Evidence map›Paper›PMID 39733862›Full record

ArticleBrain, behavior, and immunity2025

Accelerated development of cardiovascular risk factors mediates risk for major adverse cardiovascular events in posttraumatic stress disorder.

Maria Khalil, Sinead M Sinnott, Giovanni Civieri, Shady Abohashem, Simran S Grewal, Erin Hanlon, Alula Assefa, Iqra Qamar, Hui Chong Lau, Krystel Abi Karam and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Brain, behavior, and immunity, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Review
  2. Observational
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors.

Maria KhalilCardiology 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.
Sinead M SinnottCardiovascular Imaging Research Center, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; Department of Psychiatry, Harvard Medical School, Boston, MA, USA.
Giovanni CivieriCardiovascular Imaging Research Center, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
Shady AbohashemCardiovascular Imaging Research Center, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
Simran S GrewalCardiology 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.
Erin HanlonCardiovascular Imaging Research Center, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
Alula AssefaCardiovascular Imaging Research Center, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
Iqra QamarCardiology 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.
Hui Chong LauCardiology 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.
Krystel Abi KaramCardiovascular Imaging Research Center, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
Wesam AldosokyCardiovascular Imaging Research Center, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
Lisa M ShinDepartment of Psychology, Tufts University, Medford, MA, USA.
Ahmed TawakolCardiology 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.
Antonia V SeligowskiCardiovascular Imaging Research Center, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; Department of Psychiatry, Harvard Medical School, Boston, MA, USA.
Michael T OsborneCardiology 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. Electronic address: mosborne@mgh.harvard.edu.

Funding

Translational imaging and nanomedicine in inflammatory atherosclerosisP01HL131478 · NHLBI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI Zahi A. Fayad · 2017 to 2026
$24.3M
Reducing Arterial Inflammation and Improving Metabolic Health by Dual CCR2 and CCR5 Antagonism in People Living with HIVR01HL149516 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI LO, JANET, TAWAKOL, AHMED A · 2020 to 2024
$3.9M
Impact of Treating Asymptomatic CMV Replication on Cardiovascular Risk in Treated HIV InfectionR01HL152957 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI PETER W HUNT, Priscilla Y. Hsue · 2020 to 2026
$3.7M
Novel PET/CT and Treatment Strategies to reduce PTS following DVTR01HL137913 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI JAFFER, FAROUC AMIN, TAWAKOL, AHMED A · 2017 to 2020
$3.3M
Neuroimaging Measures of Psychosocial Stress as Predictors of Articular and Arterial Inflammation, Cardiometabolic Disease, and Treatment Response in Rheumatoid ArthritisR01AR077187 · NIAMS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI JON T GILES, AHMED A TAWAKOL · 2021 to 2026
$2.3M
The Effect of Mindfulness on Vascular Inflammation in Stable Coronary Disease: A Multi-System PET/MRI StudyK23HL151909 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI OSBORNE, MICHAEL THOMAS · 2021 to 2025
$997k
A Multi-Modal Investigation of Neurophysiological Deficits in PTSDK23MH125920 · NIMH · MCLEAN HOSPITAL · PI SELIGOWSKI, ANTONIA · 2021 to 2025
$870k
NHLBI NIH HHS K23 HL151909NHLBI NIH HHS P01 HL131478NHLBI NIH HHS R01 HL137913NHLBI NIH HHS R01 HL149516NHLBI NIH HHS R01 HL152957NIAMS NIH HHS R01 AR077187NIMH NIH HHS K23 MH125920
6 · The paper itself

Abstract

backgroundIndividuals 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.

objectiveWe 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 activity [SNA], ventromedial prefrontal cortex [vmPFC] activity, heart rate variability [HRV], and C-reactive protein [CRP]).

methodsSubjects (N = 84,343) in the Mass General Brigham Biobank were studied over 10 years. PTSD, CVDRFs, and MACE were identified by diagnostic codes. From participants with available clinical data, neural, autonomic, and inflammatory mediators (e.g., SNA, vmPFC, HRV, and CRP) were assessed.

resultsPTSD independently predicted incident CVDRFs (hazard ratio [95 % confidence interval] = (1.432 [1.287, 1.592], p < 0.001) and associated with the accelerated development of a new CVDRF by ∼ 4 months versus those without PTSD. The development of new CVDRFs predicted incident MACE (1.736 [1.652, 1.823, p < 0.001) and mediated the link between PTSD and MACE (p < 0.05) by up to 36.4 %. Additionally, lower vmPFC activity, lower HRV, and higher CRP were associated with the development of CVDRFs. HRV and CRP significantly mediated the PTSD-CVDRF link.

conclusionsThe PTSD-MACE link was partially explained by the accelerated development of CVDRFs. Alterations in neural, autonomic, and inflammatory intermediaries contributed to this association. These findings suggest that greater clinical attention to CVDRFs in individuals with PTSD may attenuate MACE risk.

Indexed as

Cardiovascular DiseasesStress Disorders, Post-TraumaticAdultAgedAutonomic Nervous SystemC-Reactive ProteinFemaleHeart Disease Risk FactorsHeart RateHumansMaleMiddle AgedPrefrontal CortexRisk FactorsC-Reactive ProteinCardiovascular DiseaseCardiovascular Risk FactorsCRPHRVMACEPET/CTPTSDStress-Neural ActivityvmPFC

Identifiers

PMID39733862
PMCPMC11903154

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.