PDF(Pubmed)
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.
摘要：
中风会导致心律失常等心脏并发症,心肌损伤，和心脏功能障碍，统称为中风-心脏综合征（SHS）。这些心脏改变通常在中风发作的72小时内达到峰值，并且可能对心脏功能产生长期影响。卒中后心脏并发症严重影响预后，是卒中患者死亡的第二常见原因。虽然传统的血管危险因素有助于SHS，由卒中间接诱发的其他潜在机制也已得到认可。越来越多的临床和实验证据强调中枢自主神经网络紊乱和炎症是SHS的关键病理生理机制。因此,有必要对卒中后心脏自主神经失调进行评估.目前,制定SHS的治疗策略是一项至关重要但具有挑战性的任务.识别SHS的潜在关键介质和信号通路对于开发治疗靶标至关重要。针对病理生理机制的疗法可能是有希望的。远程缺血调节通过体液，神经,和免疫炎症调节机制，有可能阻止SHS的发展。在未来,需要精心设计的试验来验证其临床疗效。这篇全面的综述为未来的研究提供了有价值的见解。
