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瓣膜性心脏病中心房心肌病:从分子生物学到临床视角。

Atrial Cardiomyopathy in Valvular Heart Disease: From Molecular Biology to Clinical Perspectives.

机构信息

Heart and Vascular Center, Semmelweis University, 1122 Budapest, Hungary.

出版信息

Cells. 2023 Jul 6;12(13):1796. doi: 10.3390/cells12131796.

DOI:10.3390/cells12131796
PMID:37443830
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10340254/
Abstract

This review discusses the evolving topic of atrial cardiomyopathy concerning valvular heart disease. The pathogenesis of atrial cardiomyopathy involves multiple factors, such as valvular disease leading to atrial structural and functional remodeling due to pressure and volume overload. Atrial enlargement and dysfunction can trigger atrial tachyarrhythmia. The complex interaction between valvular disease and atrial cardiomyopathy creates a vicious cycle of aggravating atrial enlargement, dysfunction, and valvular disease severity. Furthermore, atrial remodeling and arrhythmia can predispose to atrial thrombus formation and stroke. The underlying pathomechanism of atrial myopathy involves molecular, cellular, and subcellular alterations resulting in chronic inflammation, atrial fibrosis, and electrophysiological changes. Atrial dysfunction has emerged as an essential determinant of outcomes in valvular disease and heart failure. Despite its predictive value, the detection of atrial fibrosis and dysfunction is challenging and is not included in the clinical routine. Transthoracic echocardiography and cardiac magnetic resonance imaging are the main diagnostic tools for atrial cardiomyopathy. Recently published data have revealed that both left atrial volumes and functional parameters are independent predictors of cardiovascular events in valvular disease. The integration of atrial function assessment in clinical practice might help in early cardiovascular risk estimation, promoting early therapeutic intervention in valvular disease.

摘要

这篇综述讨论了与心脏瓣膜病相关的心房心肌病这一不断发展的主题。心房心肌病的发病机制涉及多种因素,如瓣膜病导致的压力和容量超负荷引起的心房结构和功能重塑。心房扩大和功能障碍可引发房性快速性心律失常。瓣膜病和心房心肌病之间的复杂相互作用形成了一个加剧心房扩大、功能障碍和瓣膜病严重程度的恶性循环。此外,心房重构和心律失常可导致心房血栓形成和卒中。心房肌病的潜在病理机制涉及分子、细胞和亚细胞的改变,导致慢性炎症、心房纤维化和电生理变化。心房功能障碍已成为瓣膜病和心力衰竭结局的重要决定因素。尽管具有预测价值,但心房纤维化和功能障碍的检测具有挑战性,并未纳入临床常规。经胸超声心动图和心脏磁共振成像(CMR)是诊断心房心肌病的主要工具。最近发表的数据显示,左心房容积和功能参数均是瓣膜病心血管事件的独立预测因子。在临床实践中整合心房功能评估可能有助于早期心血管风险评估,促进瓣膜病的早期治疗干预。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e11/10340254/117c68847488/cells-12-01796-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e11/10340254/2285186cd267/cells-12-01796-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e11/10340254/e0866a0d6fd3/cells-12-01796-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e11/10340254/eccbe915cbe0/cells-12-01796-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e11/10340254/54743bfeaa83/cells-12-01796-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e11/10340254/117c68847488/cells-12-01796-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e11/10340254/2285186cd267/cells-12-01796-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e11/10340254/e0866a0d6fd3/cells-12-01796-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e11/10340254/eccbe915cbe0/cells-12-01796-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e11/10340254/54743bfeaa83/cells-12-01796-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e11/10340254/117c68847488/cells-12-01796-g005.jpg

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