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Background <p>Stroke-heart syndrome (SHS) represents a serious complication after stroke that significantly elevates mortality risk, especially in the short term. The primary initiating pathological event in SHS is acute ischemic stroke, which subsequently triggers secondary cardiac dysfunction through a complex and continuous interplay among the brain, the immune system, and systemic metabolism. </p> Pathophysiological mechanisms <p>In the acute phase, an acute surge of stress hormones such as norepinephrine induces calcium overload and subsequent myocardial damage. Meanwhile, a progressive cardiac remodeling process begins, which continues to evolve over subsequent weeks. Subacutely, systemic immune activation drives splenic leukocyte mobilization and the formation of neutrophil extracellular traps (NETs), thereby exacerbating inflammation and plaque instability. Over time, gut microbiota derived metabolites, particularly phenylacetylglutamine (PAGln), may further aggravate thrombotic risk and cardiac metabolic vulnerability. </p> Endophenotype-based framework and interventions <p>To address this multifactorial complexity, this review proposes a hypothesis-generating conceptual framework that categorizes SHS into three endophenotypes, including neurogenic arrhythmic (Type I), inflammatory thrombotic (Type II), and metabolic remodeling (Type III). Potential phenotype-specific interventions include beta blockers for neural stabilization, NETs degradation for immunomodulation, and metabolic pathway antagonists. </p> Challenges and perspectives <p>Although interventions like remote ischemic conditioning (RIC) demonstrate promising biological activity and safety in preclinical evaluations, translating these exploratory findings into consistent clinical outcomes remains a significant translational challenge. Furthermore, sex specific mechanisms, notably the altered estrogen signaling in women, highlight the potential need for tailored therapeutic strategies. Transitioning toward this etiology-based paradigm provides an essential foundation for future precision therapeutics, aiming to mitigate targeted pathophysiological drivers rather than relying solely on generalized cardioprotection.</p>

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Stroke Heart Syndrome: Neuroimmune and Metabolic Crosstalk with Conceptual Approaches for Precision Therapeutics

  • 期刊论文

  • 发表日期：

    2026年8月5日

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  • Qiwen Nie,
  • Wang Guo,
  • Zhihao Wang,
  • Hongxin Li,
  • Hongyu Li

摘要

Background

Stroke-heart syndrome (SHS) represents a serious complication after stroke that significantly elevates mortality risk, especially in the short term. The primary initiating pathological event in SHS is acute ischemic stroke, which subsequently triggers secondary cardiac dysfunction through a complex and continuous interplay among the brain, the immune system, and systemic metabolism.

Pathophysiological mechanisms

In the acute phase, an acute surge of stress hormones such as norepinephrine induces calcium overload and subsequent myocardial damage. Meanwhile, a progressive cardiac remodeling process begins, which continues to evolve over subsequent weeks. Subacutely, systemic immune activation drives splenic leukocyte mobilization and the formation of neutrophil extracellular traps (NETs), thereby exacerbating inflammation and plaque instability. Over time, gut microbiota derived metabolites, particularly phenylacetylglutamine (PAGln), may further aggravate thrombotic risk and cardiac metabolic vulnerability.

Endophenotype-based framework and interventions

To address this multifactorial complexity, this review proposes a hypothesis-generating conceptual framework that categorizes SHS into three endophenotypes, including neurogenic arrhythmic (Type I), inflammatory thrombotic (Type II), and metabolic remodeling (Type III). Potential phenotype-specific interventions include beta blockers for neural stabilization, NETs degradation for immunomodulation, and metabolic pathway antagonists.

Challenges and perspectives

Although interventions like remote ischemic conditioning (RIC) demonstrate promising biological activity and safety in preclinical evaluations, translating these exploratory findings into consistent clinical outcomes remains a significant translational challenge. Furthermore, sex specific mechanisms, notably the altered estrogen signaling in women, highlight the potential need for tailored therapeutic strategies. Transitioning toward this etiology-based paradigm provides an essential foundation for future precision therapeutics, aiming to mitigate targeted pathophysiological drivers rather than relying solely on generalized cardioprotection.