Key result
Higher METS-VF linked to ~79% greater risk of new-onset AVC per unit increase.
Why the study?
Obesity influences aortic valve calcification, but the relationship between the Metabolic Score for Visceral Fat and aortic valve calcification remained largely unclear.
Does higher Metabolic Score for Visceral Fat (METS-VF) increase the risk of aortic valve calcification prevalence, new-onset, and progression in individuals without overt CVD?
Does higher Metabolic Score for Visceral Fat (METS-VF) increase the risk of aortic valve calcification prevalence, new-onset, and progression in individuals without overt CVD?
METS-VF independently predicts the prevalence, new-onset, and progression of aortic valve calcification, and Mendelian randomization supports visceral adipose tissue as a causal factor for calcific aortic valve stenosis.
Obesity significantly influences aortic valve calcification (AVC). However, the relationship between Metabolic Score for Visceral Fat (METS-VF), an indicator of visceral adiposity, and AVC remains largely unclear. Therefore, this study investigated the correlations between METS-VF with AVC prevalence, new-onset, and progression, as well as the causal association between visceral adipose tissue (VAT) and calcific aortic valve stenosis (CAVS). The analysis included a cohort of 5,245 individuals drawn from the Multi-Ethnic Study of Atherosclerosis (MESA) database. Associations between baseline METS-VF and AVC prevalence, new-onset, and progression were analyzed through logistic regression and Cox regression. The potential causal link between the VAT and CAVS was evaluated by applying a two-sample Mendelian randomization (MR) strategy. The findings indicated that a one-unit increment in METS-VF correlates with a 41% increased risk of prevalent AVC in the fully adjusted model (odds ratio [OR] = 1.41; 95% confidence interval [CI], 1.14–1.75; P = 0.002). After full adjustment in the multivariable regression analysis, a unit increase in METS-VF was correlated with a 79% higher possibility of AVC new-onset (hazard ratio [HR] = 1.79; 95% CI, 1.24–2.59; P = 0.002) and an 86% higher incident of AVC progression (HR = 1.86; 95% CI, 1.41–2.44; P < 0.001). Restricted cubic spline analysis revealed approximately linear relationships between METS-VF and AVC prevalence, new-onset, and progression. Subgroup analyses demonstrated consistent findings across groups, except for notable interactions by race (for AVC prevalence) and sex (for AVC new-onset). METS-VF outperformed other indices linked to anthropometric and metabolic characteristics in terms of predictive performance, based on receiver operating characteristic curves. Additionally, MR demonstrated that VAT had a strong causal effect on CAVS. METS-VF independently predicts AVC prevalence, new-onset, and progression, and MR analyses support VAT as a causal factor for incident CAVS. METS-VF might function as an efficient and budget-friendly screening method or early risk identification. Targeting visceral adiposity represents a promising primary prevention strategy against valvular heart disease.
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Sun et al. (2025) studied this question. A one-unit increase in METS-VF is associated with a 79% higher risk of new-onset AVC (HR 1.79) and an 86% higher risk of AVC progression (HR 1.86).
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