Neurocardiology: Brain–Heart Interactions in the Heart

Figures

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  FIGURE 1. Heart–brain interactions in Takotsubo syndrome. Physical and psychological stressors, together with predisposing factors, may disrupt brain regions involved in autonomic and emotional regulation, including the insular lobe, amygdala, and prefrontal cortex. Dysfunction within the central autonomic network, limbic system, and HPA axis may promote sympathetic overactivation, catecholamine release, and impaired emotional regulation, thereby contributing to coronary vasospasm, microvascular dysfunction, inflammation, and metabolic alterations. Integrated heart–brain management may include neuroimaging assessment, autonomic activity monitoring, cognitive behavioral therapy, exercise training, and targeted neuromodulation. CAN, central autonomic network; HPA, hypothalamic–pituitary–adrenal axis.

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  FIGURE 2. Heart–brain interactions in the epileptic heart. Acute seizures may activate the central autonomic network and induce transient cardiovascular disturbances, including abnormal heart rate, blood pressure fluctuations, respiratory dysfunction, arrhythmia, and Takotsubo syndrome. Recurrent seizures may contribute to chronic hypoxemia, catecholamine toxicity, autonomic imbalance, and antiseizure medication‐related cardiac effects, potentially contributing to myocardial fibrosis, accelerated atherosclerosis, ion channel remodeling, arrhythmias, and ventricular dysfunction. These changes are consistent with Coumel's arrhythmogenic triangle, supporting integrated strategies that combine cardiac monitoring, seizure prevention, antifibrotic therapy, and neuromodulation. BP, blood pressure; HR, heart rate.

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  FIGURE 3. Heart–brain interactions in stroke–heart syndrome. Acute stroke can cause brain injury, including blood–brain barrier disruption, neuroinflammation, glial activation, oxidative stress, and neuronal death. When the central autonomic network is involved, stroke may induce autonomic dysfunction with sympathetic activation and parasympathetic suppression. Poststroke neuroinflammation may further enhance sympathetic outflow, promoting catecholamine release and splenic nerve activation. In parallel, neuroinflammation may develop into systemic inflammatory response. Together, these neuroimmune processes promote peripheral immune cell activation and contribute to cardiac injury, including myocardial apoptosis, hypertrophy, fibrosis, calcium dysregulation, endothelial dysfunction, inflammatory cell infiltration, and metabolic alterations. These pathological changes contribute to acute myocardial injury, acute coronary syndromes, ventricular dysfunction, ECG abnormalities, arrhythmias, and sudden cardiac death. Integrated management may include early cardiac screening, risk stratification, targeted prevention and treatment, and long‐term control of stroke and cardiovascular risk factors.…

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  FIGURE 4. Heart–brain interactions in heart failure. Sympathetic activation evolves across the heart failure continuum. In the early stage, comorbidities such as obesity, hypertension, and coronary artery disease may trigger adaptive sympathetic overactivity as left ventricular function declines. With disease progression, sustained central sympathetic outflow and abnormal peripheral reflex regulation transform this compensatory response into maladaptive sympathetic overactivity, thereby further worsening cardiac dysfunction and creating a self‐perpetuating heart–brain cycle. Interventions such as exercise training, CPAP, pharmacological therapy, and neuromodulation may help interrupt this cycle. CAD, coronary artery disease; CPAP, continuous positive airway pressure; HF, heart failure; LVEDV, left ventricular end‐diastolic volume; LVEF, left ventricular ejection fraction.

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  FIGURE 5. Heart–brain interactions in cardiac dementia. Cardiac diseases may contribute to cognitive impairment through cerebral hypoperfusion, impaired cerebral blood flow regulation, cerebral embolic events, cerebral microbleeds, inflammation, and neurodegeneration. These mechanisms are associated with neuroimaging abnormalities, including reduced brain volume, hippocampal and temporal lobe atrophy, white matter hyperintensities, lacunar infarcts and silent cerebral infarcts, and abnormal functional brain networks. Integrated management may include cardiovascular risk factor control, exercise interventions and cognitive behavioral training, and disease‐specific pharmacological therapies to help delay cognitive decline in patients with cardiac disease.

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  FIGURE 6. Heart–brain interactions in psychocardiology. Cardiac diseases may contribute to psychological symptoms and disorders through autonomic imbalance, inflammation, abnormalities in cerebral perfusion or metabolism, and altered interoception. These mechanisms are associated with neuroimaging abnormalities, including amygdala hyperactivity, reduced functional connectivity within limbic networks, and regional hypometabolism in depression‐related brain areas. Integrated management may include exercise training, psychological interventions, antidepressants with favorable cardiovascular safety profiles, transcranial magnetic stimulation, and other individualized treatment strategies to alleviate psychological distress and potentially improve cardiovascular outcomes.