Stroke‐Heart Syndrome: Mechanisms, Temporal Phenotypes, and Diagnostic Reasoning

Figures

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  FIGURE 1. Mechanistic cascade from acute stroke to cardiac manifestations. Ischemic stroke, intracerebral hemorrhage, and subarachnoid hemorrhage can disrupt insular‐limbic, hypothalamic, and brainstem autonomic networks. Sympathetic activation, parasympathetic withdrawal, neuroendocrine stress, NF‐κB/NLRP3 and ZBP1‐NLRP3 signaling, endothelial injury, microvascular dysfunction, and oxygen supply‐demand mismatch may converge on myocardial injury, electrical instability, ventricular dysfunction, Takotsubo‐like cardiomyopathy, heart failure, and death. Abbreviations: ADH, antidiuretic hormone; ECG, electrocardiogram; HPA, hypothalamic‐pituitary‐adrenal; HRV, heart‐rate variability; IL, interleukin; LVEF, left ventricular ejection fraction; NF‐κB, nuclear factor‐κB; NLRP3, NOD‐like receptor protein 3; RAAS, renin‐angiotensin‐aldosterone system; SHS, stroke‐heart syndrome; TNF‐α, tumor necrosis factor‐α; ZBP1, Z‐DNA‐binding protein 1.

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  FIGURE 2. Temporal framework for SHS manifestations and outcomes. Premorbid cardiac and systemic vulnerability precedes stroke. Hyperacute and early findings include troponin change, electrocardiographic abnormalities, arrhythmia, autonomic disturbance, and ventricular dysfunction. Readmission, recurrent vascular events, heart failure, cognitive impairment, disability, and death are downstream outcomes, not defining acute manifestations. Abbreviations: ACS, acute coronary syndrome; AF, atrial fibrillation; APRI, aspartate aminotransferase‐to‐platelet ratio index; CRP, C‐reactive protein; ECG, electrocardiogram; FIB‐4, fibrosis‐4 index; HF, heart failure; IL, interleukin; LAE, left‐atrial enlargement; LV, left ventricular; MI, myocardial infarction; SHS, stroke‐heart syndrome; TIA, transient ischemic attack; VT, ventricular tachycardia.

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  FIGURE 3. Diagnostic workflow for cardiac abnormalities after acute stroke. Baseline electrocardiography and cardiac troponin support initial triage but should not delay reperfusion treatment. A high‐risk electrocardiographic abnormality, elevated troponin, symptoms, or instability prompts serial biomarkers, telemetry, hemodynamic assessment, and echocardiography. Dynamic troponin identifies acute injury but does not distinguish type 1 myocardial infarction, type 2 myocardial infarction, neurogenic injury, Takotsubo syndrome, myocarditis, or hemorrhagic‐stroke‐associated injury. Absence of a culprit lesion does not prove a neurogenic mechanism. Selective coronary assessment, CMR, and specialist review are used when clinically indicated [20, 21, 73, 75, 76, 77, 78, 79, 86, 87]. Abbreviations: BP, blood pressure; CMR, cardiac magnetic resonance; ECG, electrocardiogram; HR, heart rate; HTN, hypertension; ICH, intracerebral hemorrhage; LV, left ventricular; SAH, subarachnoid hemorrhage; SHS, stroke‐heart syndrome.