Sympathetic activation in chronic anxiety: not just at the "height" of stress. Editorial Focus on "Relative burst amplitude of muscle sympathetic nerve activity is an indicator of altered sympathetic outflow in chronic anxiety".
Sympathetic activation in chronic anxiety: not just at the "height" of stress. Editorial Focus on "Relative burst amplitude of muscle sympathetic nerve activity is an indicator of altered sympathetic outflow in chronic anxiety".
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慢性焦虑中的交感神经激活：不仅仅是在压力“高度”时。
DOI：
10.1152/jn.00220.2018
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发表时间：
2018
影响因子：
2.5
通讯作者：
M. Wenner
中科院分区：
文献类型：
--
作者：
M. Wenner
慢性焦虑是美国常见的心理健康问题，每年影响约18%的成年人（Kessler等人，2005）。焦虑与心血管疾病的患病率较高相关，并可预测未来的高血压和致死性冠状动脉疾病（Jonas et al. 1997; Kawachi et al. 1994）。焦虑和心血管疾病之间的联系机制尚不清楚，但交感神经系统的改变被认为是一个关键特征。然而，目前尚不清楚慢性焦虑的成年人是否表现出交感神经流出的改变。这是一个重要的临床问题，因为已经充分认识到异常交感神经流出与心血管疾病有关，因为在诸如高血压和心力衰竭的疾病状态中已经证明了过度的交感神经反应性。然而，也有证据表明，交感神经反应性的改变发生在其他方面健康但未来有疾病风险的人群中（Fonkoue et al. 2016; Greaney et al. 2015）。了解高危人群未来疾病的预测机制对于预防心血管疾病非常重要。在本期《神经生理学杂志》中，Holwerda及其同事研究了患有慢性焦虑症的成年人的交感神经流出（Holwerda等人。2018）。他们假设，与健康对照组相比，急性压力会导致慢性焦虑患者的交感神经流出过度。精神科医生进行了结构化的诊断访谈，以确认患者组的慢性焦虑。多单位传出肌肉交感神经活动（MSNA）记录在休息和两个常用的实验室应激源，冷加压试验和心算。评估了24小时动态血压，并对男性和女性进行了测试。这项研究的主要新发现是，患有慢性焦虑症的成年人对生理和精神压力都有更大的交感神经反应。有趣的是，只有相对突发幅度（即，身高/体型）在慢性焦虑患者中增加，而不是爆发频率或发生率。这表明MSNA爆发振幅的选择性增强是该患者组中交感神经失调的独特标志物。慢性焦虑患者的这种特征性反应可能为未来的心血管疾病奠定基础。这项研究有几个重要和有趣的方面。首先，两组之间的交感神经活动基线是相似的，差异只出现在压力源的使用上。第二，这些差异在对压力源的预期中也很明显（下文对此进行了详细介绍）。第三，相对MSNA爆发振幅与从神经精神访谈中获得的焦虑措施相关。第四，慢性焦虑症的这些数据与我们已经知道的关于被诊断患有恐慌症（一种严重的焦虑症）的人的交感神经调节改变的情况“吻合”，并且可能对未来患心血管疾病的风险有影响。总的来说，这些数据是第一个证明慢性焦虑成年人异常交感神经流出。预期压力源的反应增强可能是重要的，并且显然是由于“前馈”机制，因为反应发生在扰动之前。刺激交感神经系统的压力是日常生活的一个组成部分。虽然我们不会经常将手浸入冰水中，或者在人们面前进行心算，但这些实验室扰动可能会模仿身体对身体和精神压力的自主反应。对于那些患有慢性焦虑症的人来说，我们很容易想象这种适应不良的急性预期反应每天都会发生，最终增加长期心血管风险。这种夸张的同情反应如何转化为更高的风险？交感神经流出的发作性激增可能转化为血压变异性增加，已知这会增加心血管风险（Mancia等人，2007）。然而，作者报告两组的血压变异性无差异，评估为24小时内收缩压的标准差。有趣的是，与对照组相比，焦虑症患者夜间收缩压下降减弱，这可能是导致其风险升高的另一个因素。爆发大小或幅度的变化具有生理和临床意义，因为爆发幅度的增加可能反映了不同招募的重要性。重印请求和其他通信地址：M。M.温纳，部门运动学和应用生理学，特拉华州大学，540南学院大道，星星健康科学综合楼201 N，纽瓦克，DE 19713（电子邮件：mwenner@udel.edu）。J Neurophysiol 120：7-8，2018.首次出版于2018年4月18日; doi：10.1152/jn.00220.2018。
Chronic anxiety is a common mental health problem in the US, affecting ~18% of adults per year (Kessler et al. 2005). Anxiety is associated with a greater prevalence of cardiovascular disease and is predictive of future hypertension and fatal coronary artery disease (Jonas et al. 1997; Kawachi et al. 1994). The mechanisms linking anxiety and cardiovascular disease are unclear, but alterations in the sympathetic nervous system have been hypothesized to be a key feature. However, it is not known whether adults with chronic anxiety display altered sympathetic outflow. This is an important clinical question since it is well appreciated that aberrant sympathetic outflow is linked to cardiovascular disease, as exaggerated sympathetic reactivity has been demonstrated in disease states such as hypertension and heart failure. However, there is also evidence that alterations in sympathetic reactivity occur in populations that are otherwise healthy but at risk for future disease (Fonkoue et al. 2016; Greaney et al. 2015). Understanding mechanisms predictive of future disease in at-risk populations is important for preventing cardiovascular disease. In this issue of the Journal of Neurophysiology, Holwerda and colleagues examine sympathetic outflow in adults with chronic anxiety (Holwerda et al. 2018). They hypothesized that acute stress would result in exaggerated sympathetic outflow in patients with chronic anxiety compared with a healthy control