Genetically predicted visceral adipose tissue mass was causally associated with an increased risk of coronary artery disease (OR 1.573), heart failure, and other cardiovascular outcomes.
Observational
Does genetically predicted visceral adipose tissue mass increase the risk of cardiovascular diseases and metabolic risk factors?
Genetically predicted visceral adipose tissue mass is causally associated with a wide range of cardiovascular diseases and metabolic risk factors, potentially mediated by specific circulating proteins.
Odds Ratio: 1.573 (95% CI 1.439–1.72)
p-value: p=2.6e-23
Aim: To evaluate the genetic associations of visceral adipose tissue (VAT) mass with metabolic risk factors and cardiovascular disease (CVD) endpoints and to construct a network analysis about the underlying mechanism using Mendelian randomization (MR) analysis. Methods and Results: Using summary statistics from genome-wide association studies (GWAS), we conducted the two-sample MR to assess the effects of VAT mass on 10 metabolic risk factors and 53 CVD endpoints. Genetically predicted VAT mass was associated with metabolic risk factors, including triglyceride (odds ratio, OR, 1.263 95% confidence interval, CI, 1.203–1.326), high-density lipoprotein cholesterol (OR, 0.719 95% CI, 0.678–0.763), type 2 diabetes (OR, 2.397 95% CI, 1.965–2.923), fasting glucose (OR, 1.079 95% CI, 1.046–1.113), fasting insulin (OR, 1.194 95% CI, 1.16–1.229), and insulin resistance (OR, 1.204 95% CI, 1.16–1.25). Genetically predicted VAT mass was associated with CVD endpoints, including atrial fibrillation (OR, 1.414 95% CI, 1.332 = 1.5), coronary artery disease (OR, 1.573 95% CI, 1.439 = 1.72), myocardial infarction (OR, 1.633 95% CI, 1.484 =1.796), heart failure (OR, 1.711 95% CI, 1.599–1.832), any stroke (OR, 1.29 1.193–1.394), ischemic stroke (OR, 1.292 1.189–1.404), large artery stroke (OR, 1.483 1.206–1.823), cardioembolic stroke (OR, 1.261 1.096–1.452), and intracranial aneurysm (OR, 1.475 1.235–1.762). In the FinnGen study, the relevance of VAT mass to coronary heart disease, stroke, cardiac arrhythmia, vascular diseases, hypertensive heart disease, and cardiac death was found. In network analysis to identify the underlying mechanism between VAT and CVDs, VAT mass was positively associated with 23 cardiovascular-related proteins (e.g., Leptin, Hepatocyte growth factor, interleukin-16), and inversely with 6 proteins (e.g., Galanin peptides, Endothelial cell-specific molecule 1). These proteins were further associated with 32 CVD outcomes. Conclusion: Mendelian randomization analysis has shown that VAT mass was associated with a wide range of CVD outcomes including coronary heart disease, cardiac arrhythmia, vascular diseases, and stroke. A few circulating proteins may be the mediators between VAT and CVDs.
Huang et al. (Thu,) conducted a observational in Cardiovascular diseases. Genetically predicted visceral adipose tissue (VAT) mass vs. Lower VAT mass was evaluated on Coronary artery disease (OR 1.573, 95% CI 1.439-1.72, p=2.6e-23). Genetically predicted visceral adipose tissue mass was causally associated with an increased risk of coronary artery disease (OR 1.573), heart failure, and other cardiovascular outcomes.
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