Ontology highlight
ABSTRACT: Background
Individuals with posttraumatic stress disorder (PTSD) have high rates of cardiovascular disease (CVD) and increased cardiometabolic CVD risk factors (CVDRFs, e.g., hypertension, hyperlipidemia, or diabetes mellitus). Nevertheless, it remains unknown whether PTSD accelerates CVDRF development and how that impacts the development of major adverse cardiovascular events (MACE) in a broad population. Furthermore, the underlying mechanisms remain incompletely characterized.Objective
We hypothesized that 1) PTSD accelerates CVDRF development, 2) accelerated CVDRF development mediates the PTSD-MACE relationship, and 3) accelerated CVDRF development is partially explained by alterations in neural, autonomic, and inflammatory intermediaries (e.g., stress-associated neural
SUBMITTER: Khalil M
PROVIDER: S-EPMC11903154 | biostudies-literature | 2025 Mar
REPOSITORIES: biostudies-literature