The relationship among central obesity, systemic inflammation, and left ventricular diastolic dysfunction as determined by structural equation modeling.

The purpose of this study was to investigate the associations among central obesity, inflammation, and left ventricular (LV) diastolic dysfunction by structural equation modeling. Echocardiographic parameters were assessed in 102 otherwise-healthy adults over age 30. The participants were classified as having LV diastolic dysfunction by echocardiographic findings including mitral inflow E/A ratio <1, deceleration time >220 cm/s, or decreased peak annular early diastolic velocity in tissue Doppler imaging or otherwise the control group. Serum C-reactive protein (CRP) and lipid profile were also measured. The homeostasis model of insulin resistance (HOMA) was calculated. Central obesity was assessed by computerized tomography (CT) at the L4 level. In a multivariate regression analysis, the relationship between visceral adipose tissue (VAT) and LV diastolic dysfunction became insignificant when CRP was introduced into the model, although CRP itself was significantly associated with LV diastolic dysfunction (odds ratio (OR): 1.32, 95% confidence interval (CI): 1.01-1.72, P = 0.04). A significant correlation was also found between VAT and CRP (r = 0.70; P < 0.001). We then performed path analysis as illustrated by the structural equation model. This proved our hypotheses that VAT might affect LV diastolic dysfunction through the effect of CRP (total fat load with inflammation (B = 1.133, P < 0.001) and that inflammation might affect LV diastolic dysfunction (B = 0.373. P < 0.001)). Using structural equation modeling, we concluded that higher amounts of VAT were associated with low-grade inflammation and this may lead to subclinical LV diastolic dysfunction in otherwise-healthy subjects.