Key result
Dietary weight-management intervention reduces LVEDD by ~4.4 mm over 15 months in obese diabetic HF.
Why the study?
Obesity is associated with adverse cardiac remodeling in heart failure, but changes in left ventricular structure and function during dietary weight management are not well described.
Does a hypocaloric diet (high-protein vs. standard-protein) improve left ventricular structure and function in adults with chronic heart failure, type 2 diabetes, and obesity?
RCT (n=92)
Single-blind
Allocation algorithm balanced by study site, age, sex, race/ethnicity, and baseline exercise capacity
Yes
Does a hypocaloric diet (high-protein vs. standard-protein) improve left ventricular structure and function in adults with chronic heart failure, type 2 diabetes, and obesity?
Mean Difference: -4.44 (95% CI -6.86–-2.02)
p-value: p=nominal p < 0.001; Holm-adjusted p = 0.002
A structured hypocaloric dietary intervention over 15 months was associated with a modest reduction in left ventricular end-diastolic dimension in patients with heart failure, type 2 diabetes, and obesity, regardless of dietary protein composition.
Supports dietary weight loss for LV remodeling in obese HF with T2D; extends RCT evidence on hypocaloric diets independent of protein content.
Background: Obesity is associated with adverse cardiac remodeling in heart failure (HF), but changes during dietary weight management are not well described. We examined longitudinal changes in left ventricular (LV) structure and systolic function during a dietary weight-management intervention. Methods: Pro-HEART participants were randomized to high-protein or standard-protein hypocaloric diets. LV end-diastolic dimension (LVEDD), ejection fraction (LVEF), and posterior wall thickness (LVPWT) were assessed at baseline, 3 months, and 15 months. Linear mixed-effects models tested time and diet effects. Results: At 15 months, LVEDD data were available for 31 of 92 participants (33.7%). Achieved protein intake was similar between randomized groups. Among 92 participants, LVEDD changed significantly over time (F(2, 51.20) = 7.45, p = 0.001), with model-estimated mean LVEDD decreasing from 59.00 mm at baseline to 54.56 mm at 15 months. LVEDD decreased from 3 to 15 months (−4.42 mm; 95% CI, −7.52 to −1.33; nominal p = 0.006; Holm-adjusted p = 0.012) and from baseline to 15 months (−4.44 mm; 95% CI, −6.86 to −2.02; nominal p < 0.001; Holm-adjusted p = 0.002). LVEF did not change significantly over time (overall p = 0.074); an exploratory baseline-to-15-month contrast was +4.11 percentage points (95% CI, 0.55–7.67; Holm-adjusted p = 0.072). LVPWT did not change significantly, and no diet group × time interactions were observed. Conclusions: LVEDD was lower at longer-term follow-up. LVEF did not change significantly over time, although an exploratory baseline-to-15-month contrast suggested an increase. Because both groups received hypocaloric diets, there was no non-dietary control group, and longitudinal HF medication data were unavailable, the observed cardiac changes cannot be attributed specifically to weight loss or the dietary intervention.
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Evangelista et al. (2026) conducted an RCT in Chronic heart failure, type 2 diabetes, and overweight or obesity (n=92). High-protein hypocaloric diet vs. Standard-protein hypocaloric diet (15% protein, 55% carbohydrate, 30% fat) was evaluated on Change in left ventricular end-diastolic dimension (LVEDD) from baseline to 15 months (EMD -4.44 mm, 95% CI -6.86 to -2.02, p=nominal p < 0.001; Holm-adjusted p = 0.002). A dietary weight-management intervention reduced left ventricular end-diastolic dimension by a mean of 4.44 mm over 15 months in adults with heart failure, type 2 diabetes, and obesity.
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