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射血分数保留的心力衰竭患者:关于临床进展的问题

Heart Failure in Patients with Preserved Ejection Fraction: Questions Concerning Clinical Progression.

作者信息

Louridas George E, Lourida Katerina G

机构信息

Department of Cardiology, University General Hospital AHEPA, Aristotle University, Thessaloniki 54124, Greece.

出版信息

J Cardiovasc Dev Dis. 2016 Sep 8;3(3):27. doi: 10.3390/jcdd3030027.

DOI:10.3390/jcdd3030027
PMID:29367571
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5715675/
Abstract

Over the last two decades, important advances have been made in explaining some pathophysiological aspects of heart failure with preserved ejection fraction (HFpEF) with repercussions for the successful clinical management of the syndrome. Despite these gains, our knowledge for the natural history of clinical progression from the pre-clinical diastolic dysfunction (PDD) until the final clinical stages is significantly limited. The subclinical progression of PDD to the clinical phenotype of HFpEF and the further clinical progression to some more complex clinical models with multi-organ involvement, similar to heart failure with reduced ejection fraction (HFrEF), continue to be poorly understood. Prospective studies are needed to elucidate the natural history of clinical progression in patients with HFpEF and to identify the exact left ventricular remodeling mechanism that underlies this progression.

摘要

在过去二十年中,在解释射血分数保留的心力衰竭(HFpEF)的一些病理生理方面取得了重要进展,这对该综合征的成功临床管理产生了影响。尽管有这些进展,但我们对从临床前舒张功能障碍(PDD)到最终临床阶段的临床进展自然史的了解仍然非常有限。PDD向HFpEF临床表型的亚临床进展以及进一步向一些更复杂的多器官受累临床模型的临床进展,类似于射血分数降低的心力衰竭(HFrEF),仍然知之甚少。需要进行前瞻性研究来阐明HFpEF患者临床进展的自然史,并确定这种进展背后的确切左心室重塑机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5e3/5715675/9257f0336863/jcdd-03-00027-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5e3/5715675/adedb1f53cfd/jcdd-03-00027-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5e3/5715675/9257f0336863/jcdd-03-00027-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5e3/5715675/adedb1f53cfd/jcdd-03-00027-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5e3/5715675/9257f0336863/jcdd-03-00027-g002.jpg

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本文引用的文献

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JAMA Cardiol. 2016 Aug 1;1(5):510-8. doi: 10.1001/jamacardio.2016.1325.
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Animal models of heart failure with preserved ejection fraction.射血分数保留的心力衰竭动物模型。
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Is enhancing cGMP-PKG signalling a promising therapeutic target for heart failure with preserved ejection fraction?
随着左心室压力逐渐过载,心肌微观结构和力学的变化。
JACC Basic Transl Sci. 2020 Apr 29;5(5):463-480. doi: 10.1016/j.jacbts.2020.02.007. eCollection 2020 May.
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Conceptual Foundations of Systems Biology Explaining Complex Cardiac Diseases.系统生物学解释复杂心脏疾病的概念基础
Healthcare (Basel). 2017 Feb 21;5(1):10. doi: 10.3390/healthcare5010010.
增强cGMP-PKG信号传导是否是射血分数保留的心力衰竭的一个有前景的治疗靶点?
Neth Heart J. 2016 Apr;24(4):268-74. doi: 10.1007/s12471-016-0814-x. Epub 2016 Feb 29.
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The role of titin and extracellular matrix remodelling in heart failure with preserved ejection fraction.肌联蛋白和细胞外基质重塑在射血分数保留的心力衰竭中的作用。
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Heart failure preserved ejection fraction (HFpEF): an integrated and strategic review.射血分数保留的心力衰竭(HFpEF):一项综合的策略性综述。
Heart Fail Rev. 2015 Nov;20(6):643-53. doi: 10.1007/s10741-015-9506-7.
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Left Ventricular Ejection Fraction (EF) of 55% as Cutoff for Late Transition From Heart Failure (HF) With Preserved EF to HF With Mildly Reduced EF.左心室射血分数(EF)55%作为从射血分数保留的心衰(HF)晚期转变为轻度射血分数降低的心衰的临界值。
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