Key result
Larger visceral fat area is linked to LVDD without differences in adipose cytokine expression.
Why the study?
Little data exist regarding how qualitative and quantitative abnormalities of visceral fat contribute to left ventricular diastolic dysfunction.
Does visceral adiposity (quantitative area and qualitative inflammation) associate with left ventricular diastolic dysfunction in patients undergoing abdominal surgery?
Observational (n=77)
Blinded CT measurements
No
Does visceral adiposity (quantitative area and qualitative inflammation) associate with left ventricular diastolic dysfunction in patients undergoing abdominal surgery?
Quantitative abnormalities in visceral adiposity are associated with left ventricular diastolic dysfunction, independent of local inflammatory cytokine expression in non-obese populations.
Visceral fat area associates with LVDD independent of cytokine expression; leaves open causal mechanisms and therapeutic implications.
BACKGROUND: Visceral fat produces inflammatory cytokines and may play a major role in heart failure with preserved ejection fraction (HFpEF). However, little data exist regarding how qualitative and quantitative abnormalities of visceral fat would contribute to left ventricular diastolic dysfunction (LVDD). METHODS: We studied 77 participants who underwent open abdominal surgery for intra-abdominal tumors (LVDD, n = 44; controls without LVDD, n = 33). Visceral fat samples were obtained during the surgery, and mRNA levels of inflammatory cytokines were measured. Visceral and subcutaneous fat areas were measured using abdominal computed tomography. RESULTS: Patients with significant LVDD had greater LV remodeling and worse LVDD than controls. While body weight, body mass index, and subcutaneous fat area were similar in patients with LVDD and controls, the visceral fat area was larger in patients with LVDD than in controls. The visceral fat area was correlated with BNP levels, LV mass index, mitral e' velocity, and E/e' ratio. There were no significant differences in the mRNA expressions of visceral adipose tissue cytokines (IL-2, -6, -8, and -1β, TNFα, CRP, TGFβ, IFNγ, leptin, and adiponectin) between the groups. CONCLUSIONS: Our data may suggest the pathophysiological contribution of visceral adiposity to LVDD.
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Nagata et al. (2023) conducted an observational in Left Ventricular Diastolic Dysfunction (LVDD) / HFpEF (n=77). Visceral adiposity vs. Controls without LVDD was evaluated on mRNA expressions of visceral adipose tissue cytokines and visceral fat area. Visceral fat area was larger in patients with LVDD than in controls, whereas there were no significant differences in mRNA expressions of visceral adipose tissue cytokines between the groups.
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