Hopper James W, Spinazzola Joseph, Simpson William B, van der Kolk Bessel A
Department of Psychiatry, Boston University School of Medicine, Boston, MA, United States.
J Psychosom Res. 2006 Jan;60(1):83-90. doi: 10.1016/j.jpsychores.2005.06.002.
Evidence of elevated basal heart rate (HR) in posttraumatic stress disorder (PTSD) has been interpreted in terms of elevated sympathetic cardiac activity, as have possible increased cardiovascular disease risks and outcomes associated with elevated HR. Yet it is well-established that the parasympathetic branch of the autonomic nervous system not only influences HR independently of the sympathetic branch, but makes a greater contribution to HR, including resting HR. Additionally, abnormally low tonic parasympathetic activity on the heart has been implicated in cardiovascular disease and hypertension. This study addressed a potential parasympathetic contribution to elevated basal HR in PTSD.
We used a descriptive and subgroup differences approach to investigate relationships between parasympathetic activity and basal HR in 59 adults (50 females) with PTSD, all of whom were participants in a treatment outcome study and assessed prior to exposure to trauma-related script-driven imagery. Consistent with the well-known relationship between parasympathetic activity and HR, we hypothesized that basal respiratory sinus arrhythmia (RSA), a measure of parasympathetic cardiac activity, would be negatively correlated with basal HR. More important, we predicted that pathologically elevated HRs previously associated with PTSD would only characterize a low-RSA subgroup. Potential confounds of age, respiration rate, and aerobic fitness were addressed.
As predicted, mean HR was 80.5 bpm in the low-RSA tercile group, similar to mean HRs of PTSD groups in prior research and significantly higher than 69 and 65 bpm in the middle- and high-RSA groups, respectively, which are typical of non-PTSD controls.
These findings suggest that a substantial proportion of those with PTSD may not have elevated basal HRs. Furthermore, among those who do exhibit elevated HR, there may be a parasympathetic contribution that is independent of any sympathetic one. Only measuring both branches at once, ideally with autonomic blockades, can definitively address these issues.
创伤后应激障碍(PTSD)患者基础心率(HR)升高的证据被解释为交感神经对心脏的活动增强,HR升高可能还会增加心血管疾病风险及相关后果。然而,众所周知,自主神经系统的副交感神经分支不仅独立于交感神经分支影响心率,而且对心率的影响更大,包括静息心率。此外,心脏副交感神经张力异常降低与心血管疾病和高血压有关。本研究探讨了副交感神经对PTSD患者基础HR升高的潜在作用。
我们采用描述性和亚组差异方法,调查了59名患有PTSD的成年人(50名女性)副交感神经活动与基础HR之间的关系,所有这些人都是一项治疗结果研究的参与者,并在接触与创伤相关的脚本驱动意象之前进行了评估。鉴于副交感神经活动与HR之间的已知关系,我们假设基础呼吸性窦性心律不齐(RSA),一种副交感神经对心脏活动的测量指标,将与基础HR呈负相关。更重要的是,我们预测先前与PTSD相关的病理性HR升高仅表现在低RSA亚组中。研究还考虑了年龄、呼吸频率和有氧适能等潜在混杂因素。
正如预测的那样,低RSA三分位数组的平均HR为80.5次/分钟,与先前研究中PTSD组的平均HR相似,并且显著高于中RSA组和高RSA组的69次/分钟和65次/分钟,后两者为非PTSD对照组的典型数值。
这些发现表明,相当一部分PTSD患者可能没有基础HR升高。此外,在那些确实表现出HR升高的患者中,可能存在独立于任何交感神经作用的副交感神经作用。只有同时测量两个分支,理想情况下使用自主神经阻滞,才能明确解决这些问题。