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The SGLT2 inhibitor also displayed its efficacy in reducing left ventricular myocardial fibrosis and volume, as well as improving diastolic filling dynamics.
Dapagliflozin has proven its efficacy in substantially reducing epicardial adipose tissue (EAT), left ventricular (LV) myocardial fibrosis and volume, and improved diastolic filling dynamics in patients with asymptomatic heart failure (HF).1
Data from the DAPA-EAT trial were presented at the American Heart Association’s Scientific Sessions 2025 in New Orleans, Louisiana, by Akira Taruya, MD, assistant professor of cardiovascular medicine at Wakayama Medical University and lead study author.1
Previous research has indicated dapagliflozin’s comparative efficacy in heart failure with both preserved and reduced ejection fraction. For instance, the DELIVER trial in 2022 evaluated a broad patient group, showing a lower risk of worsening HF or cardiovascular death compared to placebo. However, little research has been conducted on dapagliflozin, or SGLT2 inhibitors in general, in terms of asymptomatic HF.2
“Epicardial adipose tissue is a metabolically active visceral fat depot implicated in the pathogenesis of heart failure, even at asymptomatic stages,” Taruya and colleagues wrote. “Although SGLT2 inhibitors have demonstrated benefits in symptomatic HF, their effects on EAT and early cardiac remodeling in asymptomatic HF remains unclear.”1
DAPA-EAT was a multicenter, randomized, open-label trial enrolling 229 patients with asymptomatic HF. It was conducted across 8 hospitals in Wakayama, Japan, and although treatment allocation was open-label, evaluators of computed tomography and echocardiography, biomarker analysts, and statisticians were blinded to ensure unbiased assessments.3
Patients eligible for inclusion were aged ≥20 years with stage B HF, excluding those with severe valvular heart disease. Those on preventive heart failure therapy with no medication changes for ≥2 weeks were also eligible.3
At index, patients underwent anthropometry, blood tests, a transthoracic echocardiogram, and computed tomography. They were then randomly assigned in a 1:1 ratio to either dapagliflozin (n = 114) or standard therapy (n = 115) for 24 weeks. The primary endpoint was a change in EAT volume from baseline to 24 weeks, which was assessed via cardiac computed tomography. Secondary endpoints included changes in LV myocardial fibrosis and volume, echocardiographic indices, biomarkers such as NT-proBNP and high-sensitivity CRP, and clinical outcomes.1,3
Ultimately, Taruya and colleagues found that dapagliflozin substantially reduced EAT volume compared to the control cohort (-15.6 mL vs 9.6 mL; between-group difference, -25.2 mL; 95% CI, -30.83 to -19.57; P <.001). LV myocardial fibrosis volume (P <.001), and LV myocardial volume (P <.001) also decreased substantially.1
The majority of echocardiographic parameters showed no significant differences, however. E/A ratio improved significantly, but no substantial changes were observed in the biomarkers. Composite cardiovascular events – defined as symptomatic HF and sudden death – occurred in 1 patient in the dapagliflozin group and in 5 patients in control. Investigators reported only rare serious adverse events, noting that they were unrelated to the study group.1
Ultimately, among patients with asymptomatic HF, Taruya and colleagues found a significant reduction in EAT volume, LV myocardial fibrosis and volume, and improved diastolic filling dynamics, all without significant safety concerns.1
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