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A Rat Model of Pressure Overload Induced Moderate Remodeling and Systolic Dysfunction as Opposed to Overt Systolic Heart Failure
Published on: April 30, 2020
Cardiac Remodeling and Dysfunction Associated in Populations With Obesity: An Analysis of Cardiac Structure and
Shaun Khanna1,2, Dylan Wilson3, Gurkeerat Mann3
1The George Institute for Global Health, UNSW Sydney, Kensington, NSW, Australia.
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.
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