Key result
Obesity is linked to increased epicardial fat volume and impaired GLS.
Why the study?
Obesity is linked to adverse cardiovascular outcomes, but subclinical cardiac remodeling patterns remain incompletely characterized.
Does obesity alter CMR-derived cardiac structure and function compared to controls without obesity?
Meta-Analysis (n=2,655)
Does obesity alter CMR-derived cardiac structure and function compared to controls without obesity?
Obesity is associated with a distinct CMR phenotype characterized by concentric ventricular remodeling, excess epicardial adiposity, and early subclinical myocardial dysfunction despite preserved ejection fraction.
Answers are grounded in this paper and cite their sources.
May prompt closer monitoring for subclinical dysfunction in obesity; reinforces obesity as a driver of adverse CMR remodeling.
BACKGROUND: Obesity links to adverse cardiovascular outcomes, but subclinical cardiac remodeling patterns remain incompletely characterized. Cardiac magnetic resonance (CMR) provides reproducible assessments of myocardial structure, function, tissue characterization, and adiposity. We conducted a systematic review and meta-analysis to define the obesity-related CMR phenotype. METHODS: PubMed, MEDLINE, EMBASE, Cochrane, Web of Science, and Scopus were searched (2000-2025) for studies comparing CMR-derived cardiac parameters in adults with obesity (WHO criteria) versus controls without obesity. Standardized mean differences (SMDs) were pooled using random-effects meta-analysis. Sensitivity analyses and meta-regression explored heterogeneity. RESULTS: Twenty studies (1395 individuals with obesity, 1260 controls) were included. Obesity was associated with increased epicardial fat volume (SMD 0.74, 95% CI 0.46-1.01; p < 0.001), higher left ventricular mass/end-diastolic volume ratio (SMD 0.51, 95% CI 0.27-0.75; p < 0.001), increased left ventricular mass index (SMD 0.33, 95% CI 0.13-0.53; p = 0.001), and higher stroke volume (SMD 0.40, 95% CI 0.20-0.61; p < 0.001). Despite preserved left ventricular ejection fraction, global longitudinal strain (GLS) was impaired (SMD -0.44, 95% CI -0.67 to -0.20; p < 0.001), indicating subclinical systolic dysfunction. Sensitivity analyses excluding cohorts with cardiometabolic disease demonstrated consistent findings. Meta-regression identified body mass index as a modifier of GLS (p = 0.02), whereas age influenced left ventricular mass remodeling. CONCLUSIONS: Obesity is characterized by a distinct CMR phenotype of concentric ventricular remodeling, excess epicardial adiposity, increased hemodynamic adaptation, and early subclinical myocardial dysfunction despite preserved ejection fraction. These findings highlight potentially reversible early cardiac adaptations contributing to the excess cardiovascular risk associated with obesity. TRIAL REGISTRATION: Registration number: PROSPERO CRD420251083324.
No takes yet. Share an insight, caveat, or question.
Khanna et al. (2026) conducted a meta-analysis in Obesity (n=2,655). Obesity vs. Controls without obesity was evaluated on Epicardial fat volume (SMD 0.74, 95% CI 0.46-1.01, p=<0.001). Obesity was associated with increased epicardial fat volume (SMD 0.74; 95% CI 0.46-1.01; P<0.001) and impaired global longitudinal strain (SMD -0.44; 95% CI -0.67 to -0.20; P<0.001).
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: