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Accelerated development of cardiovascular risk factors mediates risk for major adverse cardiovascular events in

Maria Khalil1, Sinead M Sinnott2, Giovanni Civieri3

  • 1Cardiology Division, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; Cardiovascular Imaging Research Center, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.

Brain, Behavior, and Immunity
|December 29, 2024
PubMed

Insights

Posttraumatic stress disorder (PTSD) accelerates the development of cardiovascular disease risk factors (CVDRFs), which in turn increases the risk of major adverse cardiovascular events (MACE). This pathway is influenced by neural, autonomic, and inflammatory changes.

Area of Science:

  • Cardiovascular Medicine
  • Psychiatry
  • Neuroscience

Background:

  • Individuals with posttraumatic stress disorder (PTSD) exhibit high rates of cardiovascular disease (CVD) and associated risk factors (CVDRFs).
  • The impact of PTSD on the acceleration of CVDRF development and subsequent major adverse cardiovascular events (MACE) remains unclear.
  • Underlying biological mechanisms linking PTSD to cardiovascular outcomes require further characterization.

Purpose of the Study:

  • To investigate if PTSD accelerates CVDRF development.
  • To determine if accelerated CVDRF development mediates the relationship between PTSD and MACE.
  • To explore if neural, autonomic, and inflammatory factors mediate the PTSD-CVDRF association.

Main Methods:

  • A 10-year longitudinal study of 84,343 participants from the Mass General Brigham Biobank.
  • Identification of PTSD, CVDRFs, and MACE using diagnostic codes.
  • Assessment of neural (e.g., vmPFC activity), autonomic (e.g., HRV), and inflammatory (e.g., CRP) mediators in a subset of participants.

Main Results:

  • PTSD independently predicted incident CVDRFs and accelerated their development by approximately 4 months.
  • CVDRF development significantly predicted incident MACE and mediated up to 36.4% of the PTSD-MACE link.
  • Lower vmPFC activity, lower heart rate variability (HRV), and higher C-reactive protein (CRP) were associated with CVDRF development, with HRV and CRP partially mediating the PTSD-CVDRF association.

Conclusions:

  • Accelerated CVDRF development partially explains the association between PTSD and MACE.
  • Neural, autonomic, and inflammatory alterations play a role in the PTSD-CVDRF link.
  • Clinical focus on managing CVDRFs in individuals with PTSD may reduce MACE risk.
Abstract

Keywords:
CRPCardiovascular DiseaseCardiovascular Risk FactorsHRVMACEPET/CTPTSDStress-Neural ActivityvmPFC

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