Antonia V Seligowski1, Julia B Merker2, Adam P Swiercz3, Jeanie Park4, Paul J Marvar5, Kerry J Ressler6, Tanja Jovanovic7. 1. Department of Psychiatry, Harvard Medical School, Boston, MA, USA; McLean Hospital, Belmont, MA, USA. Electronic address: aseligowski@mclean.harvard.edu. 2. McLean Hospital, Belmont, MA, USA. 3. Department of Pharmacology and Physiology, George Washington University, Washington, DC, USA. 4. Emory University School of Medicine Renal Division and the Atlanta Veterans Administration Hospital, Atlanta, GA, USA. 5. Department of Pharmacology and Physiology, George Washington University, Washington, DC, USA; Department of Psychiatry and Behavioral Sciences, George Washington University, Washington, DC, USA. 6. Department of Psychiatry, Harvard Medical School, Boston, MA, USA; McLean Hospital, Belmont, MA, USA. 7. Department of Psychiatry and Behavioral Neurosciences, Wayne State University School of Medicine, Detroit, MI, USA.
Abstract
BACKGROUND: Trauma and symptoms of posttraumatic stress disorder (PTSD) have repeatedly been linked to impaired cardiovascular functioning. Poor fear extinction is a well-established biomarker of PTSD that may provide insight into mechanisms underlying cardiovascular risk. The current study probed the cardiovascular response to extinction in a sample of trauma-exposed individuals. METHODS: Participants were 51 trauma-exposed women who underwent a fear conditioning paradigm. Heart rate (HR) during extinction was examined in response to a conditioned stimulus that was previously paired with an aversive unconditioned stimulus (CS+) and one that was never paired (CS-). Heart rate variability (HRV) was calculated at baseline and during the extinction session. RESULTS: Consistent with fear bradycardia, initial HR deceleration (.5-2s) after CS + onset occurred during early extinction and appeared to extinguish over time. Higher baseline HRV was significantly associated with greater fear bradycardia during early extinction. CONCLUSIONS: This is the first study to demonstrate a pattern of fear bradycardia in early extinction, which was associated with higher HRV levels and decreased over the course of the extinction phase. These results suggest that increased fear bradycardia may be indicative of greater vagal control (i.e., HRV), both of which are psychophysiological biomarkers that may influence cardiovascular and autonomic disease risk in trauma-exposed individuals.
BACKGROUND:Trauma and symptoms of posttraumatic stress disorder (PTSD) have repeatedly been linked to impaired cardiovascular functioning. Poor fear extinction is a well-established biomarker of PTSD that may provide insight into mechanisms underlying cardiovascular risk. The current study probed the cardiovascular response to extinction in a sample of trauma-exposed individuals. METHODS:Participants were 51 trauma-exposed women who underwent a fear conditioning paradigm. Heart rate (HR) during extinction was examined in response to a conditioned stimulus that was previously paired with an aversive unconditioned stimulus (CS+) and one that was never paired (CS-). Heart rate variability (HRV) was calculated at baseline and during the extinction session. RESULTS: Consistent with fear bradycardia, initial HR deceleration (.5-2s) after CS + onset occurred during early extinction and appeared to extinguish over time. Higher baseline HRV was significantly associated with greater fear bradycardia during early extinction. CONCLUSIONS: This is the first study to demonstrate a pattern of fear bradycardia in early extinction, which was associated with higher HRV levels and decreased over the course of the extinction phase. These results suggest that increased fear bradycardia may be indicative of greater vagal control (i.e., HRV), both of which are psychophysiological biomarkers that may influence cardiovascular and autonomic disease risk in trauma-exposed individuals.
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