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正常体重肥胖患者的左心室功能障碍:腹部脂肪沉积、纤维增生状态、胰岛素敏感性降低和促炎激活的贡献。

Left ventricular function impairment in patients with normal-weight obesity: contribution of abdominal fat deposition, profibrotic state, reduced insulin sensitivity, and proinflammatory activation.

机构信息

Departments of Cardiology and Endocrinology, Wroclaw Medical University, Wroclaw, Poland.

出版信息

Circ Cardiovasc Imaging. 2012 May 1;5(3):349-56. doi: 10.1161/CIRCIMAGING.111.969956. Epub 2012 Mar 9.

DOI:10.1161/CIRCIMAGING.111.969956
PMID:22407472
Abstract

BACKGROUND

Obesity predisposes to left ventricular (LV) dysfunction and heart failure; however, the risk of these complications has not been assessed in patients with a normal body mass index (BMI) but increased body fat content (normal-weight obesity, NWO). We hypothesized that LV performance in NWO may be impaired and sought to investigate potential contributors to cardiac functional abnormalities.

METHODS AND RESULTS

One hundred sixty-eight subjects (age, 38±7 years) with BMI <25kg/m(2) and no history of any disease affecting the myocardium were classified on the basis of body fat content into 2 groups: with NWO and without NWO. Echocardiographic indices of LV systolic and diastolic function, including myocardial velocities and deformation, serological fibrosis markers, indicators of proinflammatory activation, and metabolic control, were evaluated. Subjects with NWO demonstrated impaired LV systolic and diastolic function, increased fibrosis intensity (assessed by procollagen type I carboxy-terminal propeptide [PICP]), impaired insulin sensitivity, and increased proinflammatory activation as compared with individuals with normal body fat. The independent correlates of LV systolic and diastolic function variables were as follows: for strain, IL-18 (β=-0.17, P<0.006), C-reactive protein (β=-0.20, P<0.002) and abdominal fat deposit (β=-0.20, P<0.003); for tissue S velocity, PICP (β=-0.21, P<0.002) and abdominal fat deposit (β=-0.43, P<0.0001); for tissue E velocity, abdominal fat deposit (β=-0.30, P<0.0001), PICP (β=-0.31, P<0.0001) and homeostasis model assessment of insulin resistance index (HOMA IR; β=-0.20, P<0.002); and for E/e'-PICP, IL-18 (both β=0.18, P<0.01) and HOMA IR (β=0.16, P<0.04).

CONCLUSIONS

In patients with NWO, subclinical disturbances of LV function are independently associated with the extent of abdominal fat deposit, profibrotic state (as reflected by circulating PICP), reduced insulin sensitivity, and proinflammatory activation.

摘要

背景

肥胖使左心室(LV)功能障碍和心力衰竭的风险增加;然而,在身体质量指数(BMI)正常但体脂含量增加(正常体重肥胖,NWO)的患者中,这些并发症的风险尚未得到评估。我们假设 NWO 患者的 LV 功能可能受损,并试图研究导致心脏功能异常的潜在因素。

方法和结果

168 名受试者(年龄 38±7 岁)BMI<25kg/m2,且无任何影响心肌疾病的病史,根据体脂含量分为 2 组:NWO 组和非 NWO 组。评估了 LV 收缩和舒张功能的超声心动图指数,包括心肌速度和变形、血清纤维化标志物、促炎激活标志物和代谢控制情况。与体脂正常的个体相比,NWO 患者的 LV 收缩和舒张功能受损,纤维化强度增加(通过前胶原 I 羧基末端前肽[PICP]评估),胰岛素敏感性受损,促炎激活增加。LV 收缩和舒张功能变量的独立相关因素如下:应变,白细胞介素 18(β=-0.17,P<0.006),C 反应蛋白(β=-0.20,P<0.002)和腹部脂肪沉积(β=-0.20,P<0.003);组织 S 速度,PICP(β=-0.21,P<0.002)和腹部脂肪沉积(β=-0.43,P<0.0001);组织 E 速度,腹部脂肪沉积(β=-0.30,P<0.0001),PICP(β=-0.31,P<0.0001)和稳态模型评估的胰岛素抵抗指数(HOMA IR;β=-0.20,P<0.002);E/e'-PICP,白细胞介素 18(均β=0.18,P<0.01)和 HOMA IR(β=0.16,P<0.04)。

结论

在 NWO 患者中,LV 功能的亚临床障碍与腹部脂肪沉积程度、纤维化状态(反映为循环 PICP)、胰岛素敏感性降低和促炎激活独立相关。

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