Sharon Y Lee1, Crystal L Park2, Burak T Cilhoroz3, Linda S Pescatello4. 1. Brown University, Warren Alpert Medical School, Department of Psychiatry and Human Behavior, USA. Electronic address: Sharon_Y_Lee@brown.edu. 2. University of Connecticut, Department of Psychological Sciences, USA. Electronic address: Crystal.Park@uconn.edu. 3. Syracuse University, Department of Exercise Sciences, USA. 4. University of Connecticut, Department of Kinesiology, USA. Electronic address: Linda.Pescatello@uconn.edu.
Abstract
OBJECTIVE: Posttraumatic stress disorder (PTSD) symptoms are associated with high blood pressure (BP) and decreased heart rate variability (HRV) at rest and in response to acute stress. Unique contributions of PTSD symptom clusters to cardiovascular responses to stress are rarely investigated. This study tested whether PTSD-related arousal/reactivity drives relationships of higher PTSD symptoms with higher BP and lower HRV during rest, reactivity (stressor-induced change from baseline), and recovery. METHODS: Using a cross-sectional observational design, we enrolled 84 trauma-exposed community adults (83% female; 68% White; Mage = 35) who endorsed at least one core PTSD symptom. Participants completed a physical exam, self-reports of trauma history and PTSD symptoms, and BP and HRV frequency domain measurements during rest, stressor (mental arithmetic task), and recovery. RESULTS: Arousal/reactivity was not associated with BP or HRV reactivity but associated with a higher low (LF) to high (HF) frequency (HF) ratio (LF/HF) during recovery reflecting sympathetic predominance. During the stressor, more avoidance and intrusion were associated with increased diastolic blood pressure (DBP) from baseline; more avoidance was associated with parasympathetic predominance (lower LF/HF); and more negative cognitions/mood was associated with decreased systolic blood pressure (SBP), DBP, and LF from baseline. During recovery, more intrusion and negative cognitions/mood were associated with increased SBP from baseline; less negative cognitions/mood was associated with sympathetic predominance (higher LF/HF). CONCLUSIONS: PTSD symptom clusters demonstrated differential relationships with SBP, DBP, and HRV during reactivity and recovery. Findings may inform targeted PTSD symptom reduction interventions for disrupting links between PTSD and CVD risk.
OBJECTIVE: Posttraumatic stress disorder (PTSD) symptoms are associated with high blood pressure (BP) and decreased heart rate variability (HRV) at rest and in response to acute stress. Unique contributions of PTSD symptom clusters to cardiovascular responses to stress are rarely investigated. This study tested whether PTSD-related arousal/reactivity drives relationships of higher PTSD symptoms with higher BP and lower HRV during rest, reactivity (stressor-induced change from baseline), and recovery. METHODS: Using a cross-sectional observational design, we enrolled 84 trauma-exposed community adults (83% female; 68% White; Mage = 35) who endorsed at least one core PTSD symptom. Participants completed a physical exam, self-reports of trauma history and PTSD symptoms, and BP and HRV frequency domain measurements during rest, stressor (mental arithmetic task), and recovery. RESULTS: Arousal/reactivity was not associated with BP or HRV reactivity but associated with a higher low (LF) to high (HF) frequency (HF) ratio (LF/HF) during recovery reflecting sympathetic predominance. During the stressor, more avoidance and intrusion were associated with increased diastolic blood pressure (DBP) from baseline; more avoidance was associated with parasympathetic predominance (lower LF/HF); and more negative cognitions/mood was associated with decreased systolic blood pressure (SBP), DBP, and LF from baseline. During recovery, more intrusion and negative cognitions/mood were associated with increased SBP from baseline; less negative cognitions/mood was associated with sympathetic predominance (higher LF/HF). CONCLUSIONS: PTSD symptom clusters demonstrated differential relationships with SBP, DBP, and HRV during reactivity and recovery. Findings may inform targeted PTSD symptom reduction interventions for disrupting links between PTSD and CVD risk.
Authors: Paul A Dennis; Nathan A Kimbrel; Andrew Sherwood; Patrick S Calhoun; Lana L Watkins; Michelle F Dennis; Jean C Beckham Journal: Psychosom Med Date: 2017-06 Impact factor: 4.312