Gray Marcus A, Taggart Peter, Sutton Peter M, Groves David, Holdright Diana R, Bradbury David, Brull David, Critchley Hugo D
Functional Imaging Laboratory, Wellcome Department of Imaging Neuroscience, Institute of Neurology, University College London, 12 Queen Square, London WC1N 3BG, United Kingdom.
Proc Natl Acad Sci U S A. 2007 Apr 17;104(16):6818-23. doi: 10.1073/pnas.0609509104. Epub 2007 Apr 9.
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.
情绪创伤和心理压力可通过传出交感神经驱动的致心律失常作用引发心律失常和猝死。已有心脏病的患者风险尤其高。此外,大脑自主神经中枢内促心律失常活动模式的产生可能会因功能失调心肌的传入反馈而放大。一种反映传入心脏信息的皮层电位已被描述,它反映了个体在本体感受敏感性(对自身心跳的感知)方面的差异。为了增进我们对心律失常发生机制的理解,我们扩展了这种方法,识别出与应激期间心肌功能完整性的传入信息在皮层表达相对应的皮层电位。我们在已确诊心室功能障碍的患者中,同步测量了脑电图与心脏反应的变化。实验诱导的精神压力增强了所有患者交感神经活动的心血管指标(收缩压、心率、心室射血分数和皮肤电导)。然而,心肌的功能反应各不相同;一些患者在应激期间心输出量增加,而另一些患者则减少。在所有患者中,左颞叶和外侧额叶电极位置的心跳诱发电位幅度与应激诱导的心输出量变化相关,这与应激期间心肌功能的传入皮层表征一致。此外,左颞叶区域的心跳诱发电位幅度反映了心脏的促心律失常状态(左心室复极的不均一性)。这些观察结果描绘了一种心脏功能的皮层表征,可预测心脏复极中的促心律失常异常。我们的研究结果突出了心脏和大脑在应激诱导的心血管疾病中的动态相互作用。