Icahn School of Medicine at Mount Sinai of the New York University, United States; Division of Cardiology, Elmhurst Hospital Center, New York, NY, United States.
Int J Cardiol. 2013 Oct 3;168(3):1737-8. doi: 10.1016/j.ijcard.2013.06.003. Epub 2013 Jul 3.
The pathophysiology of Takotsubo syndrome (TTS), the reversible cardiomyopathy affecting mainly the left ventricle, with primarily apical and midventricular "ballooning" and basal hypercontractility, continues to be elusive. Many etiological hypotheses have been advanced with a pivotal recent one, which has attributed the TTS to a switch of the function of the beta-2 adrenergic receptors from the canonical cardiostimulatory to cardiodepressant mode, engendered by large doses of epinephrine administration. This worthy animal model has not been explored to its fullest, and thus the author of this viewpoint proposes a series of essential experimental enhancements, in order for the model to provide additional indirect insights, pertaining to the pathophysiology of TTS in humans.
心肌顿抑综合征（TTS）的病理生理学仍然难以捉摸，TTS 是一种主要影响左心室的可逆性心肌病，主要表现为心尖和中段“球囊样”扩张伴基底段收缩力增强。目前已经提出了许多病因假说，其中一个重要的假说认为 TTS 是由于大剂量肾上腺素给药导致β-2 肾上腺素能受体的功能从经典的心肌刺激模式转变为心肌抑制模式。这种有价值的动物模型尚未被充分探索，因此本文作者提出了一系列必要的实验增强措施，以使该模型能够提供与人类 TTS 病理生理学相关的额外间接见解。
