Royal Brompton and Harefield Hospitals, Imperial College and King's College, London SW3 6NP, UK.
University Heart Center, Department of Cardiology, University Hospital Zürich, Zürich 8091, Switzerland.
Cardiovasc Res. 2023 Jul 4;119(7):1480-1494. doi: 10.1093/cvr/cvad053.
Takotsubo syndrome (TTS) accounts for between 1 and 4% of cases presenting clinically as an acute coronary syndrome. It typically presents as a transient cardiac phenotype of left ventricular dysfunction with spontaneous recovery. More dramatic presentations may include cardiogenic shock or cardiac arrest. Despite progress in the understanding of the condition since its first description in 1990, considerable questions remain into understanding underlying pathomechanisms. In this review article, we describe the current published data on potential underlying mechanisms associated with the onset of TTS including sympathetic nervous system over-stimulation, structural and functional alterations in the central nervous system, catecholamine secretion, alterations in the balance and distribution of adrenergic receptors, the additive impact of hormones including oestrogen, epicardial coronary or microvascular spasm, endothelial dysfunction, and genetics as potentially contributing to the cascade of events leading to the onset. These pathomechanisms provide suggestions for novel potential therapeutic strategies in patients with TTS including the role of cognitive behavioural therapy, beta-blockers, and endothelin-A antagonists. The underlying mechanism of TTS remains elusive. In reality, physical or emotional stressors likely trigger through the amygdala and hippocampus a central neurohumoral activation with the local and systemic secretion of excess catecholamine and other neurohormones, which exert its effect on the myocardium through a metabolic switch, altered cellular signalling, and endothelial dysfunction. These complex pathways exert a regional activation in the myocardium through the altered distribution of adrenoceptors and density of autonomic innervation as a protective mechanism from myocardial apoptosis. More research is needed to understand how these different complex mechanisms interact with each other to bring on the TTS phenotype.
心尖球形综合征（TTS）占临床上表现为急性冠状动脉综合征的病例的 1%至 4%。它通常表现为左心室功能障碍的短暂性心脏表型，具有自发恢复。更严重的表现可能包括心源性休克或心脏骤停。尽管自 1990 年首次描述以来，人们对该病的理解取得了进展，但对于潜在的发病机制仍存在许多疑问。在这篇综述文章中，我们描述了目前关于 TTS 潜在发病机制的相关研究，包括交感神经系统过度刺激、中枢神经系统的结构和功能改变、儿茶酚胺分泌、肾上腺素能受体平衡和分布的改变、包括雌激素在内的激素的附加影响、心外膜冠状动脉或微血管痉挛、内皮功能障碍和遗传学，这些都可能导致 TTS 的发生。这些发病机制为 TTS 患者提供了新的潜在治疗策略的建议，包括认知行为疗法、β受体阻滞剂和内皮素-A 拮抗剂的作用。TTS 的潜在机制仍不清楚。实际上，身体或情绪压力源可能通过杏仁核和海马体引发中枢神经体液激活，导致局部和全身过量儿茶酚胺和其他神经激素的分泌，通过代谢转换、细胞信号改变和内皮功能障碍对心肌产生作用。这些复杂的途径通过改变肾上腺素能受体的分布和自主神经支配的密度，在心肌中发挥区域性激活作用，作为心肌细胞凋亡的保护机制。需要进一步研究来了解这些不同的复杂机制如何相互作用，从而导致 TTS 表型的发生。
