Longitudinal Studies Section, Translational Gerontology Branch, NIA/NIH, Baltimore, MD, USA; Laboratory of Cardiovascular Sciences, Human Cardiovascular Studies Unit, NIA/NIH, Baltimore, MD, USA; Research Center of Cardiovascular Biology, University of Genova, Genova, Italy.
Nutr Metab Cardiovasc Dis. 2013 Dec;23(12):1263-70. doi: 10.1016/j.numecd.2013.04.003. Epub 2013 Jul 1.
It is unclear whether subcutaneous and visceral fat are differentially correlated to the decline in left ventricular (LV) diastolic function with aging. This study sought to examine the hypothesis that age-related changes in the regional fat distribution account for changes in LV diastolic function and to explore potential mediators of this association.
In this cross-sectional study, we evaluated 843 participants of the Baltimore Longitudinal Study of Aging with echocardiogram, dual-energy X-ray absorptiometry (DEXA), abdominal computed tomography (CT) and blood tests performed at the same visit. LV diastolic function was assessed by parameters of LV relaxation (E/A ratio, Em and Em/Am ratio) and LV filling pressures (E/Em ratio). Total body fat was computed by DEXA, while visceral and subcutaneous fat were determined from abdominal CT. In multivariate models adjusted for demographics, cardiovascular risk factors, antihypertensive medications, physical activity and LV mass, both visceral and subcutaneous fat were associated with LV diastolic dysfunction. When both measures of adiposity were simultaneously included in the same model, only visceral fat was significantly associated with LV diastolic dysfunction. Triglycerides and sex-hormone binding globulin, but not adiponectin and leptin, were found to be significant mediators of the relationship between visceral fat and LV diastolic function, explaining 28-47% of the association. Bootstrapping analyses confirmed the significance of these findings.
Increased visceral adiposity is associated with LV diastolic dysfunction, possibly through a metabolic pathway involving blood lipids and ectopic fat accumulation rather than adipokines.
目前尚不清楚皮下脂肪和内脏脂肪与左心室（LV）舒张功能随年龄下降的相关性是否存在差异。本研究旨在检验以下假设，即区域性脂肪分布的年龄相关性变化可解释 LV 舒张功能的变化，并探讨这种相关性的潜在介导因素。
在这项横断面研究中，我们评估了 843 名巴尔的摩纵向衰老研究参与者，他们在同一时间接受了超声心动图、双能 X 射线吸收法（DEXA）、腹部计算机断层扫描（CT）和血液检查。通过 LV 松弛参数（E/A 比、Em 和 Em/Am 比）和 LV 充盈压（E/Em 比）评估 LV 舒张功能。通过 DEXA 计算全身脂肪量，通过腹部 CT 确定内脏和皮下脂肪量。在调整了人口统计学、心血管危险因素、降压药物、体力活动和 LV 质量的多变量模型中，内脏和皮下脂肪均与 LV 舒张功能障碍相关。当同时将两种肥胖指标纳入同一模型时，只有内脏脂肪与 LV 舒张功能障碍显著相关。甘油三酯和性激素结合球蛋白，但不是脂联素和瘦素，被发现是内脏脂肪与 LV 舒张功能之间关系的重要介导因素，解释了 28-47%的关联。自举分析证实了这些发现的重要性。
内脏脂肪增加与 LV 舒张功能障碍相关，可能通过涉及血脂和异位脂肪堆积的代谢途径，而不是通过脂肪因子。
