Nuclear Medicine Unit, Department of Diagnostic Imaging, N.O.P. - S. Stefano, U.S.L. Toscana Centro, Prato, Italy.
Department of Nuclear Medicine and Molecular Imaging, University Medical Center Groningen, Groningen, Netherlands.
Curr Radiopharm. 2023;16(4):253-268. doi: 10.2174/1874471016666230515142106.
Despite substantial research, the mechanisms behind stress Tako-tsubo cardiomyopathy (TTC) remain rather elusive.
The purpose of this paper was to provide a detailed review of the mainstream factors underlying the pathophysiology of TTC, highlighting the novel contributions of molecular pathology and in-vivo molecular imaging.
A careful literature review selected all papers discussing TTC, specifically those providing novel insights from myocardial pathology and cardiac molecular imaging.
Results concerning myocardial pathology, defect extension, sites and relationships between functional parameters underline the existence of a causal relationship between a determinant (e.g., the release of catecholamines induced by stress) and an outcome for TTC, which is not limited to a reversible contractile cardiomyopathy, but it includes reversible changes in myocardial perfusion and a long-lasting residual deficit in sympathetic function. Besides, they reinforce the hypothesis that sympathetic nerves may exert a complex control on cardiac contractile function, which is likely to be direct or indirect through metabolism and microvascular perfusion changes during anaerobic and aerobic conditions.
TTC is characterized by acute transient left ventricular systolic dysfunction, which can be challenging to distinguish from myocardial infarction at presentation. Catecholamineinduced myocardial injury is the most established theory, but other factors, including myocardial metabolism and perfusion, should be considered of utmost importance. Each effort to clarify the numerous pathways and emerging abnormalities may provide novel approaches to treat the acute episode, avoid recurrences, and prevent major adverse cardiovascular events.
尽管已经进行了大量研究，但压力性 Takotsubo 心肌病（TTC）的发病机制仍然难以捉摸。
本文旨在详细回顾 TTC 病理生理学的主流因素，强调分子病理学和体内分子成像的新贡献。
仔细的文献回顾选择了所有讨论 TTC 的论文，特别是那些从心肌病理学和心脏分子成像提供新见解的论文。
关于心肌病理学、病变延伸、部位以及功能参数之间关系的结果强调了 TTC 中存在因果关系的存在，这不仅仅局限于可逆性收缩性心肌病，还包括心肌灌注的可逆变化和交感神经功能的持久残留缺陷。此外，它们强化了这样一种假设，即交感神经可能对心脏收缩功能施加复杂的控制，这种控制可能是直接的，也可能是通过代谢和微脉管灌注在厌氧和需氧条件下的变化间接产生的。
TTC 的特征是急性短暂性左心室收缩功能障碍，在出现时可能难以与心肌梗死区分。儿茶酚胺诱导的心肌损伤是最被认可的理论，但其他因素，包括心肌代谢和灌注，也应被认为至关重要。澄清众多途径和新出现的异常的每一次努力都可能为治疗急性发作、避免复发和预防主要不良心血管事件提供新的方法。
