Markers and Mechanisms of Individual Differences in Cortico-Cardiac Covariation

对潜在威胁的认知处理几乎可以立即加速心脏活动。虽然已知皮质和心脏过程相互影响并发生协变（皮质-心脏协变），但我们不知道为什么某些个体的皮质-心脏协变比其他个体更强。皮质-心脏协变的个体差异与焦虑的个体差异有关，因此对于我们理解气质性焦虑和焦虑障碍特别重要。在这里，两项研究与健康的参与者提出，试图阐明标记物和机制的皮质-心脏协变。研究1的主要目的是测试先前报告的时滞单次试验EEG和心率的受试者内相关性是否为与焦虑相关的皮质-心脏协变提供了稳定有效的特征标记。N = 67参与者执行几个范式（赌博任务，时间估计任务和恐惧条件反射范式），唤起良好的特征签名在EEG，心率和EEG-心率协变和性格焦虑的措施进行了评估。6个月后进行相同的范例。利用收集的数据，将使用多特征多方法和交叉滞后面板方法评估皮质-心脏协变的复检可靠性、收敛性、结构和预测（即焦虑）有效性，如通过各种测量（EEG-心率协变、刺激诱发的心率反应、心率变异性）和各种范例评估的。研究2的主要目的是研究皮质-心脏协变的潜在机制，并通过实验测试皮质-心脏协变的个体差异是否有助于焦虑的个体差异，反之亦然。在这项研究中，N = 148参与者在休克威胁和控制条件下执行赌博任务。重要的是，我们打算通过双盲和安慰剂对照摄入艾司西酞普兰（10 mg）来改变皮质-心脏协变，艾司西酞普兰是一种可能通过调节5-羟色胺活性来影响皮质对心脏影响的物质。通过评估（A）（电击诱发的）皮质-心脏协变的改变是否介导了预期电击期间的焦虑的主观体验，或者（B）（电击威胁诱发的）焦虑的改变是否介导了皮质-心脏协变的改变，可以推断焦虑和皮质-心脏协变之间的因果关系。结合，研究1和2，从而告知，是否皮质-心脏协变与联合EEG-心率测量评估反映了一个稳定的特质和经历焦虑的风险因素。这两项研究将提供重要的见解，大脑与心脏沟通的一般机制，并进入皮质-心脏协变的个体差异的机制。

The mere cognitive processing of a potential threat may almost immediately accelerate cardiac activity. Although cortical and cardiac processes are known to affect each other and covary (cortico-cardiac covariation), we do not know why cortico-cardiac covariation is stronger in some individuals than in others. Individual differences in cortico-cardiac covariation relate to individual differences in anxiety and are thus particularly important for our understanding of dispositional anxiety and anxiety disorders. Here, two studies with healthy participants are proposed in an attempt to shed light on markers and mechanisms of cortico-cardiac covariation. The main goal of study 1 is to test whether previously reported within-subject correlations of time-lagged single-trial EEG and heart rate provide a stable and valid trait-marker for cortico-cardiac covariation with relevance for anxiety. N = 67 participants perform several paradigms (gambling task, time estimation task and fear conditioning paradigm) that evoke well-characterized signatures in EEG, heart rate and measures of EEG-heart rate covariation and dispositional anxiety is assessed. The same paradigms are performed 6 months later. With the collected data the re-test reliability, convergent, construct and predictive (i.e. anxiety) validity of cortico-cardiac covariation as assessed with various measures (EEG-heart rate covariation, stimulus-evoked heart rate responses, heart rate variability) and various paradigms will be assessed using multi-trait-multi-method and cross-lagged panel approaches. The main goal of study 2 is to investigate underlying mechanisms of cortico-cardiac covariation and to experimentally test whether individual differences in cortico-cardiac covariation contribute to individual differences in anxiety or vice versa. In that study, N = 148 participants perform a gambling task during threat-of-shock and control conditions. Importantly, we intend to pharmacologically alter cortico-cardiac covariation by double blind and placebo-controlled intake of escitalopram (10 mg), a substance that presumably affects cortical influences on the heart by modulating serotonin activity. By assessing whether (A) (pharmacologically induced) alterations of cortico-cardiac covariation mediate the subjective experience of anxiety during the anticipation of shocks or (B) whether (threat-of-shock induced) alterations of anxiety mediate changes in cortico-cardiac covariation, inferences about causal relationships between anxiety and cortico-cardiac covariation can be made. In combination, studies 1 and 2 thus inform, whether cortico-cardiac covariation as assessed with combined EEG-heart rate measurements reflects a stable trait and a risk factor for experiencing anxiety. Both studies will provide important insights into the general mechanisms by which the brain communicates with the heart and into the mechanisms of individual variation in cortico-cardiac covariation.