A cortical potential reflecting cardiac function.
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.
Gray
Marcus A
MA
Functional 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
Taggart
Peter
P
Sutton
Peter M
PM
Groves
David
D
Holdright
Diana R
DR
Bradbury
David
D
Brull
David
D
Critchley
Hugo D
HD
D000328:Adult; D000344:Afferent Pathways / Q000502:physiology; D000368:Aged; D001145:Arrhythmias, Cardiac / Q000188:drug therapy / Q000503:physiopathology*; D002540:Cerebral Cortex / Q000502:physiology*; D004562:Electrocardiography; D004569:Electroencephalography; D005071:Evoked Potentials / Q000502:physiology*; D006339:Heart Rate / Q000502:physiology; D006801:Humans; D008297:Male; D008875:Middle Aged; D017397:Prefrontal Cortex / Q000502:physiology; D013315:Stress, Psychological / Q000503:physiopathology*; D013702:Temporal Lobe / Q000502:physiology