Symptom Severity Impacts Inflammation and Sympathetic Over‐activity in Post‐Traumatic Stress Disorder (PTSD)

Abstract

Patients with post‐traumatic stress disorder (PTSD) are at significantly higher risk of developing hypertension and cardiovascular disease. Low‐grade inflammation and overactive sympathetic nervous system (SNS) activity are suggested as contributing mechanisms. Our prior studies showed that while SNS reactivity during stress is heightened in PTSD, resting MSNA and inflammation was not elevated in young combat Veterans with PTSD as a group; however, prior results did not take into account the potential influence of PTSD symptom severity on neural cardiovascular function. The aim of the current study was to determine if PTSD patients with greater PTSD symptoms measured via the gold‐standard clinician administered PTSD scale (CAPS) have higher SNS activity and inflammation compared to PTSD patients with less severe symptoms. To answer this question, we recruited 21 veterans clinically diagnosed with PTSD (mean CAPS score, 68±4). We measured muscle sympathetic nerve activity (MSNA) via microneurography and blood pressure using standard technique. We collected blood samples to measure serum levels of two inflammatory biomarkers: highly sensitive C‐reactive protein (hsCRP) and interleukin‐6 (IL‐6). For data analysis, the participants were grouped based on the median CAPS score of 70, with the low CAPS group (L‐CAPS) having a score ≤ 70 and the high CAPS group (H‐CAPS) having a score > 70. The two groups (L‐CAPS, n=11; H‐CAPS, n=10) were matched for age, body mass index (BMI) and selective serotonin reuptake inhibitor (SSRI) prescription. Resting blood pressure and heart rate were similar between the two groups. However, the H‐CAPS group had a significantly greater MSNA at baseline when quantified as both burst frequency (26±5 vs 13±2 bursts/min, p= 0.011) and burst incidence (35±6 vs 21±3 bursts/100hb, p= 0.022) compared to the L‐CAPS group. Similarly, hsCRP (2.02±0.71 vs 0.74±0.18, p= 0.036) and IL‐6 (5.44±1.86 vs 2.35±0.73, p= 0.055) levels were higher in the H‐CAPS group compared to the L‐CAPS group. Furthermore, the levels of hsCRP (r= 0.766, p< 0.001) and IL‐6 (r= 0.594, p=0.007) were positively correlated with MSNA. When the groups were analyzed separately, the correlation between MSNA and hsCRP was stronger in the H‐CAPS group (r=0.822, p=0.012) than the L‐CAPS group (r=0.604, p=0.065). These results suggest that the severity of PTSD is associated with chronically increased MSNA and inflammation, and SNS overactivity may be mechanistically linked to inflammation in severe PTSD.Support or Funding InformationSupported by NIH HL‐098744, NIH DK‐00756, VA Merit I01CX001065, AHA 15CSA24340001This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.