Symptom severity impacts sympathetic dysregulation and inflammation in post-traumatic stress disorder (PTSD)

Ida T. Fonkoue; Paul J. Marvar; Seth Norrholm; Yunxiao Li; Melanie L. Kankam; Toure N. Jones; Monica Vemulapalli; Barbara Rothbaum; J. Douglas Bremner; Ngoc Anh Le; Jeanie Park

doi:10.1016/j.bbi.2019.10.021

Symptom severity impacts sympathetic dysregulation and inflammation in post-traumatic stress disorder (PTSD)

Ida T. Fonkoue, Paul J. Marvar, Seth Norrholm, Yunxiao Li, Melanie L. Kankam, Toure N. Jones, Monica Vemulapalli, Barbara Rothbaum, J. Douglas Bremner, Ngoc Anh Le, Jeanie Park

Research output: Contribution to journal › Article › peer-review

64 Scopus citations

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.

Original language	English (US)
Pages (from-to)	260-269
Number of pages	10
Journal	Brain, Behavior, and Immunity
Volume	83
DOIs	https://doi.org/10.1016/j.bbi.2019.10.021
State	Published - Jan 2020
Externally published	Yes

Bibliographical note

Funding Information:
This work was supported by Merit Review Award number I01CX001065 from the United States Department of Veterans Affairs (VA) Clinical Sciences Research and Development Program; American Heart Association National Affiliate , Collaborative Sciences Award 15CSA24340001 ; National Institutes of Health (NIH) R01 HL135183; NIH training grant T32 DK-00756 ; Department of Veterans Affairs, Veterans Health Administration, Office of Research and Development and the Clinical Studies Center of the Atlanta VA Health Care System, Decatur, Georgia; and Foundation for Atlanta Veterans Education and Research (FAVER).

Publisher Copyright:
© 2019

Keywords

Autonomic activity
Baroreflex sensitivity
Blood pressure
Inflammation
PTSD severity

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.bbi.2019.10.021

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@article{1e601ccb8651471da9074cc23aba43a9,

title = "Symptom severity impacts sympathetic dysregulation and inflammation in post-traumatic stress disorder (PTSD)",

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.",

keywords = "Autonomic activity, Baroreflex sensitivity, Blood pressure, Inflammation, PTSD severity",

author = "Fonkoue, {Ida T.} and Marvar, {Paul J.} and Seth Norrholm and Yunxiao Li and Kankam, {Melanie L.} and Jones, {Toure N.} and Monica Vemulapalli and Barbara Rothbaum and {Douglas Bremner}, J. and Le, {Ngoc Anh} and Jeanie Park",

note = "Funding Information: This work was supported by Merit Review Award number I01CX001065 from the United States Department of Veterans Affairs (VA) Clinical Sciences Research and Development Program; American Heart Association National Affiliate , Collaborative Sciences Award 15CSA24340001 ; National Institutes of Health (NIH) R01 HL135183; NIH training grant T32 DK-00756 ; Department of Veterans Affairs, Veterans Health Administration, Office of Research and Development and the Clinical Studies Center of the Atlanta VA Health Care System, Decatur, Georgia; and Foundation for Atlanta Veterans Education and Research (FAVER). Publisher Copyright: {\textcopyright} 2019",

year = "2020",

month = jan,

doi = "10.1016/j.bbi.2019.10.021",

language = "English (US)",

volume = "83",

pages = "260--269",

journal = "Brain, Behavior, and Immunity",

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T1 - Symptom severity impacts sympathetic dysregulation and inflammation in post-traumatic stress disorder (PTSD)

AU - Fonkoue, Ida T.

AU - Marvar, Paul J.

AU - Norrholm, Seth

AU - Li, Yunxiao

AU - Kankam, Melanie L.

AU - Jones, Toure N.

AU - Vemulapalli, Monica

AU - Rothbaum, Barbara

AU - Douglas Bremner, J.

AU - Le, Ngoc Anh

AU - Park, Jeanie

N1 - Funding Information: This work was supported by Merit Review Award number I01CX001065 from the United States Department of Veterans Affairs (VA) Clinical Sciences Research and Development Program; American Heart Association National Affiliate , Collaborative Sciences Award 15CSA24340001 ; National Institutes of Health (NIH) R01 HL135183; NIH training grant T32 DK-00756 ; Department of Veterans Affairs, Veterans Health Administration, Office of Research and Development and the Clinical Studies Center of the Atlanta VA Health Care System, Decatur, Georgia; and Foundation for Atlanta Veterans Education and Research (FAVER). Publisher Copyright: © 2019

PY - 2020/1

Y1 - 2020/1

N2 - 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.

AB - 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.

KW - Autonomic activity

KW - Baroreflex sensitivity

KW - Blood pressure

KW - Inflammation

KW - PTSD severity

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ER -

Symptom severity impacts sympathetic dysregulation and inflammation in post-traumatic stress disorder (PTSD)

Abstract

Bibliographical note

Keywords

UN SDGs

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