Department of Internal Medicine, National Taiwan University College of Medicine and Hospital Yun-Lin Branch, Yun-Lin, Taiwan.
Obesity (Silver Spring). 2012 Apr;20(4):730-7. doi: 10.1038/oby.2011.30. Epub 2011 Mar 10.
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.
本研究旨在通过结构方程模型探讨中心性肥胖、炎症与左心室（LV）舒张功能障碍之间的关系。对 102 名年龄大于 30 岁的健康成年人进行超声心动图参数评估。根据超声心动图检查结果，将参与者分为左心室舒张功能障碍组（包括二尖瓣血流 E/A 比值<1、减速时间>220cm/s 或组织多普勒成像中峰值环早期舒张速度降低）和对照组。同时还测量了血清 C 反应蛋白（CRP）和血脂谱。计算了胰岛素抵抗的稳态模型（HOMA）。采用计算机断层扫描（CT）在 L4 水平评估中心性肥胖。在多元回归分析中，当将 CRP 引入模型后，内脏脂肪组织（VAT）与 LV 舒张功能障碍之间的关系变得不显著，尽管 CRP 本身与 LV 舒张功能障碍显著相关（比值比（OR）：1.32，95%置信区间（CI）：1.01-1.72，P=0.04）。VAT 与 CRP 之间也存在显著相关性（r=0.70；P<0.001）。然后，我们按照结构方程模型进行路径分析。这证明了我们的假设，即 VAT 可能通过 CRP 的作用影响 LV 舒张功能障碍（总脂肪负荷伴炎症（B=1.133，P<0.001），并且炎症可能影响 LV 舒张功能障碍（B=0.373，P<0.001））。使用结构方程模型，我们得出结论，较高的 VAT 与低度炎症相关，这可能导致健康受试者出现亚临床 LV 舒张功能障碍。
