Brain Advance Access originally published online on October 20, 2004
Brain 2005 128(1):75-85; doi:10.1093/brain/awh324
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Brain Vol. 128 No. 1 © Guarantors of Brain 2004; all rights reserved
Mental stress and sudden cardiac death: asymmetric midbrain activity as a linking mechanism
1 Wellcome Department of Imaging Neuroscience, Institute of Neurology, University College London, 2 Autonomic Unit, National Hospital for Neurology and Neurosurgery, and Neurovascular Medicine Unit, St Mary's Hospital, Imperial College School of Medicine, 3 Department of Cardiology and Cardiothoracic Surgery, The Hatter Institute for Cardiovascular Studies, University College Hospital, 4 The Heart Hospital, University College London Hospitals, and 5 Department of Cardiological Sciences, St George's Hospital Medical School, Cranmer Terrace, London, UK
Correspondence to: Hugo D. Critchley, Wellcome Department of Imaging Neuroscience, Institute of Neurology, University College London, London WC1N 3BG, UK E-mail: h.critchley{at}fil.ion.ucl.ac.uk
Patients with specific neurological, psychiatric or cardiovascular conditions are at enhanced risk of cardiac arrhythmia and sudden death. The neurogenic mechanisms are poorly understood. However, in many cases, stress may precipitate cardiac arrhythmia and sudden death in vulnerable patients, presumably via centrally driven autonomic nervous system responses. From a cardiological perspective, the likelihood of arrhythmia is strongly associated with abnormalities in electrical repolarization (recovery) of the heart muscle after each contraction. Inhomogeneous and asymmetric repolarization, reflected in ECG T-wave abnormalities, is associated with a greatly increased risk of arrhythmia, i.e. a proarrhythmic state. We therefore undertook a study to identify the brain mechanisms by which stress can induce cardiac arrhythmia through efferent autonomic drive. We recruited a typical group of 10 out-patients attending a cardiological clinic. We simultaneously measured brain activity, using H215O PET, and the proarrhythmic state of the heart, using ECG, during mental and physical stress challenges and corresponding control conditions. Proarrhythmic changes in the heart were quantified from two ECG-derived measures of repolarization inhomogeneity and were related to changes in magnitude and lateralization of regional brain activity reflected in regional cerebral blood flow. Across the patient group, we observed a robust positive relationship between right-lateralized asymmetry in midbrain activity and proarrhythmic abnormalities of cardiac repolarization (apparent in two independent ECG measures) during stress. This association between stress-induced lateralization of midbrain activity and enhanced arrhythmic vulnerability provides empirical support for a putative mechanism for stress-induced sudden death, wherein lateralization of central autonomic drive during stress results in imbalanced activity in right and left cardiac sympathetic nerves. A right–left asymmetry in sympathetic drive across the surface of the heart disrupts the electrophysiological homogeneity of ventricular repolarization, predisposing to arrhythmia. Our findings highlight a proximal brain basis for stress-induced cardiac arrhythmic vulnerability.
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