Insulin resistance-associated decreases in left ventricular diastolic function are strongly modified by the extent of concentric remodeling in a community sample
详细信息    查看全文
文摘
Whether excess adiposity, associated metabolic abnormalities or alternative risk factors for left ventricular (LV) diastolic function are modified rather than mediated by geometric LV remodeling, is uncertain.

Methods

Echocardiographic LV mass index (LVMI), relative wall thickness (RWT) and diastolic function (lateral and septal wall myocardial tissue lengthening at the level of the mitral annulus [e′] [n = 430], ratio of early-to-late transmitral blood flow velocity (E/A), and E/e′ [n = 430]) were determined in 737 randomly recruited participants of a community-based study (43% obese).

Results

Independent of LVMI and confounders, indexes of adiposity and the homeostasis model of insulin resistance (HOMA-IR) were independently associated with LV diastolic function (p < 0.05). In addition, RWT was independently associated with LV diastolic function (p < 0.002). Importantly, an independent interaction between HOMA-IR and RWT, but not between blood pressure or age and RWT, was related to LV diastolic function (p < 0.05). This translated into an independent relationship between HOMA-IR and lateral e′ (partial r = − 0.17, p < 0.02), septal e′ (partial r = − 0.14, p = 0.05), E/A (partial r = − 0.17, p < 0.005) and E/e′ (partial r = 0.19, p < 0.01) in those with RWT above, but a lack of relationship between HOMA-IR and LV diastolic function (p > 0.59) in those with RWT below the median for the sample. Similarly, HOMA-IR was independently associated with LV diastolic dysfunction in those with RWT above (p < 0.05) but not below (p > 0.19) the median for the sample.

Conclusions

The relationship between insulin resistance, but not alternative risk factors and LV diastolic function is markedly modified by the presence of a more concentrically remodeled LV.

© 2004-2018 中国地质图书馆版权所有 京ICP备05064691号 京公网安备11010802017129号

地址:北京市海淀区学院路29号 邮编:100083

电话:办公室:(+86 10)66554848;文献借阅、咨询服务、科技查新:66554700