Pathophysiologic Contributions of Visceral Adiposity to Left Ventricular Diastolic Dysfunction
Reika Nagata1,2, Masaru Obokata1, Miki Matsui2
1Department of Cardiovascular Medicine, Gunma University Graduate School of Medicine, 3-39-22 Showa-machi, Maebashi 371-8511, Gunma, Japan.
Insights
Increased visceral fat, but not subcutaneous fat, is linked to left ventricular diastolic dysfunction (LVDD). This finding suggests visceral adiposity contributes to LVDD pathophysiology.
Area of Science:
- Cardiology
- Metabolic Syndrome
- Medical Imaging
Background:
- Visceral fat releases inflammatory cytokines, potentially contributing to heart failure with preserved ejection fraction (HFpEF).
- Limited data exist on how visceral fat abnormalities impact left ventricular diastolic dysfunction (LVDD).
Purpose of the Study:
- To investigate the relationship between visceral fat quantity and left ventricular diastolic dysfunction (LVDD).
- To explore the role of visceral adiposity in the pathophysiology of LVDD.
Main Methods:
- Studied 77 patients undergoing abdominal surgery (44 with LVDD, 33 controls).
- Assessed visceral and subcutaneous fat areas via abdominal CT scans.
- Measured mRNA levels of inflammatory cytokines in visceral fat samples.
Main Results:
- Patients with LVDD had significantly larger visceral fat areas compared to controls.
- Visceral fat area correlated with BNP levels, LV mass index, and diastolic function parameters (mitral e' velocity, E/e' ratio).
- No significant differences in visceral adipose tissue cytokine mRNA expression were found between groups.
Conclusions:
- Elevated visceral adiposity is associated with left ventricular diastolic dysfunction (LVDD).
- Visceral fat accumulation may play a pathophysiological role in LVDD.
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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