Prehypertension Augments Autonomic Imbalance in Post‐traumatic Stress Disorder (PTSD)
Authors: Fonkoue Ida T. , Kang JooHee , Marvar Paul , Park Jeanie 
Published: June 2021

Post‐traumatic stress disorder (PTSD), a major health risk for civilians and veterans, is commonly associated with prehypertension, and is characterized by a significantly increased risk of developing hypertension and cardiovascular disease. The physiological mechanisms of PTSD‐induced hypertension remain unclear, but previous data suggest an autonomic dysregulation (high sympathetic activity and blunted parasympathetic control) in patients with PTSD. However, it is not clear whether this autonomic imbalance is driven by resting blood pressure, and whether prehypertension augments autonomic dysregulation in PTSD. We hypothesized that the comorbidity of prehypertension with PTSD will increase resting sympathetic activity, reduce resting parasympathetic activity and increase sympathetic and blood pressure (BP) reactivity to mental stress. Twenty‐one (13 prehypertensive and 8 normotensive) veterans with PTSD, matched for age, race and body mass index (BMI), volunteered for this study. We recorded continuous electrocardiogram (EKG), BP and heart rate (HR) during five minutes of supine rest and three minutes of mental arithmetic. Muscle sympathetic nerve activity (MSNA) using microneurography was obtained to assess direct, real‐time measures of sympathetic activity. The time and frequency domain methods were used to calculate the following heart rate variability (HRV) indices: standard deviation of normal to normal R‐R intervals (SDNN), root mean square of the successive differences (RMSSD) and high frequency power (HF). Baseline systolic BP (127±3 vs. 112±3 mmHg, p=0.007) and diastolic BP (83±2 vs. 71±2 mmHg, p=0.001) were significantly higher in prehypertensive PTSD compared to normotensive PTSD, but HR (76±3 vs. 69±6 beats/min, p=0.277) was not different between the two groups. While resting MSNA (22±2 vs. 25±6 bursts/min, p=0.579) was comparable between the two groups, HRV was significantly lower in prehypertensive PTSD compared to normotensive PTSD (68±9 vs 103±17 ms, p=0.031; 47±8 vs 85±26 ms, p=0.047; 491±153 vs 1873±844 ms2/HZ, p=0.017) for SDNN, RMSSD and HF respectively. During mental arithmetic, minute by minute increases in systolic BP (time*status, p=0.01) and diastolic BP (time*status, p=0.04) were significantly higher in prehypertensive PTSD. The difference remained significant when adjusted for baseline BP. HR reactivity did not differ between hypertensive and normotensive PTSD (time*status, p>0.05). Likewise, MSNA reactivity was not statistically different between the two groups. However, when adjusted for baseline BP, minute by minute changes in MSNA were significantly higher (time*status*bp, p=0.03) in prehypertensive PTSD. In conclusion, our findings reveal an attenuated parasympathetic control in patients with comorbid prehypertension and PTSD coupled with an exaggerated neurohemodynamic response to stress. These early changes might be contributing to the higher risk of cardiovascular diseases in this population.

Support or Funding Information

Supported by NIH HL‐098744, NIH DK‐00756, VA Merit I01CX001065, AHA 15CSA24340001

This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.