Lipids & metabolic liver disease
Associations Between Visceral and Liver Fat and Cardiac Structure and Function: A UK Biobank Study
Authors' conclusion
We established the independent associations of VAT and PDFF with unhealthy cardiac structure and function. Furthermore, it identifies SBP and insulin resistance as important mediating factors.
Study context
- Population
- UK Biobank participants with abdominal MR-quantified visceral adipose tissue (VAT) and liver fat (PDFF) and cardiac magnetic resonance (CMR)-measured cardiac structure and function
- Participants
- 10,920 participants
- Exposure
- Higher vs lower VAT and liver fat
- Outcome
- Associations of VAT and PDFF with CMR-measured cardiac structure and function
Methodological detailsUK Biobank, multiple linear regression, multiple mediation analyses
- UK Biobank
- Multiple linear regression
- Multiple mediation analyses
Main finding
As reported in the abstract
CMR metrics
- Elevated VAT or PDFF associated with adverse left ventricular (LV) structure (increased wall thickness, concentric LV remodeling)
- Elevated VAT or PDFF associated with impaired LV function (lower LV global functional index, absolute value of LV global longitudinal strain)
- Elevated VAT or PDFF associated with diminished left atrial volumes and stroke volume (all P values significant)
Observational data: associations, not effects.
Further findings
VAT-PDFF combination groups
- All groups except low VAT-low PDFF linked to unfavorable cardiac remodeling metrics
- High VAT-high PDFF group displayed the most pronounced cardiac alterations
Mediation analyses
- VAT or PDFF related to systolic blood pressure (SBP), diabetes, dyslipidemia, lipid profile, liver function and glucose
- Potential mediating pathways primarily through SBP and triglyceride-glucose index, only partially explaining the adipose-CMR relationship
Original publication
Associations Between Visceral and Liver Fat and Cardiac Structure and Function: A UK Biobank Study. J Clin Endocrinol Metab. Published 17 September 2024. doi:10.
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