Abstract

The intricate relationship between post-traumatic stress disorder (PTSD) and cardiovascular disease (CVD) has garnered increasing attention due to its bidirectional impact and potential for significant health consequences. Epidemiological evidence suggests that PTSD may serve as a risk factor for incident CVD, while acute CVD events can trigger PTSD, subsequently increasing the risk of recurrent cardiovascular events. This dynamic interplay is characterized by the human stress response, disrupted behavioral and lifestyle factors, and potential physiological mechanisms. Notably, the immediate aftermath of a cardiovascular event presents a critical window for intervention, offering the possibility of preventing the development of PTSD and its associated physiological and behavioral sequelae. However, while candidate mechanisms linking PTSD and CVD have been identified, determining which mechanisms are most amenable to intervention remains a challenge. This article emphasizes the urgency of addressing key unanswered questions in this domain. Despite an evolving understanding of the association between PTSD and CVD, causal relationships remain to be firmly established. Comprehensive investigations into the intricate interplay of behavioral and biological mechanisms are essential for identifying precise targets for intervention. Innovations in research methodologies, including the exploration of PTSD symptom dynamics and their impact on cardiovascular function, hold the potential for identifying crucial intervention points. Drawing parallels from prior challenges in translating identified risk factors into effective interventions, the field must prioritize systematic investigations and early-phase intervention trials. By doing so, researchers and clinicians can potentially develop strategies to mitigate CVD risk in the context of PTSD and improve both cardiovascular and mental health outcomes.

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