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Stroke and heart disease are two of the leading causes of the global disease burden. However, modern research has gradually revealed a potential causal link between these two conditions. Most studies have focused on the direct role of arrhythmias in stroke. However, clinical evidence suggests that the incidence of arrhythmias increases after stroke in patients without a history of arrhythmia, and cardiac disease after stroke has become the second leading cause of death after stroke. This article focuses on arrhythmias after stroke and reviews brain-heart crosstalk after stroke. This article examines the potential mechanisms of brain-heart interactions after stroke, including increased catecholamines due to autonomic imbalance, gut microbial dysbiosis, immune response, and systemic inflammation. In addition, this article discusses the impact of arrhythmia on stroke severity and the role of brain injury sites in brain-heart interactions. To address these mechanisms, we propose that post-stroke arrhythmia is a type of stroke-induced disease distinct from primary arrhythmia. We aimed to identify new therapeutic targets and treatments, both pharmacological and non-pharmacological, to achieve targeted treatment and provide guidance for future clinical prevention and treatment.
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