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胰岛素抵抗对普通社区中正常体重及超重/肥胖日本受试者亚临床左心室功能障碍的影响

Impact of insulin resistance on subclinical left ventricular dysfunction in normal weight and overweight/obese japanese subjects in a general community.

作者信息

Hirose Kazutoshi, Nakanishi Koki, Daimon Masao, Sawada Naoko, Yoshida Yuriko, Iwama Kentaro, Yamamoto Yuko, Ishiwata Jumpei, Hirokawa Megumi, Koyama Katsuhiro, Nakao Tomoko, Morita Hiroyuki, Di Tullio Marco R, Homma Shunichi, Komuro Issei

机构信息

Department of Cardiovascular Medicine, The University of Tokyo, Tokyo, Japan.

Department of Clinical Laboratory, The University of Tokyo, Tokyo, Japan.

出版信息

Cardiovasc Diabetol. 2021 Jan 21;20(1):22. doi: 10.1186/s12933-020-01201-6.

DOI:10.1186/s12933-020-01201-6
PMID:33478525
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7818760/
Abstract

BACKGROUND

Insulin resistance carries increased risk of heart failure, although the pathophysiological mechanisms remain unclear. LV global longitudinal strain (LVGLS) assessed by speckle-tracking echocardiography has emerged as an important tool to detect early LV systolic abnormalities. This study aimed to investigate the association between insulin resistance and subclinical left ventricular (LV) dysfunction in a sample of the general population without overt cardiac disease.

METHODS

We investigated 539 participants who voluntarily underwent extensive cardiovascular health check including laboratory test and speckle-tracking echocardiography. Glycemic profiles were categorized into 3 groups according to homeostatic model assessment of insulin resistance (HOMA-IR): absence of insulin resistance (HOMA-IR < 1.5), presence of insulin resistance (HOMA-IR ≥ 1.5) and diabetes mellitus (DM). Multivariable logistic regression models were conducted to evaluate the association between abnormal glucose metabolism and impaired LVGLS (> - 16.65%).

RESULTS

Forty-five (8.3%) participants had DM and 66 (12.2%) had abnormal HOMA-IR. LV mass index and E/e' ratio did not differ between participants with and without abnormal HOMA-IR, whereas abnormal HOMA-IR group had significantly decreased LVGLS (- 17.6 ± 2.6% vs. - 19.7 ± 3.1%, p < 0.05). The prevalence of impaired LVGLS was higher in abnormal HOMA-IR group compared with normal HOMA-IR group (42.4% vs. 14.0%) and similar to that of DM (48.9%). In multivariable analyses, glycemic abnormalities were significantly associated with impaired LVGLS, independent of traditional cardiovascular risk factors and pertinent laboratory and echocardiographic parameters [adjusted odds ratio (OR) 2.38, p = 0.007 for abnormal HOMA-IR; adjusted OR 3.02, p = 0.003 for DM]. The independent association persisted even after adjustment for waist circumference as a marker of abdominal adiposity. Sub-group analyses stratified by body mass index showed significant association between abnormal HOMA-IR and impaired LVGLS in normal weight individuals (adjusted OR 4.59, p = 0.001), but not in overweight/obese individuals (adjusted OR 1.62, p = 0.300).

CONCLUSIONS

In the general population without overt cardiac disease, insulin resistance carries independent risk for subclinical LV dysfunction, especially in normal weight individuals.

摘要

背景

胰岛素抵抗会增加心力衰竭风险,但其病理生理机制仍不清楚。通过斑点追踪超声心动图评估的左心室整体纵向应变(LVGLS)已成为检测早期左心室收缩功能异常的重要工具。本研究旨在调查在无明显心脏病的普通人群样本中胰岛素抵抗与亚临床左心室(LV)功能障碍之间的关联。

方法

我们调查了539名自愿接受包括实验室检查和斑点追踪超声心动图在内的广泛心血管健康检查的参与者。根据胰岛素抵抗稳态模型评估(HOMA-IR)将血糖谱分为3组:无胰岛素抵抗(HOMA-IR<1.5)、存在胰岛素抵抗(HOMA-IR≥1.5)和糖尿病(DM)。采用多变量逻辑回归模型评估糖代谢异常与LVGLS受损(>-16.65%)之间的关联。

结果

45名(8.3%)参与者患有DM,66名(12.2%)参与者HOMA-IR异常。HOMA-IR异常和正常的参与者之间左心室质量指数和E/e'比值无差异,而HOMA-IR异常组的LVGLS显著降低(-17.6±2.6%对-19.7±3.1%,p<0.05)。与正常HOMA-IR组相比,HOMA-IR异常组LVGLS受损的患病率更高(42.4%对14.0%),与DM组相似(48.9%)。在多变量分析中,糖代谢异常与LVGLS受损显著相关,独立于传统心血管危险因素以及相关实验室和超声心动图参数[HOMA-IR异常的调整比值比(OR)为2.38,p = 0.007;DM的调整OR为3.02,p = 0.003]。即使将腰围作为腹部肥胖的标志物进行调整后,这种独立关联仍然存在。按体重指数分层的亚组分析显示,在正常体重个体中,HOMA-IR异常与LVGLS受损之间存在显著关联(调整OR为4.59,p = 0.001),但在超重/肥胖个体中无此关联(调整OR为1.62,p = 0.300)。

结论

在无明显心脏病的普通人群中,胰岛素抵抗是亚临床左心室功能障碍的独立危险因素,尤其是在正常体重个体中。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0b3/7818760/4c58ea0c7a54/12933_2020_1201_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0b3/7818760/85b1166ee34d/12933_2020_1201_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0b3/7818760/9a860d52879e/12933_2020_1201_Fig2_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0b3/7818760/4c58ea0c7a54/12933_2020_1201_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0b3/7818760/85b1166ee34d/12933_2020_1201_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0b3/7818760/9a860d52879e/12933_2020_1201_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0b3/7818760/03f102347f89/12933_2020_1201_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0b3/7818760/4c58ea0c7a54/12933_2020_1201_Fig4_HTML.jpg

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