The relationship among central obesity, systemic inflammation, and left ventricular diastolic dysfunction as
Cho-Kai Wu1, Chung-Yi Yang, Jou-Wei Lin
1Department of Internal Medicine, National Taiwan University College of Medicine and Hospital Yun-Lin Branch, Yun-Lin, Taiwan.
Obesity (Silver Spring, Md.)
|March 12, 2011
Summary
Central obesity, measured by visceral adipose tissue (VAT), is linked to low-grade inflammation (C-reactive protein or CRP). This inflammation may cause subclinical left ventricular (LV) diastolic dysfunction in healthy adults.
Area of Science:
- Cardiology
- Metabolic Syndrome
- Inflammation Research
Background:
- Central obesity is a growing health concern.
- Inflammation plays a role in cardiovascular disease.
- Subclinical left ventricular (LV) diastolic dysfunction can precede heart failure.
Purpose of the Study:
- To investigate the associations among central obesity, inflammation, and LV diastolic dysfunction.
- To explore the mediating role of inflammation in the relationship between central obesity and LV diastolic dysfunction using structural equation modeling.
Main Methods:
- Assessed echocardiographic parameters in 102 healthy adults over 30.
- Measured serum C-reactive protein (CRP) and lipid profiles.
- Quantified visceral adipose tissue (VAT) using CT scans and calculated HOMA for insulin resistance.
Main Results:
- Visceral adipose tissue (VAT) was significantly correlated with CRP (r=0.70, P<0.001).
- CRP was significantly associated with LV diastolic dysfunction (OR: 1.32, P=0.04).
- Structural equation modeling indicated VAT affects LV diastolic dysfunction via CRP (B=1.133, P<0.001), and CRP affects LV diastolic dysfunction (B=0.373, P<0.001).
Conclusions:
- Higher visceral adipose tissue (VAT) is associated with low-grade inflammation (CRP).
- This inflammation may lead to subclinical left ventricular (LV) diastolic dysfunction.
- Structural equation modeling confirms inflammation as a mediator between central obesity and LV diastolic dysfunction.
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