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Updated: Jul 4, 2025

A Thrombotic Stroke Model Based On Transient Cerebral Hypoxia-ischemia
Published on: August 18, 2015
Stroke Related Brain-Heart Crosstalk: Pathophysiology, Clinical Implications, and Underlying Mechanisms
Xuehui Fan1,2,3, Jianyang Cao4,5, Mingxia Li4,5
1Key Laboratory of Medical Electrophysiology, Ministry of Education and Medical Electrophysiological Key Laboratory of Sichuan Province, Collaborative Innovation Center for Prevention of Cardiovascular Diseases, Institute of Cardiovascular Research, Southwest Medical University, Luzhou, 646000, China.
Insights
Acute ischemic stroke (AIS) can cause severe heart problems due to brain-heart axis interactions. Understanding these mechanisms is key to preventing and managing cardiovascular dysfunctions after stroke.
Area of Science:
- Neuroscience
- Cardiology
- Pathophysiology
Background:
- Acute ischemic stroke (AIS) significantly impacts cardiovascular function, leading to a range of complications like heart attack and heart failure.
- The brain-heart axis describes the bidirectional communication between the central nervous system and the cardiovascular system, crucial in stroke outcomes.
- Understanding this interaction is vital for improving patient prognosis and reducing mortality.
Purpose of the Study:
- To review the current understanding of pathophysiological mechanisms linking AIS and cardiovascular dysfunctions.
- To explore the role of the brain-heart axis in stroke-related cardiac complications.
- To suggest management strategies for these dysfunctions.
Main Methods:
- Review of preclinical and clinical research on AIS-induced cardiovascular dysfunctions.
- Analysis of neurohumoral pathways, including the hypothalamic-pituitary-adrenal (HPA) axis, autonomic nervous system, and inflammatory responses.
- Examination of existing therapeutic interventions and their limitations.
Main Results:
- AIS triggers cardiovascular complications through mechanisms involving the HPA axis, sympathetic/parasympathetic imbalance, inflammation, and gut dysbiosis.
- These factors collectively influence the stroke-related brain-heart axis, contributing to adverse cardiac events.
- Current treatments for hypertension and arrhythmias show limitations, with therapeutic targets remaining elusive.
Conclusions:
- The brain-heart axis plays a critical role in cardiovascular complications following AIS.
- Further research is needed to identify effective therapeutic targets for managing these complex interactions.
- A comprehensive understanding of these mechanisms is essential for developing novel treatment strategies.
Abstract:
The emergence of acute ischemic stroke (AIS) induced cardiovascular dysfunctions as a bidirectional interaction has gained paramount importance in understanding the intricate relationship between the brain and heart. Post AIS, the ensuing cardiovascular dysfunctions encompass a spectrum of complications, including heart attack, congestive heart failure, systolic or diastolic dysfunction, arrhythmias, electrocardiographic anomalies, hemodynamic instability, cardiac arrest, among others, all of which are correlated with adverse outcomes and mortality. Mounting evidence underscores the intimate crosstalk between the heart and the brain, facilitated by intricate physiological and neurohumoral complex networks. The primary pathophysiological mechanisms contributing to these severe cardiac complications involve the hypothalamic-pituitary-adrenal (HPA) axis, sympathetic and parasympathetic hyperactivity, immune and inflammatory responses, and gut dysbiosis, collectively shaping the stroke-related brain-heart axis. Ongoing research endeavors are concentrated on devising strategies to prevent AIS-induced cardiovascular dysfunctions. Notably, labetalol, nicardipine, and nitroprusside are recommended for hypertension control, while β-blockers are employed to avert chronic remodeling and address arrhythmias. However, despite these therapeutic interventions, therapeutic targets remain elusive, necessitating further investigations into this complex challenge. This review aims to delineate the state-of-the-art pathophysiological mechanisms in AIS through preclinical and clinical research, unraveling their intricate interplay within the brain-heart axis, and offering pragmatic suggestions for managing AIS-induced cardiovascular dysfunctions.
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