group. A psychiatrist performed structured diagnostic interviews to confirm chronic anxiety in the patient group. Multiunit efferent muscle sympathetic nerve activity (MSNA) was recorded at rest and in response to two commonly used laboratory stressors, the cold pressor test and mental arithmetic. Ambulatory 24-h blood pressures were assessed, and both men and women were tested. The main novel finding of the study was that adults with chronic anxiety had a greater sympathetic response to both physiological and mental stress. Interestingly, only relative burst amplitude (i.e., height/size) was increased in the chronic anxiety patients, not burst frequency or incidence. This suggests that selective augmentation of MSNA burst amplitude is a unique marker of sympathetic dysregulation in this patient group. This signature response in patients with chronic anxiety may set the stage for future cardiovascular disease. There are several important and interesting aspects to this study. First, baseline sympathetic activity was similar between the groups—differences emerged only with use of stressors. Second, these differences were also evident in anticipation of the stressors (more on this below). Third, relative MSNA burst amplitude was correlated to measures of anxiety obtained from the neuropsychiatric interview. And fourth, these data in chronic anxiety “fit” with what we already know about altered sympathetic regulation in those diagnosed with panic disorder, a severe form of anxiety, and likely have implications for future risk of cardiovascular disease. Collectively, these data are the first to demonstrate aberrant sympathetic outflow in adults with chronic anxiety. The heightened response in anticipation of the stressor may be important and is clearly due to a “feedforward” mechanism, since the response occurred before the perturbations. Stress that activates the sympathetic nervous system is a component of everyday life. While we do not routinely immerse our hands in ice water, or perform mental arithmetic in front of people, these laboratory perturbations may mimic the body’s autonomic response to physical and mental stress. In the case of those with chronic anxiety, we can easily envision this maladaptive acute anticipatory response occurring daily, ultimately increasing long-term cardiovascular risk. How would this exaggerated sympathetic response translate to heightened risk? Episodic surges in sympathetic outflow may translate to increased blood pressure variability, which is known to increase cardiovascular risk (Mancia et al. 2007). However, the authors reported no differences in blood pressure variability in the two groups, assessed as the standard deviation of the systolic blood pressure over 24 h. Interestingly, those with anxiety had attenuated nighttime systolic blood pressure dipping compared with the control subjects, which may be another factor contributing to their heightened risk profile. Changes in burst size or amplitude are both physiologically and clinically meaningful, as increases in burst amplitude may reflect the importance of different recruitment Address for reprint requests and other correspondence: M. M. Wenner, Dept. of Kinesiology and Applied Physiology, Univ. of Delaware, 540 South College Ave., STAR Health Sciences Complex Rm. 201N, Newark, DE 19713 (e-mail: mwenner@udel.edu). J Neurophysiol 120: 7–8, 2018. First published April 18, 2018; doi:10.1152/jn.00220.2018.
影响因子：
--
作者：
Kessler, RC;Berglund, P;Walters, EE
通讯作者：
Walters, EE
DOI：
10.1152/ajpheart.00378.2016
发表时间：
2016-08-01
影响因子：
4.8
作者：
Fonkoue, Ida T.;Wang, Min;Carter, Jason R.
通讯作者：
Carter, Jason R.