Diminished vagal activity and blunted diurnal variation of heart rate dynamics in posttraumatic stress disorder

Abstract

Affected autonomic heart regulation is implicated in the pathophysiology of cardiovascular diseases and is associated with posttraumatic stress disorder (PTSD). However, although sympathetic hyperactivation has been repeatedly shown in PTSD, research has neglected parasympathetic function. The objective of this study is the long-term assessment of heart rate (HR) dynamics and its diurnal changes as an index of autonomic imbalance in PTSD. Since tonic parasympathetic activity underlies long-range correlation of heartbeat interval fluctuations in the healthy state, we included nonlinear (unifractal) analysis as an important and sensitive readout to assess functional alterations. We conducted electrocardiogram recordings over a 24-h period in 15 deployed male subjects with moderate to high levels of combat exposure (PTSD: n = 7; combat controls: n = 8) in the supine position. HR dynamics were assessed in two 5-h sub-epochs in the time and frequency domains, and by nonlinear analysis based on detrended fluctuation analysis. Psychiatric symptoms were assessed using structured interviews, including the Clinician Administered PTSD Scale. Subjects with PTSD showed significantly higher baseline HR, higher LF/HF ratio in the frequency domain, blunted differences between day and night-time measures, as well as a higher scaling coefficient αfast during the day, indicating diminished tonic parasympathetic activity. Diminished diurnal differences and blunted tonic parasympathetic activity altering HR dynamics suggest central neuroautonomic dysregulation that could represent a possible link to increased cardiovascular disease in PTSD.

Posttraumatic Stress, Heart Rate Variability, and the Mediating Role of Behavioral Health Risks

“…Consistent with previous work (4, 5, 23-27), PTSD symptoms were negatively related to a combination of short- and long-term measures of HRV. A novel finding was that nearly all of this relationship was explained by increased smoking, lifetime alcohol dependence, and sleep disturbance.…”

“…The majority of prior studies linking PTSD with HRV used short-term laboratory measures of HRV, which carry less prognostic power than long-term ECG data (48). Those few studies that have employed 24-hour ECG monitoring (4, 27, 50) have produced somewhat inconsistent results, likely due to small sample size (27) and restricted sampling (50). One recent investigation, a large-scale twin study of middle-aged combat veterans (4), did, however, demonstrate significantly lower 24-hour HRV in high- and low-frequency spectra amongst individuals with PTSD.…”

“…Thus, suppressed PNS activity and consequently reduced HRV are implied in individuals with anxiety or trauma-related disorders such as PTSD. Indeed, individuals with PTSD exhibit reduced HRV in both short-term laboratory-based measurements of HRV (5, 23-26) and 24-hour ambulatory measures (4, 27). In turn, individuals with PTSD are more likely than those without PTSD to develop cardiovascular disease (28) and face an increased risk of cardiac death (29).…”

Ecological assessment of heart rate complexity: Differences between high- and low-anxious adolescents

“…DFA calculates both short-term α1 (4 to 11 heart beats) and long-term α2 (N 11 beats) scaling exponents in heartbeat time series. Beyond the field of cardiovascular diseases, the need to distinguish between these two scaling exponents has proved useful in emotion regulation studies , anxiety disorders (Agorastos et al, 2013;Baumert et al, 2008), and aging studies (Beckers et al, 2005).…”

Concerns Over Divergent Approaches in the Diagnostics of Posttraumatic Stress Disorder

“…40,98 The most replicated biomarker so far is a hypothalamic-pituitary-adrenal axis finding of low plasma cortisol (especially at the nadir), and increased glucocorticoid receptor sensitivity, a finding opposite that of MDD, despite commonalities that include central nervous system hyperarousal, increased amygdalar reactivity, and diminished parasympathetic outflow. 27,39,[99][100][101] Further potential PTSD biomarkers may be found in imaging, psychological, endocrine, and molecular categories that will be classified into risk, disease, and therapy markers (eg, amygdala dysregulation, hippocampal integrity, fear prediction, 102 hypocorticolaemia, enhanced startle, impairment of cognitive functions, hippocampal integrity) that can create a long-lasting state of physiological reactivity that amplifies and exacerbates the effects of daily life (ie, allostatic load 103 ). These factors affect not only individual genes and biomolecules, but also entire biological networks, which in turn increase or decrease the risk of illness or affect illness severity.…”