A review of the interplay between Takotsubo cardiomyopathy and adrenal insufficiency: Catecholamine surge and glucocorticoid deficiency.
Autor: | Heidari A; School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran; Health Policy Research Center, Shiraz University of Medical Sciences, Shiraz, Iran. Electronic address: afshin.heidari@live.com., Ghorbani M; Health Policy Research Center, Shiraz University of Medical Sciences, Shiraz, Iran; Orthopedic Research Center, Mashhad University of Medical Sciences, Mashhad, Iran., Hassanzadeh S; School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran; Health Policy Research Center, Shiraz University of Medical Sciences, Shiraz, Iran; Department of Radiology, Mayo Clinic College of Medicine and Science, Rochester, MN, USA., Rahmanipour E; Health Policy Research Center, Shiraz University of Medical Sciences, Shiraz, Iran; Immunology Research Center, Mashhad University of Medical Sciences, Mashhad, Iran. |
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Jazyk: | angličtina |
Zdroj: | Progress in cardiovascular diseases [Prog Cardiovasc Dis] 2024 Nov-Dec; Vol. 87, pp. 18-25. Date of Electronic Publication: 2024 Oct 09. |
DOI: | 10.1016/j.pcad.2024.10.001 |
Abstrakt: | Background: 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. Methods: 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. Results: 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. Conclusions: 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. Competing Interests: Declaration of competing interest None. (Copyright © 2024 Elsevier Inc. All rights reserved.) |
Databáze: | MEDLINE |
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