Heidari Afshin, Ghorbani Mohammad, Hassanzadeh Sara, Rahmanipour Elham
School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran; Health Policy Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
Health Policy Research Center, Shiraz University of Medical Sciences, Shiraz, Iran; Orthopedic Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
Prog Cardiovasc Dis. 2024 Nov-Dec;87:18-25. doi: 10.1016/j.pcad.2024.10.001. Epub 2024 Oct 9.
Takotsubo Cardiomyopathy (TCM) is a transient heart condition often precipitated by stress and characterized by atypical ventricular ballooning. The interplay between TCM and Adrenal Insufficiency (AI), particularly the influence of catecholamine excess and glucocorticoid deficiency on TCM's pathogenesis in individuals with AI, warrants comprehensive exploration for a better understanding of TCM pathophysiology and establishment of potential therapeutic strategies.
We conducted an extensive literature search via PubMed and Google Scholar, targeting reports on AI, heart failure, and cardiomyopathy, supplemented by forward and backward citation tracing. We analyzed 46 cases from 45 reports, assessing the clinical presentation and outcomes in the context of AI categorization.
In patients with AI, a glucocorticoid deficit appears to exacerbate the myocardial vulnerability to catecholamine toxicity, precipitating TCM. Most conditions were reversible; however, three pre-1990 cases resulted in irreversible outcomes.
The investigation into the AI and TCM intersection highlights the pathogenic significance of catecholamines in the absence of glucocorticoids. The data consolidates the hypothesis that glucocorticoid scarcity exacerbates the cardiac susceptibility to catecholaminergic toxicity, potentially triggering TCM. The study affirms glucocorticoids' cardioprotective roles and elucidates how catecholamine surges contribute to TCM pathogenesis, suggesting strategic clinical management adjustments for AI patients to reduce TCM incidence.
应激性心肌病（TCM）是一种常由应激诱发的短暂性心脏疾病，其特征为非典型心室扩张。应激性心肌病与肾上腺功能不全（AI）之间的相互作用，尤其是儿茶酚胺过量和糖皮质激素缺乏对AI患者应激性心肌病发病机制的影响，需要进行全面探究，以更好地理解应激性心肌病的病理生理学并制定潜在的治疗策略。
我们通过PubMed和谷歌学术进行了广泛的文献检索，以AI、心力衰竭和心肌病的报告为目标，并通过正向和反向引文追踪进行补充。我们分析了45篇报告中的46例病例，在AI分类的背景下评估临床表现和结果。
在AI患者中，糖皮质激素缺乏似乎会加剧心肌对儿茶酚胺毒性的易感性，从而引发应激性心肌病。大多数情况是可逆的；然而，1990年前的3例病例导致了不可逆的结果。
对AI与应激性心肌病交叉领域的研究突出了在缺乏糖皮质激素的情况下儿茶酚胺的致病意义。这些数据强化了糖皮质激素缺乏会加剧心脏对儿茶酚胺能毒性的易感性、可能引发应激性心肌病的假说。该研究证实了糖皮质激素的心脏保护作用，并阐明了儿茶酚胺激增如何导致应激性心肌病的发病机制，建议对AI患者进行战略临床管理调整以降低应激性心肌病的发病率。
