This review elucidates the mechanistic role of the central autonomic network, particularly the insula and limbic system, in Stroke-Heart Syndrome, highlighting potential neuroimaging biomarkers and targeted therapies.
Stroke-Heart Syndrome describes cardiac dysfunction following acute cerebrovascular events, with injury to the central autonomic network being a key pathological mechanism. The insular cortex and limbic system act as central hubs for neuro-cardiac regulation, integrating autonomic, neuroendocrine, and immune signals. This review summarizes the structural and functional organization of the central autonomic network, emphasizing the insula's subregional specialization and its hemispheric bias in autonomic regulation. Generally, the right insula is more often linked to sympathetic predominance and the left to parasympathetic modulation, though this pattern is not absolute but rather contingent on subregional and methodological factors. Clinical and experimental evidence links lesions in the insula and limbic system to arrhythmias, QT interval prolongation, and myocardial injury through autonomic imbalance. Advances in neuroimaging, such as functional magnetic resonance imaging and diffusion tensor imaging, provide novel biomarkers for early cardiac risk stratification after stroke. Furthermore, emerging interventions including heart rate variability biofeedback and non-invasive vagus nerve stimulation show therapeutic potential by targeting these central circuits. Elucidating the mechanisms of central autonomic network injury, particularly involving the insula and limbic system, is essential for improving risk assessment and developing targeted therapies for Stroke-Heart Syndrome.
Li et al. (Wed,) studied this question.