Alvarenga Marlies E, Richards Jeffrey C, Lambert Gavin, Esler Murray D
Faculty of Medicine, Monash University & Cardiovascular Neurosciences Division, Baker Heart Research Institute, Baker Heart Research Institute, Prahran, Victoria, Australia.
Psychosom Med. 2006 Jan-Feb;68(1):8-16. doi: 10.1097/01.psy.0000195872.00987.db.
The risk of adverse clinical cardiac events is increased in patients with panic disorder (PD). We evaluated possible mechanistic links between PD and heart disease. We estimated cardiac vagal activity from heart rate variability (HRV) measurements and quantified sympathetic nervous system (SNS) activity using plasma noradrenaline tracer kinetics methodology.
Thirty-nine people with PD and 39 age- and gender-matched healthy volunteers were studied. In 19 participants with PD, both HRV and plasma noradrenaline kinetics were tested; in 20 with PD and 20 healthy volunteers, HRV measurements only were made, whereas in 19 healthy volunteers, noradrenaline kinetics only was tested. All panic disorder participants completed psychological measures of anxiety sensitivity and state and trait anxiety; healthy volunteers in whom HRV was measured also provided psychological measures.
Sympathetic nervous tone in the heart, based on rates of cardiac noradrenaline spillover, was normal in PD. Noradrenaline and adrenaline plasma clearance and plasma tritiated noradrenaline and adrenaline extraction in transit through the heart, all dependent on the noradrenaline transporter (NET), were reduced in PD. Psychometric testing linked inhibition of anger to this deficit in NET functioning. Anxiety sensitivity was specifically associated with impaired cardiac NET. High- and low-frequency heart rate spectral power was unrelated to all plasma noradrenaline kinetics measurements.
Defective neuronal reuptake of noradrenaline, by augmenting the sympathetic neural signal in the heart, might have a dual effect, sensitizing the heart such as to lead to symptom development (and thus perhaps causing panic disorder) and, second, potentially contributing to adverse cardiac events in established PD.
惊恐障碍（PD）患者发生临床不良心脏事件的风险增加。我们评估了PD与心脏病之间可能的机制联系。我们通过心率变异性（HRV）测量来估计心脏迷走神经活动，并使用血浆去甲肾上腺素示踪动力学方法对交感神经系统（SNS）活动进行量化。
对39名PD患者和39名年龄及性别匹配的健康志愿者进行了研究。在19名PD患者中，同时测试了HRV和血浆去甲肾上腺素动力学；在20名PD患者和20名健康志愿者中，仅进行了HRV测量，而在19名健康志愿者中，仅测试了去甲肾上腺素动力学。所有惊恐障碍参与者均完成了焦虑敏感性以及状态和特质焦虑的心理测量；测量了HRV的健康志愿者也提供了心理测量数据。
基于心脏去甲肾上腺素溢出率，PD患者心脏的交感神经张力正常。去甲肾上腺素和肾上腺素的血浆清除率以及经心脏转运过程中的血浆氚标记去甲肾上腺素和肾上腺素提取率，均依赖于去甲肾上腺素转运体（NET），在PD患者中均降低。心理测量测试表明，愤怒抑制与NET功能的这种缺陷有关。焦虑敏感性与心脏NET受损特别相关。高频和低频心率频谱功率与所有血浆去甲肾上腺素动力学测量均无关。
去甲肾上腺素的神经元再摄取缺陷通过增强心脏交感神经信号可能具有双重作用，使心脏敏感化从而导致症状发展（进而可能导致惊恐障碍），其次，可能在已确诊的PD中促成不良心脏事件。
