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交感神经驱动刺激舒张功能障碍?

Sympathetic drive stimulating diastolic dysfunction?

机构信息

Division of Cardiology, Department of Internal Medicine, University of Cincinnati, Cincinnati, OH, USA.

Division of Cardiovascular Diseases, University of Cincinnati, 231 Albert Sabin Way, Mail location MLB 052, Cincinnati, OH, 45267-0542, USA.

出版信息

J Nucl Cardiol. 2018 Aug;25(4):1110-1113. doi: 10.1007/s12350-017-0809-z. Epub 2017 Feb 9.

DOI:10.1007/s12350-017-0809-z
PMID:28185233
Abstract

Diastolic heart failure accounts for half of the heart failure population and its pathophysiology remains an area of active research. The renin angiotensin and aldosterone axis has been the focus of clinical trials to treat patients with heart failure with preserved ejection fraction, however with limited yield in terms of clinical success. Sympathetic activity has been considered a plausible cause for the molecular changes that lead to diastolic dysfunction. Based on this understanding the study by Gimelli et al uses MIBG to evaluate for association between diastolic dysfunction and sympathetic denervation. The results of this study set the stage for a follow up study for evaluation of sympathetic denervation in isolated diastolic dysfunction.

摘要

舒张性心力衰竭占心力衰竭患者的一半,其病理生理学仍是一个活跃的研究领域。肾素-血管紧张素-醛固酮轴一直是治疗射血分数保留心力衰竭患者的临床试验的重点,但在临床成功方面收效有限。交感神经活动被认为是导致舒张功能障碍的分子变化的一个合理原因。基于这一认识,Gimelli 等人的研究使用 MIBG 来评估舒张功能障碍与交感神经去神经支配之间的关系。这项研究的结果为后续研究孤立性舒张性心力衰竭患者的交感神经去神经支配奠定了基础。

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本文引用的文献

1
Relationships between left ventricular sympathetic innervation and diastolic dysfunction: the role of myocardial innervation/perfusion mismatch.左心室交感神经支配与舒张功能障碍的关系:心肌神经支配/灌注不匹配的作用。
J Nucl Cardiol. 2018 Aug;25(4):1101-1109. doi: 10.1007/s12350-016-0753-3. Epub 2016 Dec 27.
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Lessons from the TOPCAT trial.
绝经后女性射血分数保留的心力衰竭的优势:由雌激素缺乏构建的心肌细胞内和细胞外适应性不良改变。
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N Engl J Med. 2009 Aug 27;361(9):932-4. doi: 10.1056/NEJMc0904179.
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Sympathetic and baroreflex cardiovascular control in hypertension-related left ventricular dysfunction.高血压相关左心室功能障碍中的交感神经与压力反射性心血管控制
Hypertension. 2009 Feb;53(2):205-9. doi: 10.1161/HYPERTENSIONAHA.108.121467. Epub 2009 Jan 5.
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G protein-coupled receptor kinase 2 ablation in cardiac myocytes before or after myocardial infarction prevents heart failure.在心肌梗死之前或之后,心肌细胞中G蛋白偶联受体激酶2的缺失可预防心力衰竭。
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Impaired chronotropic and vasodilator reserves limit exercise capacity in patients with heart failure and a preserved ejection fraction.变时性和血管舒张储备受损限制了射血分数保留的心力衰竭患者的运动能力。
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