REVIEW article
Front. Cardiovasc. Med.
Sec. Cardioneurology
Volume 12 - 2025 | doi: 10.3389/fcvm.2025.1632704
This article is part of the Research TopicExploring Heart-Brain Interactions: Autonomic Imbalance and Neuromodulation Strategies in Cardiovascular DiseaseView all 5 articles
Sympathetic overactivation and catecholamine toxicity: mechanisms and therapeutic strategies for neurogenic heart injury following acute ischemic stroke
Provisionally accepted- 1Heilongjiang University of Chinese Medicine, Harbin, China
- 2The Second Affiliated Hospital of Heilongjiang University of Chinese Medicine, Harbin, China
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Acute ischemic stroke (AIS) may trigger a spectrum of cardiac complications spanning arrhythmias, troponin elevation, Takotsubo cardiomyopathy, heart failure, and myocardial fibrosis and other acute or chronic cardiac lesions. These complications seriously affect the prognosis of patients. Existing studies have shown that the excessive excitation of the sympathetic neural network after cerebral ischemic injury leads to an increase in catecholamine levels, which may be a key factor triggering neurogenic cardiac damage after AIS. Therefore, evaluating the trigger areas of sympathetic nerve excitation and monitoring related cardiac damage indicators play a key role in patient management. Inhibiting excessive excitation of the sympathetic nerve, alleviating inflammatory responses and oxidative stress, is expected to become the core strategy for the prevention and treatment of neurogenic cardiac injury after AIS. Future research still needs to deeply explore the mechanism of cardiotoxicity mediated by the sympathetic neuro-catecholamine system after AIS, and at the same time promote clinical trials targeting the mechanism to verify treatment paradigms through translational models. This review aims to provide a useful reference direction for subsequent in-depth research.
Keywords: Acute ischemic stroke, Sympathetic nervous, catecholamine, neurogenic heart injury, Cardiac Injury
Received: 21 May 2025; Accepted: 24 Sep 2025.
Copyright: © 2025 Guo, Li, Li, Nie, Wang, Li and Tang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Qiang Tang, tangqiang1963@163.com
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