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本文引用的文献

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2
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3
From Inflammation to Fibrosis-Molecular and Cellular Mechanisms of Myocardial Tissue Remodelling and Perspectives on Differential Treatment Opportunities.从炎症到纤维化——心肌组织重塑的分子和细胞机制及差异化治疗机会展望
Curr Heart Fail Rep. 2017 Aug;14(4):235-250. doi: 10.1007/s11897-017-0343-y.
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2017 ACC/AHA/HFSA Focused Update of the 2013 ACCF/AHA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Failure Society of America.2017年美国心脏病学会/美国心脏协会/美国心力衰竭学会对2013年美国心脏病学会基金会/美国心脏协会心力衰竭管理指南的重点更新:美国心脏病学会/美国心脏协会临床实践指南特别工作组及美国心力衰竭学会的报告
Circulation. 2017 Aug 8;136(6):e137-e161. doi: 10.1161/CIR.0000000000000509. Epub 2017 Apr 28.
5
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Sex differences in inflammation during atherosclerosis.动脉粥样硬化过程中炎症的性别差异。
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Diffuse Myocardial Fibrosis and Inflammation in Rheumatoid Arthritis: Insights From CMR T1 Mapping.类风湿关节炎的弥漫性心肌纤维化和炎症:CMR T1 映射的见解。
JACC Cardiovasc Imaging. 2015 May;8(5):526-536. doi: 10.1016/j.jcmg.2014.12.025. Epub 2015 Apr 15.
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炎症标志物与心肌纤维化的关系。

Association Between Inflammatory Markers and Myocardial Fibrosis.

机构信息

From the Department of Medicine (M.D.M., V.N., H.D.V., J.A.C.L.), Johns Hopkins University, Baltimore, MD.

Department of Internal Medicine, Federal University of Santa Maria, Rio Grande do Sul, Brazil (M.D.M.).

出版信息

Hypertension. 2018 Oct;72(4):902-908. doi: 10.1161/HYPERTENSIONAHA.118.11463.

DOI:10.1161/HYPERTENSIONAHA.118.11463
PMID:30354713
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6205739/
Abstract

Inflammation promotes adverse ventricular remodeling. T1 mapping has been used to noninvasively assess interstitial myocardial fibrosis. We examined the association of baseline markers of systemic inflammation with interstitial myocardial fibrosis measured by extracellular volume fraction (ECV) and native T1 mapping at 10-year follow-up in the MESA (Multi-Ethnic Study of Atherosclerosis). Seven hundred seventy-two participants had complete baseline data and underwent cardiac magnetic resonance imaging. All analyses were stratified by sex. Multivariable linear regression models were constructed to assess the associations of baseline CRP (C-reactive protein), IL (interleukin)-6, and fibrinogen with native T1 time and ECV. Longer native T1 times and higher percentages of ECV represent increasing myocardial fibrosis. A 1-SD increment of log-transformed IL-6 levels was associated with 0.4% higher ECV in men (β=0.4; P=0.05). CRP and fibrinogen were not associated to ECV. A 1-SD increment in the log-transformed CRP levels was associated with 4.9 ms higher native T1 (β=4.9; P=0.03). In women, the inflammatory markers did not demonstrate association with native T1 nor ECV. Higher IL-6 and CRP levels are associated with increased interstitial myocardial fibrosis assessed by cardiac magnetic resonance in men. However, no inflammatory markers were associated to myocardial fibrosis in women.

摘要

炎症促进不良的心室重构。T1 映射已被用于无创评估间质心肌纤维化。我们研究了基线全身性炎症标志物与通过细胞外容积分数 (ECV) 和 10 年随访时的固有 T1 映射测量的间质心肌纤维化之间的关联,这项研究来自于动脉粥样硬化多民族研究 (MESA)。772 名参与者具有完整的基线数据,并接受了心脏磁共振成像。所有分析均按性别分层。构建了多变量线性回归模型,以评估基线 CRP(C 反应蛋白)、IL(白细胞介素)-6 和纤维蛋白原与固有 T1 时间和 ECV 的相关性。固有 T1 时间延长和 ECV 百分比升高代表心肌纤维化增加。男性中,IL-6 水平的对数转换增加 1-SD,与 ECV 增加 0.4%相关(β=0.4;P=0.05)。CRP 和纤维蛋白原与 ECV 无关。CRP 水平的对数转换增加 1-SD,与固有 T1 增加 4.9 ms 相关(β=4.9;P=0.03)。在女性中,炎症标志物与固有 T1 或 ECV 均无相关性。较高的 IL-6 和 CRP 水平与男性心脏磁共振评估的间质心肌纤维化增加相关。然而,在女性中,没有炎症标志物与心肌纤维化相关。