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塔科苏博综合征的病理生理学

Francesco Pelliccia¹, Juan Carlos Kaski¹, Filippo Crea¹

¹From Department of Cardiovascular Sciences, Sapienza University, Rome, Italy (F.P.); Molecular and Clinical Sciences Research Institute, St George's, University of London, UK (J.C.K.); Institute of Cardiology, Catholic University, Rome, Italy (F.C.); and Vita-Salute University and San Raffaele Hospital, Milan, Italy (P.G.C.).

|June 14, 2017

概括

塔科苏博综合征 (TTS) 涉及急性心肌功能障碍,通常是由压力引起的. 虽然这不是典型的心脏病发作,但它带有很大的死亡风险,神经系统在它的发展中发挥着关键作用.

科学领域:

心脏病学
神经科学
病理生理学

背景情况:

塔科苏博综合征 (TTS) 首次描述于20世纪90年代,模仿急性心肌梗塞,但冠状动脉正常,左心室功能障碍过渡.
最初被认为是良性的TTS现在被认为具有显著的短期和长期死亡率,与ST段升高的心肌梗塞相当.
目前尚不完全了解TTS的确切原因和病因, 需要对其潜在机制进行进一步研究.

研究的目的:

审查塔科苏博综合征 (TTS) 的病理生理学.
强调中枢神经系统和自主神经系统在TTS发展中的关键作用.
探索压力对心肌损伤的影响,

主要方法:

专注于塔科苏博综合征的神经生物学和心血管方面的文献综述.
对研究心理压力因素与TTS发病之间的联系进行分析.
检查catecholamines,皮质醇和自主神经系统激活在TTS病变的作用.

主要成果:

情绪和心理压力会激活中枢神经系统,导致皮质醇和甲醇胺水平升高.
通过直接毒性,受体介导作用和冠状动脉收缩,增加的循环和局部释放的甲醇胺会导致心肌损伤.
这种过渡性左心室气球,是TTS的特征,由此导致儿科胺激增和心脏工作量增加.

结论:

中枢神经系统和自主神经系统在塔科苏博综合征的病理生理学中起着关键作用.
由压力因素引起的catecholamine激增是TTS心肌损伤和左心室功能障碍的主要驱动因素.
绝经后妇女的雌激素缺乏等因素可能会使个体易患TTS,可能是通过内皮功能障碍,尽管知识差距仍然存在.

关键词:

塔科苏博心肌病自主神经系统心肌疾病类甲基胺冠状动脉循环心脏疾病缺血性心脏病

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