Stroke‐Heart Syndrome: Mechanisms, Temporal Phenotypes, and Diagnostic Reasoning
Fa Lin, Jian Lyu, Yanci Liu, Zhiyuan Feng, Jie Bao, Wenxiong Song, Bingcheng Zhu, Minghao Liu, Jionghao Xue, Jiadi Weng, Jiani Zhang, Jizong Zhao, Xiaolin Chen, Bin DongABSTRACT
Stroke‐heart syndrome (SHS) encompasses new or worsened cardiac abnormalities that arise after acute stroke, most often within the first 30 days and with an early peak. Its spectrum includes acute myocardial injury, electrocardiographic changes, arrhythmia, ventricular dysfunction, Takotsubo syndrome, and heart failure, but similar findings may reflect antecedent cardiac disease or systemic illness. This Review defines the accepted clinical boundaries of SHS and integrates central autonomic network disruption, neuroendocrine stress, inflammation, endothelial and microvascular dysfunction, oxygen supply‐demand imbalance, and premorbid substrate into a time‐resolved framework. Eight provisional, non‐mutually‐exclusive phenotypic domains are proposed to organize current evidence without implying validated endotypes. A diagnostic approach based on symptom chronology, prior cardiac data, serial troponin and electrocardiography, rhythm monitoring, echocardiography, selective coronary assessment, and cardiac magnetic resonance is presented to distinguish stroke‐triggered injury from recent myocardial infarction, pre‐existing atrial fibrillation, chronic myocardial injury, and established heart failure. No syndrome‐specific treatment is validated; care should prioritize recognized cardiac emergencies, correction of reversible stressors, and coordinated stroke‐cardiology decision‐making. Prospective studies with documented premorbid status, standardized time points, and blinded adjudication are needed to validate the proposed phenotypes and determine whether they improve outcomes.