Sympathetic and Cardiovascular Response to Device Guided Slow Breathing Acutely Depends on Post‐Traumatic Stress Disorder (PTSD) Severity

Abstract

Post‐traumatic stress disorder (PTSD) is associated with an increased risk for developing hypertension and cardiovascular disease. We previously showed that device guided slow breathing (DGB) using the RESPeRATE device acutely lowers muscle sympathetic nerve activity (MSNA) and improves baroreflex sensitivity and hemodynamics in patients with PTSD. However, it remains unclear whether the physiological responses to DGB depend on the severity of the disorder. We hypothesized that neural and cardiovascular response to acute DGB will be heightened in PTSD participants with a greater severity of PTSD symptoms. To test our hypothesis, we recruited 25 veterans (age 36 ± 2 years; BMI 29 ± 2 kg/m2) with PTSD. The clinician‐administered PTSD scale (CAPS) was used to confirm the diagnosis of PTSD (CAPS score ≥45) and the severity of PTSD symptoms. The CAPS scores in our sample ranged from 45 to 95 with a median score of 70 that was used to separate our study participants into two groups (group effect): Moderate (CAPS ≤70, n=13) and Severe (CAPS >70, n=12). Within each group, participants were randomized to either breathing with the DGB device (at a rate of 5–6 breaths/min) or breathing with an identical Sham device (at 12–14 breaths/min) (device effect) for 15 minutes. In the Moderate group, 5 participants used DGB and 8 used Sham; while in the Severe group, 6 used DGB and 6 used Sham. Beat‐to‐beat blood pressure (BP) via finger plethysmography, heart rate (HR) via EKG, heart rate variability (HRV) and muscle sympathetic nerve activity (MSNA) using microneurography were measured continuously at baseline and after 10 minutes of breathing (time effect). Age, BMI, resting BP and HR (all p>0.05) were similar between groups. In response to the breathing intervention, systolic BP (time*group*device, p=0.352) and diastolic BP (time*group*device, p=0.552) responses to DGB compared to Sham were comparable between the Moderate and Severe groups. However, as we hypothesized, HR decreased more with DGB (75 ± 4 to 62 ± 3 beats/min) than Sham (73 ± 6 to 75 ± 5 beats/min) in the Severe group when compared to the Moderate group (time*group*device, p=0.049). Likewise, MSNA decreased more (time*group*device, p=0.025) with DGB (38 ± 7 to 24 ± 4 bursts/min) compared to Sham (17 ± 2 to 14 ± 2 bursts/min) in the Severe group compared to the Moderate group. Unlike MSNA, HRV responses were not different between the groups. In summary, we found that DGB decreases HR and MSNA more in participants with a higher CAPS score, i.e. more severe PTSD. These results suggest that DGB may have greater beneficial effects on sympathetic overactivity and hemodynamics in PTSD patients with severe symptoms. Whether DGB leads to long‐term benefits on neural and cardiovascular function in severe PTSD should be studied in the future.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.