Publication: Effects of traumatic stress on endothelial and cardiac autonomic functions
| dc.contributor.department | School of Medicine | |
| dc.contributor.kuauthor | Aslan, Gamze | |
| dc.contributor.kuauthor | Kanbay, Mehmet | |
| dc.contributor.kuauthor | Yurtseven, Ece | |
| dc.contributor.kuauthor | Yaycıoğlu, Arda | |
| dc.contributor.kuauthor | Aytekin, Saide | |
| dc.contributor.kuauthor | Aytekin, Vedat | |
| dc.contributor.kuauthor | Şar, Vedat | |
| dc.contributor.schoolcollegeinstitute | SCHOOL OF MEDICINE | |
| dc.date.accessioned | 2026-02-26T07:11:37Z | |
| dc.date.available | 2026-02-25 | |
| dc.date.issued | 2026 | |
| dc.description.abstract | Traumatic stress is a psychobiological response to an overwhelming life event that exceeds the individual's capacity to cope. Emerging evidence suggests that exposure to traumatic stress: whether or not it results in post-traumatic stress disorder (PTSD) is associated with increased cardiovascular risk. This study aimed to examine the relationship between trauma-related psychiatric symptoms and markers of endothelial and cardiac autonomic function. A list of potentially traumatic life events and the self-report PTSD Symptom Checklist-5 were administered to 132 adults. To evaluate the endothelial function, carotid intima media thickness (CIMT) and flow mediated dilatation were measured for all participants. Additionally, the Ewing test results, heart rate (HR), blood pressure, and biochemical parameters were collected. Those who reported at least 1 stressor event of traumatic scope (n = 48, 36%) were compared to those who did not (n = 84, 64%) alongside participants with and without a diagnosis of PTSD. Carotid intima media thickness (0.61 mm [0.32-0.82] vs 0.41 mm [0.28-0.69], P < .0005), systolic blood pressure (SBP) (125 mm Hg [109-130] vs 114 mm Hg [95-130], P < .0005), morning HR (81 bpm [61-96] vs 77 bpm [50-100], P = .042), serum C-reactive protein (CRP, 1.40 mg/L [0.30-5.30] vs 0.30 mg/L [0.30-4.10], P = .014) values were significantly increased in the traumatic stressor group compared to the non-stressor group. Flow mediated dilatation values (8% [4-16] vs 11% [4-23], P < .0005) were lower in the traumatic stressor group than the non-stressor group. Presence of traumatic stress was positively correlated with CIMT (R = 0.56, P < .0005), CRP (R = 0.22, P = .03), and SBP (R = 0.41, P < .0005). Presence of traumatic stress was negatively correlated with flow mediated dilatation (r = -0.35, P < .0005). According to the logistic regression analysis, SBP, CIMT, and flow mediated dilatation values were independently associated with traumatic stress. The Diagnostic and Statistical Manual of Mental Disorders-5 diagnosis of PTSD (n = 19, 14%) and PTSD symptom total scores (mean = 22.3, SD = 16.1) were, however, not associated with any of the assessed biological variables. Trauma exposure regardless of PTSD diagnosis was independently associated with early signs of vascular dysfunction and elevated cardiovascular risk markers (SBP, CIMT, and flow mediated dilatation). Morever, morning HR and serum CRP values were found significantly different between the participants with and without a history of traumatic stress. These findings underscore the need to consider trauma history in cardiovascular risk assessment, even in the absence of clinically diagnosed PTSD. Copyright © 2026 the Author(s). Published by Wolters Kluwer Health, Inc. | |
| dc.description.fulltext | Yes | |
| dc.description.harvestedfrom | Manual | |
| dc.description.indexedby | WOS | |
| dc.description.indexedby | Scopus | |
| dc.description.indexedby | PubMed | |
| dc.description.openaccess | Gold OA | |
| dc.description.peerreviewstatus | N/A | |
| dc.description.publisherscope | International | |
| dc.description.readpublish | N/A | |
| dc.description.sponsoredbyTubitakEu | N/A | |
| dc.description.version | N/A | |
| dc.identifier.doi | 10.1097/MD.0000000000047028 | |
| dc.identifier.embargo | No | |
| dc.identifier.issn | 1536-5964 | |
| dc.identifier.issue | 2 | |
| dc.identifier.pubmed | 41517656 | |
| dc.identifier.quartile | Q1 | |
| dc.identifier.scopus | 2-s2.0-105027042576 | |
| dc.identifier.startpage | e47028 | |
| dc.identifier.uri | https://doi.org/10.1097/MD.0000000000047028 | |
| dc.identifier.uri | https://hdl.handle.net/20.500.14288/32417 | |
| dc.identifier.volume | 105 | |
| dc.identifier.wos | 001680447700014 | |
| dc.keywords | Cardiac autonomic functions | |
| dc.keywords | Endothelial dysfunction | |
| dc.keywords | Traumatic stress | |
| dc.language.iso | eng | |
| dc.publisher | Wolters Kluwer Health | |
| dc.relation.affiliation | Koç University | |
| dc.relation.collection | Koç University Institutional Repository | |
| dc.relation.ispartof | Medicine | |
| dc.relation.openaccess | Yes | |
| dc.rights | CC BY-NC-ND (Attribution-NonCommercial-NoDerivs) | |
| dc.rights.uri | Attribution, Non-commercial, No Derivative Works (CC-BY-NC-ND) | |
| dc.subject | Psychiatry | |
| dc.subject | Cardiovascular medicine | |
| dc.title | Effects of traumatic stress on endothelial and cardiac autonomic functions | |
| dc.type | Journal Article | |
| dspace.entity.type | Publication | |
| relation.isOrgUnitOfPublication | d02929e1-2a70-44f0-ae17-7819f587bedd | |
| relation.isOrgUnitOfPublication.latestForDiscovery | d02929e1-2a70-44f0-ae17-7819f587bedd | |
| relation.isParentOrgUnitOfPublication | 17f2dc8e-6e54-4fa8-b5e0-d6415123a93e | |
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