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Some individuals who are exposed to traumatic events experience both psychological and cardiovascular changes that affect their health and well-being. The purpose of this study is to learn more about how reducing the psychological symptoms (such as those that occur with posttraumatic stress disorder, or PTSD) affects cardiovascular systems that regulate heart and blood pressure.
There is a fundamental gap in the understanding of how a diagnosis of post-traumatic stress disorder (PTSD) portends excess risk of coronary heart disease (CHD). This is primarily because of two reasons: (1) the core studies which provide support for an association between PTSD and CHD risk depended on lengthy follow-up periods with no repeat measurement of either PTSD or other related cardiovascular risk factors; (2) PTSD is highly comorbid with both adverse health behaviors and with psychiatric comorbidity that also vary across time and could largely explain the association between PTSD and increased risk of CHD. The long-term goal is to better understand whether there is a direct link between PTSD and CHD risk, as well as to ascertain the role of candidate pathophysiological mechanisms. The study proposed in this application is designed to examine how changes in PTSD symptoms following an established therapeutic intervention (Cognitive Processing Therapy) affect CHD disease pathways in individuals with PTSD. This design will permit an evaluation of the hypothesis that individuals who show significant improvement in PTSD symptoms will also show improvement in CHD risk biomarkers, and individuals who fail to show improvement or show worsening PTSD symptoms, will show no change or worsening in CHD biomarker activity. The study will also provide an evaluation of the role of key stress-related CHD biomarkers as mechanisms underlying the increased CHD risk burden associated with PTSD. Choice of CHD biomarkers focused on the established association of PTSD with chronic activation of stress response systems and includes autonomic nervous system dysregulation, chronic systemic inflammation, and vascular endothelial dysfunction. The proposed research is significant because it is expected to provide knowledge of the role of both the direct impact of PTSD symptoms on CHD risk pathways and the role of these systems as candidate mechanisms underlying the relationship between PTSD and CHD risk. By better defining how PTSD is a risk factor for CHD, as well as identifying the disease pathways involved, the proposed study will help inform strategies for CHD prevention, as well as guide optimal medical management for vulnerable men and women with PTSD, especially in those who refrain or who are refractory to psychiatric treatment.
Age
40 - 65 years
Sex
ALL
Healthy Volunteers
No
Duke University Medical Center
Durham, North Carolina, United States
Start Date
April 1, 2016
Primary Completion Date
July 20, 2021
Completion Date
July 20, 2021
Last Updated
April 17, 2024
112
ACTUAL participants
Cognitive Processing Therapy - Cognitive
BEHAVIORAL
Lead Sponsor
Duke University
NCT07010757
NCT07462312
Data Source & Attribution
This clinical trial information is sourced from ClinicalTrials.gov, a service of the U.S. National Institutes of Health.
Modifications: This data has been reformatted for display purposes. Eligibility criteria have been parsed into inclusion/exclusion sections. Location data has been geocoded to enable distance-based search. For the authoritative and most current information, please visit ClinicalTrials.gov.
Neither the United States Government nor Clareo Health make any warranties regarding the data. Check ClinicalTrials.gov frequently for updates.
View ClinicalTrials.gov Terms and ConditionsNCT07447089