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Updated: Jul 15, 2026

In Silico Clinical Trials for Cardiovascular Disease
Published on: May 27, 2022
A cortical potential reflecting cardiac function
Marcus A Gray1, Peter Taggart, Peter M Sutton
1Functional Imaging Laboratory, Wellcome Department of Imaging Neuroscience, Institute of Neurology, University College London, 12 Queen Square, London WC1N 3BG, United Kingdom. M.A.Gray@bsms.ac.uk
Insights
Mental stress impacts heart function, influencing cardiac output and potentially causing arrhythmias. Brain activity, measured via electroencephalography, reflects the heart
Area of Science:
- Neuroscience
- Cardiology
- Psychophysiology
Background:
- Psychological stress and emotional trauma can trigger cardiac arrhythmias and sudden death via sympathetic nervous system activation.
- Individuals with pre-existing heart conditions are more susceptible to stress-induced cardiac events.
- Cerebral autonomic centers can amplify proarrhythmic signals through feedback from a compromised heart.
Purpose of the Study:
- To investigate the cortical representation of afferent cardiac information during stress.
- To identify electrocortical potentials linked to myocardial function during psychological stress.
- To understand the brain-heart interaction in stress-induced cardiovascular morbidity.
Main Methods:
- Simultaneous measurement of cardiac response and electroencephalography (EEG) in patients with ventricular dysfunction.
- Experimentally induced mental stress to assess cardiovascular and electrocortical changes.
- Analysis of heartbeat-evoked potential (HEP) amplitude in relation to cardiac output and repolarization.
Main Results:
- Mental stress increased sympathetic activity markers (blood pressure, heart rate, ejection fraction, skin conductance).
- Cardiac output response to stress varied among patients (increase or decrease).
- HEP amplitude at specific electrode locations correlated with stress-induced cardiac output changes and reflected proarrhythmic status.
Conclusions:
- A cortical representation of myocardial function during stress exists, detectable via EEG.
- Heartbeat-evoked potential amplitude is predictive of proarrhythmic abnormalities, specifically left ventricular repolarization inhomogeneity.
- Findings underscore the critical interplay between the heart and brain in the context of stress-related cardiovascular disease.
Abstract:
Emotional trauma and psychological stress can precipitate cardiac arrhythmia and sudden death through arrhythmogenic effects of efferent sympathetic drive. Patients with preexisting heart disease are particularly at risk. Moreover, generation of proarrhythmic activity patterns within cerebral autonomic centers may be amplified by afferent feedback from a dysfunctional myocardium. An electrocortical potential reflecting afferent cardiac information has been described, reflecting individual differences in interoceptive sensitivity (awareness of one's own heartbeats). To inform our understanding of mechanisms underlying arrhythmogenesis, we extended this approach, identifying electrocortical potentials corresponding to the cortical expression of afferent information about the integrity of myocardial function during stress. We measured changes in cardiac response simultaneously with electroencephalography in patients with established ventricular dysfunction. Experimentally induced mental stress enhanced cardiovascular indices of sympathetic activity (systolic blood pressure, heart rate, ventricular ejection fraction, and skin conductance) across all patients. However, the functional response of the myocardium varied; some patients increased, whereas others decreased, cardiac output during stress. Across patients, heartbeat-evoked potential amplitude at left temporal and lateral frontal electrode locations correlated with stress-induced changes in cardiac output, consistent with an afferent cortical representation of myocardial function during stress. Moreover, the amplitude of the heartbeat-evoked potential in the left temporal region reflected the proarrhythmic status of the heart (inhomogeneity of left ventricular repolarization). These observations delineate a cortical representation of cardiac function predictive of proarrhythmic abnormalities in cardiac repolarization. Our findings highlight the dynamic interaction of heart and brain in stress-induced cardiovascular morbidity.
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