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<p>Bidirectional, multilevel communication between the heart and the brain is pivotal for the beat-to-beat regulation of cardiac function and the close titration of cardiac output to&#xa0;meet metabolic demand. Given this bidirectional communication, it is perhaps not surprising that cardiac pathologies lead to changes in the central and peripheral autonomic nervous system, which in turn lead to further progression of cardiovascular disease. Within the CNS, structural and functional changes have been reported in the setting of hypertension and heart failure in multiple autonomic regions and nuclei, including the spinal cord, brainstem, hypothalamus&#xa0;and higher centres, such as the amygdala and thalamus. These&#xa0;alterations enhance the excitability of sympathetic neuronal populations and diminish the&#xa0;excitability of neurons&#xa0;within the parasympathetic nuclei, resulting in sympathovagal imbalance. The&#xa0;primary&#xa0;drivers of these structural and functional changes appear to be a combination of increased angiotensin signalling (both central and peripheral), neuroinflammation,&#xa0;oxidative stress and glial activation. Targeting the CNS in the setting of cardiovascular disease presents an exciting avenue for the field of neuromodulation.</p>

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The brain–heart axis: effects of cardiovascular disease on the CNS and opportunities for central neuromodulation

  • 期刊论文

  • 发表日期：

    2025年12月11日

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  • Valerie Y. H. van Weperen,
  • Marmar Vaseghi

摘要

Bidirectional, multilevel communication between the heart and the brain is pivotal for the beat-to-beat regulation of cardiac function and the close titration of cardiac output to meet metabolic demand. Given this bidirectional communication, it is perhaps not surprising that cardiac pathologies lead to changes in the central and peripheral autonomic nervous system, which in turn lead to further progression of cardiovascular disease. Within the CNS, structural and functional changes have been reported in the setting of hypertension and heart failure in multiple autonomic regions and nuclei, including the spinal cord, brainstem, hypothalamus and higher centres, such as the amygdala and thalamus. These alterations enhance the excitability of sympathetic neuronal populations and diminish the excitability of neurons within the parasympathetic nuclei, resulting in sympathovagal imbalance. The primary drivers of these structural and functional changes appear to be a combination of increased angiotensin signalling (both central and peripheral), neuroinflammation, oxidative stress and glial activation. Targeting the CNS in the setting of cardiovascular disease presents an exciting avenue for the field of neuromodulation.