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心房基质重构在主动脉瓣狭窄伴心房颤动患者中的研究。

Atrial matrix remodeling in atrial fibrillation patients with aortic stenosis.

机构信息

Cardiovascular Research and Development Center, Faculty of Medicine, University of Porto, Alameda Professor Hernani Monteiro, 4200, Porto, Portugal.

Department of Clinical Pathology, São João University Hospital Centre, Porto, Portugal.

出版信息

BMC Cardiovasc Disord. 2020 Oct 31;20(1):468. doi: 10.1186/s12872-020-01754-0.

DOI:10.1186/s12872-020-01754-0
PMID:33129260
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7603735/
Abstract

BACKGROUND

This study aimed to evaluate atrium extracellular matrix remodeling in atrial fibrillation (AF) patients with severe aortic stenosis, through histological fibrosis quantification and extracellular matrix gene expression analysis, as well as serum quantification of selected protein targets.

METHODS

A posthoc analysis of a prospective study was performed in a cohort of aortic stenosis patients. Between 2014 and 2019, 56 patients with severe aortic stenosis submitted to aortic valve replacement surgery in a tertiary hospital were selected.

RESULTS

Fibrosis was significantly increased in the AF group when compared to sinus rhythm (SR) patients (p = 0.024). Moreover, cardiomyocyte area was significantly higher in AF patients versus SR patients (p = 0.008). Conversely, collagen III gene expression was increased in AF patients (p = 0.038). TIMP1 was less expressed in the atria of AF patients. MMP16/TIMP4 ratio was significantly decreased in AF patients (p = 0.006). TIMP1 (p = 0.004) and TIMP2 (p = 0.012) were significantly increased in the serum of AF patients. Aortic valve maximum (p = 0.0159) and mean (p = 0.031) gradients demonstrated a negative association with serum TIMP1.

CONCLUSIONS

Atrial fibrillation patients with severe aortic stenosis present increased atrial fibrosis and collagen type III synthesis, with extracellular matrix remodelling demonstrated by a decrease in the MMP16/TIMP4 ratio, along with an increased serum TIMP1 and TIMP2 proteins.

摘要

背景

本研究旨在通过组织学纤维化定量和细胞外基质基因表达分析以及选定蛋白靶标的血清定量，评估严重主动脉瓣狭窄伴房颤（AF）患者的心房细胞外基质重塑。

方法

对一家三级医院接受主动脉瓣置换术的主动脉瓣狭窄患者的前瞻性研究进行了事后分析。2014 年至 2019 年间，共选择了 56 例严重主动脉瓣狭窄患者。

结果

与窦性心律（SR）患者相比，AF 组的纤维化显著增加（p=0.024）。此外，AF 患者的心肌细胞面积明显高于 SR 患者（p=0.008）。相反，AF 患者的胶原蛋白 III 基因表达增加（p=0.038）。TIMP1 在 AF 患者心房中的表达减少。AF 患者的 MMP16/TIMP4 比值显著降低（p=0.006）。TIMP1（p=0.004）和 TIMP2（p=0.012）在 AF 患者的血清中显著增加。主动脉瓣最大（p=0.0159）和平均（p=0.031）梯度与血清 TIMP1 呈负相关。

结论

患有严重主动脉瓣狭窄的房颤患者表现出心房纤维化和 III 型胶原蛋白合成增加，细胞外基质重塑表现为 MMP16/TIMP4 比值降低，同时血清 TIMP1 和 TIMP2 蛋白增加。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ea8/7603735/3a76be4114fe/12872_2020_1754_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ea8/7603735/bf60c855d925/12872_2020_1754_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ea8/7603735/85de20dfa21d/12872_2020_1754_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ea8/7603735/8d6a25c55dc3/12872_2020_1754_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ea8/7603735/34545c8fb861/12872_2020_1754_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ea8/7603735/ef056264e2ef/12872_2020_1754_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ea8/7603735/38ca155bb1dd/12872_2020_1754_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ea8/7603735/f69d57f65d29/12872_2020_1754_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ea8/7603735/c49241a193c4/12872_2020_1754_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ea8/7603735/3a76be4114fe/12872_2020_1754_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ea8/7603735/bf60c855d925/12872_2020_1754_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ea8/7603735/85de20dfa21d/12872_2020_1754_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ea8/7603735/8d6a25c55dc3/12872_2020_1754_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ea8/7603735/34545c8fb861/12872_2020_1754_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ea8/7603735/ef056264e2ef/12872_2020_1754_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ea8/7603735/38ca155bb1dd/12872_2020_1754_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ea8/7603735/f69d57f65d29/12872_2020_1754_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ea8/7603735/c49241a193c4/12872_2020_1754_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ea8/7603735/3a76be4114fe/12872_2020_1754_Fig9_HTML.jpg

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