Abstract：
The pathophysiology of TTS is still elusive. This viewpoint proposes that TTS is an acute coronary syndrome, engendered by an ASNS/catecholamine-induced LVOTO, which results in an enhanced wall stress and afterload-based supply/demand mismatch, culminating in a segmental myocardial ischemic injury state, in susceptible individuals. Such individuals are felt to be particularly women with chronic hypertension, known or latent HCM, or non-HCM segmental myocardial hypertrophy, and certain structural abnormalities involving the LV and the MV apparatus. Recommendations are provided to explore further this hypothesis, while maintaining our focus on all other advanced TTS pathophysiology hypotheses for all patients, or those who do not experience LVOTO, men, the young, and patients with reverse, mid-ventricular, or right ventricular TTS, in whom more prolonged hyperadrenergic stimulation and/or larger amounts of blood-ridden catecholamines, segmental particularities of cardiac innervation and/or density of α-, and β-adrenergic receptors, pheochromocytoma, neurological chronic or acute comorbidities/catastrophies, coronary epicardial/microvascular vasospasm, and CMD.
摘要：
TTS的病理生理学仍然难以捉摸。这种观点认为TTS是一种急性冠脉综合征,由ASNS/儿茶酚胺诱导的LVOTO引起，这导致了增强的墙体应力和基于后负荷的供需不匹配，最终导致节段性心肌缺血损伤状态，在易感个体中。这些人尤其被认为是患有慢性高血压的女性，已知或潜在的HCM，或非HCM节段性心肌肥厚，以及涉及LV和MV设备的某些结构异常。提供了进一步探索这一假设的建议，同时保持我们对所有患者的所有其他高级TTS病理生理学假设的关注，或那些没有经历过LVOTO的人，男人,年轻人,和反向患者，中室,或右心室TTS，在其中更长时间的高肾上腺素能刺激和/或更大量的充血儿茶酚胺，心脏神经支配的节段特殊性和/或α-的密度，和β-肾上腺素能受体，嗜铬细胞瘤,神经慢性或急性合并症/灾难，冠状动脉心外膜/微血管血管痉挛，和CMD。
