Posttraumatic Stress Disorder Treatment Effects on Cardiovascular Physiology: A Systematic Review and Agenda for Future Research.

Journal Article (Systematic Review;Journal Article)

Posttraumatic stress disorder (PTSD) is linked to both altered physiological functioning and poorer cardiovascular health outcomes, including an increased risk for cardiovascular disease and cardiovascular-related mortality. An important question is whether interventions for PTSD might ameliorate the risk for poorer health by improving cardiovascular physiological intermediaries. To begin to characterize the literature addressing this question, we conducted a systematic review of empirical studies examining the impact of PTSD interventions on cardiovascular physiological intermediaries, including blood pressure (BP), heart rate (HR), cardiac impedance, and subclinical atherosclerosis. Outcomes included both tonic (i.e., resting) cardiovascular functioning and cardiovascular reactivity (CVR). A total of 44 studies met the inclusion criteria. There was mixed evidence regarding whether PTSD treatment improved tonic cardiovascular functioning. There was stronger evidence that PTSD treatments reduced CVR to trauma-related stressors, particularly for higher-quality studies of cognitive behavioral interventions. No studies examined cardiac impedance or subclinical atherosclerosis. The studies had a high degree of heterogeneity in the populations sampled and interventions tested. Moreover, they generally included small sample sizes and lacked control conditions. Interventions for PTSD may improve cardiovascular physiological outcomes, particularly CVR to trauma cues, although additional methodologically rigorous studies are needed. We outline changes to future research that would improve the literature regarding this important question, including the more frequent use of control groups and larger sample sizes.

Full Text

Duke Authors

Cited Authors

  • Bourassa, KJ; Hendrickson, RC; Reger, GM; Norr, AM

Published Date

  • April 2021

Published In

Volume / Issue

  • 34 / 2

Start / End Page

  • 384 - 393

PubMed ID

  • 33277952

Pubmed Central ID

  • PMC8035275

Electronic International Standard Serial Number (EISSN)

  • 1573-6598

International Standard Serial Number (ISSN)

  • 0894-9867

Digital Object Identifier (DOI)

  • 10.1002/jts.22637


  • eng