SynthesisCardiovascular diabetology2026
Association between body mass index reduction and epicardial adipose tissue changes across pharmacological and lifestyle interventions: a multilevel meta-regression analysis.
Synthesis in Cardiovascular diabetology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEpicardial adipose tissue (EAT) is a metabolically active visceral fat depot implicated in cardiometabolic disease. Although EAT reductions are commonly attributed to weight loss, the extent to which EAT change is explained by body mass index (BMI) reduction versus intervention-specific effects remains unclear.
methodsWe performed a systematic review and multilevel meta-regression of interventional studies reporting pre- and post-intervention changes in EAT and BMI. MEDLINE, Embase, and Cochrane CENTRAL were searched from inception to April 2026. Standardized mean change using pre-test standardization (SMCR) was calculated for both outcomes. Multilevel meta-regression assessed the association between BMI and EAT change while adjusting for intervention class, follow-up duration, and imaging modality. BMI-adjusted residual analyses were used descriptively to evaluate deviations from model-predicted EAT responses.
resultsForty-two studies comprising 50 intervention arms and 1,890 participants were included. Across all interventions, both EAT and BMI decreased significantly. In the multivariable meta-regression model, BMI reduction was associated with EAT reduction (β = 0.19, p = 0.03), although BMI explained only a limited proportion of variability in EAT response. Intervention class remained a significant moderator of EAT change (p < 0.001). Larger observed reductions in EAT were seen with dietary interventions, GLP-1 receptor agonists, and bariatric surgery. In descriptive residual analyses, dietary interventions and GLP-1 receptor agonists demonstrated greater-than-predicted reductions in EAT relative to the overall study-level BMI-EAT relationship. These findings should be interpreted cautiously because intervention-specific comparisons were exploratory and do not constitute formal comparative efficacy estimates. DISCUSSION: EAT reduction is only partially explained by systemic weight loss, and substantial heterogeneity exists across intervention classes. These findings support the concept that EAT remodeling may be influenced by factors beyond generalized adiposity reduction. However, intervention-specific patterns observed in this study are descriptive and hypothesis-generating and require confirmation in adequately powered comparative studies. Moreover, overall certainty of evidence was low for pooled EAT reduction and very low for intervention-specific comparative patterns.
trial registrationPROSPERO (CRD420261367140).
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.