Wang Ti, Xiong Ting, Yang Yuxue, Zuo Bangyun, Chen Xiwei, Wang Daxin
The Hospital Affiliated to Medical School of Yangzhou University (Taizhou People's Hospital), Taizhou, Jiangsu, China.
Department of Cardiology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Front Cardiovasc Med. 2022 Nov 24;9:1060070. doi: 10.3389/fcvm.2022.1060070. eCollection 2022.
The heart requires a large and constant supply of energy that is mainly the result of an efficient metabolic machinery that converges on mitochondrial oxidative metabolism to maintain its continuous mechanical work. Perturbations in these metabolic processes may therefore affect energy generation and contractile function directly. Metabolism characteristics in takotsubo syndrome (TTS) reveals several metabolic alterations called metabolic remodeling, including the hyperactivity of sympathetic metabolism, derangements of substrate utilization, effector subcellular dysfunction and systemic metabolic disorders, ultimately contributing to the progression of the disease and the development of a persistent and long-term heart failure (HF) phenotype. In this review, we explore the current literature investigating the pathological metabolic alterations in TTS. Although the metabolic dysfunction in takotsubo hearts is initially recognized as a myocardial metabolic inflexibility, we suggest that the widespread alterations of systemic metabolism with complex interplay between the heart and peripheral tissues rather than just cardiometabolic disorders account for long-term maladaptive metabolic, functional and structural impairment under this condition. Therapeutic strategies with the recent evidence from small clinical and animal researches, especially for targeting substrate utilization and/or oxidative stress, might be promising tools to improve the outcome of patients with TTS beyond that achieved with traditional sympathetic inhibition and symptomatic therapies.
心脏需要大量持续的能量供应，这主要是高效代谢机制的结果，该机制汇聚于线粒体氧化代谢以维持其持续的机械工作。因此，这些代谢过程的紊乱可能直接影响能量生成和收缩功能。应激性心肌病（TTS）的代谢特征揭示了几种称为代谢重塑的代谢改变，包括交感代谢亢进、底物利用紊乱、效应器亚细胞功能障碍和全身代谢紊乱，最终导致疾病进展以及持续性和长期心力衰竭（HF）表型的发展。在本综述中，我们探讨了当前研究TTS病理代谢改变的文献。尽管应激性心肌病心脏的代谢功能障碍最初被认为是心肌代谢灵活性不足，但我们认为，全身代谢的广泛改变以及心脏与外周组织之间复杂的相互作用，而非仅仅是心脏代谢紊乱，导致了这种情况下长期的适应性不良代谢、功能和结构损害。基于小型临床和动物研究的最新证据的治疗策略，特别是针对底物利用和/或氧化应激的策略，可能是改善TTS患者预后的有前景的工具，其效果可能优于传统的交感神经抑制和对症治疗。
