Preliminary evidence of parasympathetic influence on basal heart rate in posttraumatic stress disorder.
OBJECTIVE
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.


METHODS
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.


RESULTS
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.


CONCLUSIONS
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.
Hopper
James W
JW
Department of Psychiatry, Boston University School of Medicine, Boston, MA, United States. jhopper@mclean.harvard.edu
Spinazzola
Joseph
J
Simpson
William B
WB
van der Kolk
Bessel A
BA
D000328:Adult; D001007:Anxiety / Q000453:epidemiology; D004562:Electrocardiography; D005260:Female; D006339:Heart Rate / Q000502:physiology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D010275:Parasympathetic Nervous System / Q000503:physiopathology*; D011594:Psychometrics / Q000706:statistics & numerical data; D012720:Severity of Illness Index; D018709:Statistics, Nonparametric; D013313:Stress Disorders, Post-Traumatic / Q000175:diagnosis / Q000453:epidemiology / Q000503:physiopathology*; D011795:Surveys and Questionnaires