Brief report

Power spectral analysis of heart rate variability in posttraumatic stress disorder patients

The enigma of post-traumatic stress disorder (PTSD) is embedded in a complex array of physiological responses to stressful situations that result in disruptions in arousal and cognitions that characterise the psychological disorder. Deciphering these physiological patterns is complex, which has seen the use of machine learning (ML) grow in popularity. However, it is unclear to what extent ML has been used with physiological data, specifically, the electroencephalogram (EEG) and electrocardiogram (ECG) to further understand the physiological responses associated with PTSD. To better understand the use of EEG and ECG biomarkers, with and without ML, a scoping review was undertaken. A total of 124 papers based on adult samples were identified comprising 19 ML studies involving EEG and ECG. A further 21 studies using EEG data, and 84 studies employing ECG meeting all other criteria but not employing ML were included for comparison. Identified studies indicate classical ML methodologies currently dominate EEG and ECG biomarkers research, with derived biomarkers holding clinically relevant diagnostic implications for PTSD. Discussion of the emerging trends, algorithms used and their success is provided, along with areas for future research.

Cardiovascular and psychiatric disorders are among the most commonly treated conditions worldwide. Research in neurocardiology, psychiatry, and epidemiology have defined bidirectional relationships between psychiatric disorders and heart disease, affirming the role of impaired autonomic nervous system, or dysautonomia in the prognosis and development in these disorders. These studies have fueled rapid clinical translation of experimental findings, with potential to complement existing pharmacological therapies. In this review, we comprehensively discuss the state-of-the-art investigations and novel treatment approaches for stress-related dysautonomias, emphasizing the effects of stress on the cardiac neuronal hierarchy. Increasing evidence suggests that autonomic modulation stands as an attractive therapeutic strategy in the treatment of dysautonomias that could complement existing therapies and possibly reduce the burden of drug-related side effects and treatment-resistant conditions. Further investigations regarding treatment optimization, selectivity, usability, and ethical concerns are required.

Cross-sectional studies have found that individuals with posttraumatic stress disorder (PTSD) exhibit deficits in autonomic functioning. While PTSD rates are twice as high in women compared to men, sex differences in autonomic functioning are relatively unknown among trauma-exposed populations. The current study used a prospective design to examine sex differences in posttraumatic autonomic functioning.

192 participants were recruited from emergency departments following trauma exposure (Mean age = 35.88, 68.2% female). Skin conductance was measured in the emergency department; fear conditioning was completed two weeks later and included measures of blood pressure (BP), heart rate (HR), and high frequency heart rate variability (HF-HRV). PTSD symptoms were assessed 8 weeks after trauma.

2-week systolic BP was significantly higher in men, while 2-week HR was significantly higher in women, and a sex by PTSD interaction suggested that women who developed PTSD demonstrated the highest HR levels. Two-week HF-HRV was significantly lower in women, and a sex by PTSD interaction suggested that women with PTSD demonstrated the lowest HF-HRV levels. Skin conductance response in the emergency department was associated with 2-week HR and HF-HRV only among women who developed PTSD.

Our results indicate that there are notable sex differences in autonomic functioning among trauma-exposed individuals. Differences in sympathetic biomarkers (BP and HR) may have implications for cardiovascular disease risk given that sympathetic arousal is a mechanism implicated in this risk among PTSD populations. Future research examining differential pathways between PTSD and cardiovascular risk among men versus women is warranted.

Heart rate variability (HRV), a measure of the variability in intervals between subsequent heart beats, is now widely considered an index of emotion regulatory capacity and the ability to adapt flexibly to changing environmental demands. Abnormalities in HRV are implicated in a host of psychopathologies, making it a potentially powerful transdiagnostic biobehavioral change mechanism in treatment interventions. While most mental illnesses are associated with low HRV, eating disorders have been linked to elevated HRV. We examined 62 research articles on HRV in psychopathology to test the hypothesis that there is an “ideal range” of HRV that predicts optimal functioning. Relationships between symptom severity and parameters that quantify HRV were examined graphically. More extreme time-domain HRV measures, both high and low, were associated with psychopathology, whereas healthy controls displayed mid-range values. Findings preliminarily support the hypothesis that there is an “ideal range” of HRV that could be targeted in biofeedback interventions.

Deficits in safety signal learning are well-established in fear-related disorders (e.g., PTSD, phobias). The current study used a fear conditioning paradigm to test associations among eye blink startle and event-related brain potential (ERP) latency measures of safety signal learning, as well as the role of cardiac vagal control (a measure of top-down inhibition necessary for safety learning).

Participants were 49 trauma-exposed women ages 17 to 28 years. Eyeblink startle response and ERP amplitudes/latencies were derived for conditioned stimuli associated (CS+) and not associated (CS-) with an aversive unconditioned stimulus. ERPs included the P100 and late positive potential (LPP), which index early visual processing and sustained emotional encoding, respectively. Cardiac vagal control was assessed with resting heart rate variability (HRV).

P100 and LPP latencies for the CS- (safety signal stimulus) were significantly negatively associated with startle to the CS-, but not the CS + . LPP CS- latencies were significantly negatively associated with PTSD Intrusion scores, and this relationship was moderated by vagal control, such that the effect was only present among those with low HRV.

ERP-based markers of safety signal learning were associated with startle response to the CS- (but not CS+) and PTSD symptoms, indicating that these markers may have relevance for fear-related disorders. Cardiac vagal control indexed by HRV is a moderating factor in these associations and may be relevant to safety signal learning.

Trauma and symptoms of posttraumatic stress disorder (PTSD) have repeatedly been linked to impaired cardiovascular functioning. Poor fear extinction is a well-established biomarker of PTSD that may provide insight into mechanisms underlying cardiovascular risk. The current study probed the cardiovascular response to extinction in a sample of trauma-exposed individuals.

Participants were 51 trauma-exposed women who underwent a fear conditioning paradigm. Heart rate (HR) during extinction was examined in response to a conditioned stimulus that was previously paired with an aversive unconditioned stimulus (CS+) and one that was never paired (CS-). Heart rate variability (HRV) was calculated at baseline and during the extinction session.

Consistent with fear bradycardia, initial HR deceleration (.5-2s) after CS + onset occurred during early extinction and appeared to extinguish over time. Higher baseline HRV was significantly associated with greater fear bradycardia during early extinction.

This is the first study to demonstrate a pattern of fear bradycardia in early extinction, which was associated with higher HRV levels and decreased over the course of the extinction phase. These results suggest that increased fear bradycardia may be indicative of greater vagal control (i.e., HRV), both of which are psychophysiological biomarkers that may influence cardiovascular and autonomic disease risk in trauma-exposed individuals.