Knez Rajna, Niksic Milan, Omerovic Elmir
Gillberg Neuropsychiatry Centre, Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Research and Development, Department of Women's and Child Health, Skaraborg Hospital, Skövde, Sweden.
Front Cardiovasc Med. 2022 Nov 3;9:1016369. doi: 10.3389/fcvm.2022.1016369. eCollection 2022.
Takotsubo syndrome (TTS) is an acute heart failure syndrome. Emotional or physical stressors are believed to precipitate TTS, while the pathophysiological mechanism is not yet completely understood. During the coronavirus disease (COVID-19) pandemic, an increased incidence of TTS has been reported in some countries; however, the precise pathophysiological mechanism for developing TTS with acute COVID-19 infection is unknown. Nevertheless, observing the symptoms of COVID-19 might lead to new perspectives in understanding TTS pathophysiology, as some of the symptoms of the COVID-19 infection could be assessed in the context of an orexin/hypocretin-system dysfunction. Orexin/hypocretin is a cardiorespiratory neuromodulator that acts on two orexin receptors widely distributed in the brain and peripheral tissues. In COVID-19 patients, autoantibodies against one of these orexin receptors have been reported. Orexin-system dysfunction affects a variety of systems in an organism. Here, we review the influence of orexin-system dysfunction on the cardiovascular system to propose its connection with TTS. We propose that orexin-system dysfunction is a potential novel explanation for the pathophysiology of TTS due to direct or indirect dynamics of orexin signaling, which could influence cardiac contractility. This is in line with the conceptualization of TTS as a cardiovascular syndrome rather than merely a cardiac abnormality or cardiomyopathy. To the best of our knowledge, this is the first publication to present a plausible connection between TTS and orexin-system dysfunction. We hope that this novel hypothesis will inspire comprehensive studies regarding orexin's role in TTS pathophysiology. Furthermore, confirmation of this plausible pathophysiological mechanism could contribute to the development of orexin-based therapeutics in the treatment and prevention of TTS.
应激性心肌病(TTS)是一种急性心力衰竭综合征。情绪或身体应激源被认为会诱发TTS,但其病理生理机制尚未完全明确。在冠状病毒病(COVID-19)大流行期间,一些国家报告了TTS发病率的上升;然而,急性COVID-19感染导致TTS的确切病理生理机制尚不清楚。尽管如此,观察COVID-19的症状可能会为理解TTS的病理生理学带来新的视角,因为COVID-19感染的一些症状可以在食欲素/下丘脑泌素系统功能障碍的背景下进行评估。食欲素/下丘脑泌素是一种心肺神经调节剂,作用于广泛分布于大脑和外周组织的两种食欲素受体。在COVID-19患者中,已报告了针对其中一种食欲素受体的自身抗体。食欲素系统功能障碍会影响生物体的多种系统。在此,我们综述食欲素系统功能障碍对心血管系统的影响,以提出其与TTS的关联。我们提出,由于食欲素信号的直接或间接动态变化,食欲素系统功能障碍是TTS病理生理学的一种潜在新解释,这可能会影响心脏收缩力。这与将TTS概念化为心血管综合征而非仅仅是心脏异常或心肌病相一致。据我们所知,这是首次发表的提出TTS与食欲素系统功能障碍之间合理关联的文章。我们希望这一新假设将激发关于食欲素在TTS病理生理学中作用的全面研究。此外,对这种合理病理生理机制的证实可能有助于开发基于食欲素的疗法来治疗和预防TTS。