Premium
Effects of Device‐Guided Slow Breathing on Hemodynamics in Pre‐Hypertensive Post‐Traumatic Stress Disorder Patients
Author(s) -
Kang Joohee,
Fonkoue Ida T.,
Kankam Melanie,
DaCosta Dana,
Park Jeanie
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2018.32.1_supplement.737.3
Subject(s) - medicine , prehypertension , blood pressure , heart rate , cardiology , heart rate variability , autonomic nervous system , baroreflex , respiratory rate , hemodynamics , anesthesia , breathing , mean arterial pressure , respiratory system
Post‐traumatic stress disorder (PTSD) is associated with an increased risk for developing hypertension and cardiovascular (CV) disease, but the mechanisms underlying this risk remain unknown. Patients with PTSD have higher resting heart rate and blood pressure (BP) and decreased heart rate variability (HRV), suggesting a state of increased sympathetic nervous system (SNS) and decreased parasympathetic nervous system (PNS) activity. Prior studies have shown that device‐guided slow breathing (DGB) may lower BP and SNS activity in hypertensive patients; however, the potential beneficial effects of DGB on PNS have not previously been explored in PTSD or prehypertension. We hypothesized that DGB will lower BP and improve autonomic function in PTSD patients. We recruited 21 prehypertensive veterans with PTSD and 13 prehypertensive veterans without PTSD (controls). The PTSD group was randomly assigned to the DGB (PTSD+DGB, N=13) during which respiratory rates were monitored and lowered using a biofeedback device to sub‐physiologic levels (~5 breaths/min) versus an identical sham device (PTSD+SHAM, N=8) in which respiratory rates were held at a normal rate of 14 breaths/min. All control participants without PTSD were assigned to the DGB device (CON+DGB, N=13). Continuous EKG and beat‐to‐beat arterial blood pressure was monitored for 10 minutes at rest, followed by 10 minutes of breathing with either DGB or sham. All study participants had prehypertension (mean BP, 125±2/80±2 mmHg). From baseline to the end of 10 minutes of DGB, the PTSD+DGB group had a significant reduction in systolic blood pressure (SBP, −11±3 mmHg, p =0.001), diastolic blood pressure (DBP, −6.5±2 mmHg, p =0.003), and mean arterial pressure (MAP, −8±2 mmHg, p =0.001). In the CON+DGB group, we observed a significant reduction in SBP (−7±3 mmHg, p =0.029) in controls during DGB, and a trend towards reduced DBP and MAP. In the PTSD+sham group, there was no significant reduction in SBP, DBP, and MAP with the sham device in PTSD patients. There was no significant change in HR ( p =0.093), RMSSD ( p =0.143), and pNN50 ( p =0.203) with DGB or sham in either group. DGB acutely lowers blood pressure in prehypertensive PTSD patients and controls, but does not improve heart rate variability measures of PNS in either group. Long‐term studies are needed to determine if DGB could represent a novel therapeutic intervention to improve hemodynamics and autonomic physiology in PTSD patients. Support or Funding Information This work was supported by National Institutes of Health Grant K23 HL‐098744 and R01 HL135183; Satellite Health Care, a not‐for‐profit renal care provider; the Department of Veterans Affairs, Veterans Health Administration, Office of Research and Development, Clinical Studies Center, Decatur, Georgia; the Atlanta Research and Education Foundation; and Public Health Service Grant UL1 RR‐025008 from the Clinical and Translational Science Award program, National Institutes of Health, National Center for Research Resources. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .