Elevated Resting Blood Pressure Augments Autonomic Imbalance in Posttraumatic Stress Disorder (PTSD).

Posttraumatic stress disorder (PTSD) is characterized by increased sympathetic nervous system (SNS) activity, blunted parasympathetic nervous system (PNS) activity, and impaired baroreflex sensitivity (BRS) that contribute to accelerated cardiovascular disease (CVD). PTSD patients also have chronic stress-related elevations in resting blood pressure (BP), often in the prehypertensive range; yet, it is unclear if elevated resting blood pressure (ERBP) augments these autonomic derangements in PTSD. We hypothesized that compared to normotensive PTSD (N-PTSD), those with ERBP (E-PTSD) have further increased SNS, decreased PNS activity and impaired BRS at rest, and exaggerated SNS reactivity, PNS withdrawal, and pressor responses during stress. In 16 E-PTSD and 17 matched N-PTSD, we measured continuous BP, ECG, muscle sympathetic nerve activity (MSNA), and heart rate variability (HRV) markers reflecting cardiac PNS activity (standard deviation of R-R intervals (SDNN), root mean square of differences in successive R-R intervals (RMSSD), and high frequency power (HF)) during five minutes of rest and three minutes of mental arithmetic. Resting MSNA (p=0.943), sympathetic BRS (p=0.189) and cardiovagal BRS (p=0.332) were similar between groups. However, baseline SDNN (56±6 vs 78±8ms, p=0.019), RMSSD (39±6 vs 63±9 ms, p=0.018), and HF (378±103 vs 693±92 ms2 , p=0.015) were lower in E-PTSD vs. N-PTSD. During mental stress, the systolic blood pressure response (p=0.011) was augmented in E-PTSD. While MSNA reactivity was not different (p>0.05), the E-PTSD group had an exaggerated reduction in HRV during mental stress (p<0.05). PTSD with ERBP have attenuated resting cardiac PNS activity, coupled with exaggerated BP reactivity and PNS withdrawal during stress.