Endothelial Dysfunction, PTSD, Trauma
Conditions
Keywords
Trauma, PTSD, Endothelial Dysfunction
Brief summary
This study will test whether endothelial dysfunction could be the early subclinical mechanism by which posttraumatic stress disorder (PTSD) increases cardiovascular disease (CVD) risk, and whether posttraumatic fear-a key component of PTSD-or another PTSD dimension could be the target to offset that risk. The results of this study may help trauma-exposed individuals who are at risk of having CVD events.
Detailed description
Posttraumatic stress disorder (PTSD) increases risk of incident cardiovascular disease (CVD) by 25-50%. Most individuals (50-90%) experience a traumatic event in their lifetime, and PTSD is the fifth most common psychiatric disorder. Experts have now called for increased CVD surveillance after trauma and for PTSD treatment trials powered to reduce CVD risk. However, both CVD risk and PTSD are complex phenomena that likely interact in nuanced ways. This study will determine which PTSD dimension(s) contribute to endothelial dysfunction, one of the earliest modifiable precursors to CVD. The investigators will examine cross-sectional and longitudinal associations of PTSD and its underlying dimensions with functional and, secondarily, cellular measures of endothelial dysfunction (FMD and circulating endothelial cell-derived microparticles, respectively) in a community-dwelling sample of CVD-free adult men and women with a history of trauma (50% with current PTSD).
Interventions
BEHAVIORALPsychophysiological fear conditioning and extinction task
Behavioral task to assess psychophysiological measures of fear
BEHAVIORALEyetracking task
Behavioral task to assess dysphoria-relevant attention allocation
Sponsors
University of California, Los Angeles
National Heart, Lung, and Blood Institute (NHLBI)
Study design
Observational model
CASE_CONTROL
Time perspective
CROSS_SECTIONAL
Eligibility
Sex/Gender
ALL
Age
18 Years to No maximum
Healthy volunteers
No
Inclusion criteria
* Aged 18+ years * History of exposure to a psychological trauma (e.g., natural disaster, physical assault) * Fluent in English * Willing to and capable of providing informed consent Additional Inclusion Criteria for the PTSD Group * Diagnosed with current PTSD (duration of at least 1 month) using the Clinician-Administered PTSD Scale for Diagnostic and Statistical Manual 5th Edition (DSM-5) (CAPS-5) at the diagnostic interview assessment
Exclusion criteria
* History of CVD (i.e., diagnosis of myocardial infarction, unstable angina, heart failure, peripheral artery disease, or stroke) * Deemed unable to comply with the protocol (either self-selected or by indicating during screening that could not complete all requested tasks) * Current bipolar disorder or psychotic disorder * Mild or more severe cognitive impairment \[Mini-Mental State Exam (MMSE)3 score ≤18\] * Current moderate or severe substance use disorder * Acute, unstable, or severe medical disorder or pregnancy * Deemed to need immediate psychiatric intervention (e.g., active suicidality) * Use of antipsychotic, mood stabilizer, antidepressant, or stimulant medication in the past 4 weeks * Daily benzodiazepine use in the past 2 weeks Additional
Design outcomes
Primary
| Measure | Time frame | Description |
|---|---|---|
| Flow-mediated Dilation of the Brachial Artery (FMD) % | Baseline | FMD is the percent difference in diameter of the brachial artery, before and after occlusion. Impaired endothelial function occurs when blood vessels are unable to dilate fully in response to nitric oxide synthesis and release, which is manifested as impaired endothelium-dependent vasodilation (i.e., lower FMD). Lower FMD has been associated with the degree of coronary atherosclerosis and predicts CVD events. |
Secondary
| Measure | Time frame | Description |
|---|---|---|
| Circulating Endothelial Cell-derived Microparticles (EMPs) Expressing CD62E | Baseline | EMPs expressing CD62E (i.e., endothelial cell activation) and CD31 (i.e., endothelial cell apoptosis) will be measured. Assessments of circulating EMPs will be measured using flow cytometry, and total flow cytometry counts will be converted to the number of EMPs per uL of blood. Higher concentrations of EMPs expressing CD62E and CD31 indicate greater endothelial dysfunction. |
| Circulating Endothelial Cell-derived Microparticles (EMPs) Expressing CD31 | Baseline | EMPs expressing CD62E (i.e., endothelial cell activation) and CD31 (i.e., endothelial cell apoptosis) will be measured. Assessments of circulating EMPs will be measured using flow cytometry, and total flow cytometry counts will be converted to the number of EMPs per uL of blood. Higher concentrations of EMPs expressing CD62E and CD31 indicate greater endothelial dysfunction. |
Countries
United States
Contacts
PRINCIPAL_INVESTIGATORJennifer A Sumner, PhD
University of California, Los Angeles
Baseline characteristics
| Characteristic | — |
|---|---|
| Age, Continuous | 38.34 Years STANDARD_DEVIATION 14.22 |
| Ethnicity (NIH/OMB) Hispanic or Latino | 28 Participants |
| Ethnicity (NIH/OMB) Not Hispanic or Latino | 58 Participants |
| Ethnicity (NIH/OMB) Unknown or Not Reported | 0 Participants |
| Race (NIH/OMB) American Indian or Alaska Native | 1 Participants |
| Race (NIH/OMB) Asian | 36 Participants |
| Race (NIH/OMB) Black or African American | 9 Participants |
| Race (NIH/OMB) More than one race | 7 Participants |
| Race (NIH/OMB) Native Hawaiian or Other Pacific Islander | 0 Participants |
| Race (NIH/OMB) Unknown or Not Reported | 21 Participants |
| Race (NIH/OMB) White | 72 Participants |
| Sex: Female, Male Female | 45 Participants |
| Sex: Female, Male Male | 37 Participants |
Adverse events
| Event type | EG000 affected / at risk | EG001 affected / at risk |
|---|---|---|
| deaths Total, all-cause mortality | 0 / 82 | 0 / 86 |
| other Total, other adverse events | 0 / 82 | 0 / 86 |
| serious Total, serious adverse events | 0 / 82 | 0 / 86 |
Outcome results
None listed