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动脉瘤性蛛网膜下腔出血后神经源性应激性心肌病的机制

Mechanisms in neurogenic stress cardiomyopathy after aneurysmal subarachnoid hemorrhage.

作者信息

Lee Vivien H, Oh Jae K, Mulvagh Sharon L, Wijdicks Eelco F M

机构信息

Division of Critical Care Neurology, Department of Neurology, Mayo Clinic College of Medicine, Rochester, MN 55905, USA.

出版信息

Neurocrit Care. 2006;5(3):243-9. doi: 10.1385/NCC:5:3:243.

Abstract

Cardiac dysfunction after aneurysmal subarachnoid hemorrhage (SAH) is often referred to as "neurogenic stunned myocardium," which does not accurately reflect the suspected pathophysiology. We propose an alternative terminology, "neurogenic stress cardiomyopathy," as a more appropriate label based on our review of the current literature. This article will review the distinctive characteristics of SAH-induced cardiac dysfunction, hypotheses to explain the pathophysiology, and the supporting clinical and animal studies. Recognition of the unique features associated with SAH-induced cardiac complications allows optimal management of patients with SAH. We will also discuss the clinical and theoretical overlap of SAH-induced cardiac dysfunction with a syndrome known as tako-tsubo cardiomyopathy and explore therapeutic opportunities.

摘要

动脉瘤性蛛网膜下腔出血(SAH)后的心脏功能障碍通常被称为“神经源性心肌顿抑”,但这并不能准确反映所怀疑的病理生理学机制。基于我们对当前文献的综述,我们提出一个替代术语“神经源性应激性心肌病”,作为更合适的称谓。本文将综述SAH所致心脏功能障碍的独特特征、解释其病理生理学的假说,以及支持性的临床和动物研究。认识到与SAH所致心脏并发症相关的独特特征,有助于对SAH患者进行最佳管理。我们还将讨论SAH所致心脏功能障碍与一种称为应激性心肌病的综合征在临床和理论上的重叠,并探索治疗机会。

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