Stroke-heart syndrome: current progress and future outlook

Abstract

Stroke can lead to cardiac complications such as arrhythmia, myocardial injury, and cardiac dysfunction, collectively termed stroke-heart syndrome (SHS). These cardiac alterations typically peak within 72 h of stroke onset and can have long-term effects on cardiac function. Post-stroke cardiac complications seriously affect prognosis and are the second most frequent cause of death in patients with stroke. Although traditional vascular risk factors contribute to SHS, other potential mechanisms indirectly induced by stroke have also been recognized. Accumulating clinical and experimental evidence has emphasized the role of central autonomic network disorders and inflammation as key pathophysiological mechanisms of SHS. Therefore, an assessment of post-stroke cardiac dysautonomia is necessary. Currently, the development of treatment strategies for SHS is a vital but challenging task. Identifying potential key mediators and signaling pathways of SHS is essential for developing therapeutic targets. Therapies targeting pathophysiological mechanisms may be promising. Remote ischemic conditioning exerts protective effects through humoral, nerve, and immune-inflammatory regulatory mechanisms, potentially preventing the development of SHS. In the future, well-designed trials are required to verify its clinical efficacy. This comprehensive review provides valuable insights for future research.

Keywords: Acute ischemic stroke; Cardiac dysfunction; Central autonomic network; Remote ischemic conditioning; Stroke–heart syndrome.

Fig. 1

Mechanisms for stroke–heart syndrome. Stroke leads to central autonomic network dysregulation, HPA axis activation, inflammation, and immune response. These mechanisms interact with each other, ultimately resulting in cardiac damage. “Cell death signals”, miRNA, and MV are also involved in the development of SHS. HPA hypothalamic–pituitary–adrenal, MV microvesicle

Fig. 2

Diagnosis and management of myocardial injury after acute ischemic stroke. Continuous cardiac monitoring, myocardial enzyme measurements, and autonomic function assessment are necessary after stroke onset. If no contraindications exist, patients with acute myocardial infarction after acute ischemic stroke (within the time window) can be treated with reperfusion therapy. Patients with other types of myocardial injury should undergo a comprehensive etiological examination followed by treatment of the underlying cause