 2 Diabetes) trials. The primary outcome was the change in left atrial (LA) volume, with treatment effects assessed using analysis of covariance stratified by trial and body mass index (P=0.0013).
The results showed that baseline clinical and echocardiographic characteristics were balanced between participants receiving semaglutide (n = 253) and those receiving placebo (n = 238). Over the 52 weeks, semaglutide treatment attenuated the progression of LA remodeling (estimated mean difference in LA volume: −6.13 mL; 95% CI: −9.85 to −2.41 mL; P=0.0013) and reduced right ventricular (RV) enlargement (estimated mean difference in RV end-diastolic area: −1.99 cm2; 95% CI: −3.60 to −0.38 cm2; P=0.016; estimated mean difference in RV end-systolic area: −1.41 cm2; 95% CI: −2.42 to −0.40 cm2; P=0.0064) compared to placebo. Semaglutide also improved E-wave velocity (estimated MD: −5.63 cm/s; 95% CI: −9.42 to −1.84 cm/s; P=0.0037), the E/A (early/late mitral inflow velocity) ratio (estimated MD: −0.14; 95% CI: −0.24 to −0.04; P=0.0075), and the E/e′ (early mitral inflow velocity/early diastolic mitral annular velocity) average (estimated MD: −0.79; 95% CI: −1.60 to 0.01; P=0.05). Associations were not influenced by diabetes or atrial fibrillation status. Semaglutide did not affect LV dimensions, mass, or systolic function. Greater weight loss with semaglutide was associated with a more substantial reduction in LA volume (P interaction = 0.033). Still, it was not the case for changes in E-wave velocity, E/e′ average, or RV end-diastolic area.
They concluded that semaglutide may improve adverse cardiac remodeling in patients with obesity-related HFpEF.
Source: jacc.org/doi/10.1016/j.jacc.2024.08.021
