Symptom severity impacts sympathetic dysregulation and inflammation in post-traumatic stress disorder (PTSD) |
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| Institution: | 1. Renal Division, Department of Medicine, Emory University School of Medicine, Atlanta, GA, USA;2. Research Service Line, Atlanta Veterans Affairs Health Care System (VAHCS), Decatur, GA, USA;3. Department of Pharmacology and Physiology, Institute for Neuroscience, George Washington University, Washington, DC, USA;4. Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, GA, USA;5. Department of Biostatistics and Bioinformatics, Rollins School of Public Health, Emory University, Atlanta, GA, USA;6. Department of Radiology, Emory University School of Medicine, Atlanta, GA, USA;7. Biomarker Core Laboratory, Atlanta VAHCS, Decatur, GA, USA;1. San Francisco Veterans Affairs Medical Center and Mental Illness Research, Education and Clinical Center, San Francisco, CA, USA;2. Department of Internal Medicine, St. Mary’s Medical Center, San Francisco, CA, USA;3. Department of Neurology, Stanford University, Palo Alto, CA, USA;4. Department of Psychiatry, University of California, San Francisco, CA, USA;5. Department of Internal Medicine, University of California, San Francisco, CA, USA;1. Icahn School of Medicine at Mount Sinai, New York, NY, USA;2. Department of Medicine, University of California, San Francisco, CA, USA;3. Department of Psychiatry, University of California, San Francisco, CA, USA;4. Veterans Affairs Medical Center, San Francisco, CA, USA;1. University of California, San Francisco, CA, USA;2. San Francisco Veteran’s Affairs Medical Center and Northern California Institute for Research and Education, San Francisco, CA, USA;3. Columbia University Medical Center, NY, USA;1. Center for Behavioral Cardiovascular Health, Department of Medicine, Columbia University Medical Center, New York City, NY, USA;2. Department of Psychosomatic Medicine, Clinic Barmelweid, Barmelweid, Switzerland;1. Center for Behavioral Cardiovascular Health, Columbia University Medical Center, New York, New York;2. Department of Biostatistics, Columbia University Mailman School of Public Health, New York, New York;3. Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts;4. Department of Social and Behavioral Sciences, Harvard T.H. Chan School of Public Health, Boston, Massachusetts;5. Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, Massachusetts;6. Channing Division of Network Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts;7. Psychiatric and Neurodevelopmental Genetics Unit and Department of Psychiatry, Massachusetts General Hospital, Boston, Massachusetts;8. Department of Epidemiology and Biostatistics, University of California San Francisco School of Medicine, San Francisco, California;1. John Hopkins University, School of Nursing, 525 N. Wolfe Street, Baltimore, MD, 21205, USA;2. National Institutes of Health, National Institute of Nursing Research, 9000 Rockville Pike, Bethesda, MD, 20892, USA;3. Henry M. Jackson Foundation, 6720A Rockledge Drive, Bethesda, MD, 20817, USA;4. Center for Neuroscience and Regenerative Medicine, 12725 Twinbrook Parkway, Rockville, MD, 20852, USA;5. Uniformed Services University of the Health Sciences, Department of Medicine, 4301 Jones Bridge Road, Bethesda, MD, 20814, USA |
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| Abstract: | Post-traumatic stress disorder (PTSD) is associated with a greater risk of incident hypertension and cardiovascular disease. Inflammation, impaired baroreflex sensitivity (BRS) decreased parasympathetic nervous system (PNS) and overactive sympathetic nervous system (SNS) activity are suggested as contributing mechanisms. Increasing severity of PTSD symptoms has been linked to greater cardiovascular risk; however, the impact of PTSD symptom severity on inflammation and autonomic control of blood pressure has not yet been explored. We hypothesized that increasing PTSD symptom severity is linked to higher inflammation, greater SNS activity, lower PNS reactivity and impaired BRS. Seventy Veterans participated in this study: 28 with severe PTSD ((Clinical Administered PTSD Scale (CAPS) > 60; S-PTSD), 16 with moderate PTSD (CAPS ≥ 45 ≤ 60; M-PTSD) and 26 Controls (CAPS < 45; NO-PTSD). We recorded continuous blood pressure (BP), heart rate (HR) via EKG, heart rate variability (HRV) markers reflecting PNS and muscle sympathetic nerve activity (MSNA) at rest, during arterial baroreflex sensitivity (BRS) testing via the modified Oxford technique, and during 3 min of mental stress via mental arithmetic. Blood samples were analyzed for 12 biomarkers of systemic and vascular inflammation. While BP was comparable between severity groups, HR tended to be higher (p = 0.055) in S-PTSD (76 ± 2 beats/min) than in Controls (67 ± 2 beats/min) but comparable to M-PTSD (70 ± 3 beats/min). There were no differences in resting HRV and MSNA between groups; however, cardiovagal BRS was blunted (p = 0.021) in S-PTSD (10 ± 1 ms/mmHg) compared to controls (16 ± 3 ms/mmHg) but comparable to M-PTSD (12 ± 2 ms/mmHg). Veterans in the S-PTSD group had a higher (p < 0.001) combined inflammatory score compared to both M-PTSD and NO-PTSD. Likewise, while mental stress induced similar SNS and cardiovascular responses between the groups, there was a greater reduction in HRV in S-PTSD compared to both M-PTSD and NO-PTSD. In summary, individuals with severe PTSD symptoms have higher inflammation, greater impairment of BRS, a trend towards higher resting HR and exaggerated PNS withdrawal at the onset of mental stress that may contribute to cardiovascular risk in severe PTSD. |
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| Keywords: | PTSD severity Autonomic activity Baroreflex sensitivity Inflammation Blood pressure |
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