Evidence map›Paper›PMID 39228375›Full record

ArticleEuropean heart journal2024

Pre-existing maternal cardiovascular disease and the risk of offspring cardiovascular disease from infancy to early adulthood.

Muhammad Zakir Hossin, Kalliopi Kazamia, Jonas Faxén, André Rudolph, Kari Johansson, Anna Sandström, Neda Razaz

Abstract read
In one paragraph

Article in European heart journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

  1. Article
  2. Article
  3. Prediction of Cyanotic Congenital Heart Disease Risk in U.S. Births.Journal of cardiovascular development and disease · 2026
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Lactation safety of cardiovascular medications.American heart journal plus : cardiology research and practice · 2025
    Review
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

7 authors.

Muhammad Zakir HossinDepartment of Medicine Solna, Clinical Epidemiology Division, Karolinska Institutet, Karolinska University Hospital, D1: 04, Stockholm SE-171 76, Sweden.ORCID 0000-0002-9078-419X
Kalliopi KazamiaDepartment of Pediatric Cardiology, Stockholm-Uppsala, Karolinska University Hospital, Stockholm, Sweden.
Jonas FaxénDepartment of Cardiology, Karolinska University Hospital, Stockholm, Sweden.
André RudolphDepartment of Pediatric Cardiology, Stockholm-Uppsala, Karolinska University Hospital, Stockholm, Sweden.
Kari JohanssonDepartment of Medicine Solna, Clinical Epidemiology Division, Karolinska Institutet, Karolinska University Hospital, D1: 04, Stockholm SE-171 76, Sweden.
Anna SandströmDepartment of Medicine Solna, Clinical Epidemiology Division, Karolinska Institutet, Karolinska University Hospital, D1: 04, Stockholm SE-171 76, Sweden.
Neda RazazDepartment of Medicine Solna, Clinical Epidemiology Division, Karolinska Institutet, Karolinska University Hospital, D1: 04, Stockholm SE-171 76, Sweden.

Funding

Swedish Heart and Lung Foundation No. 3581/2020Swedish Research Council for Health, Working life and Welfare 2023-01238 and 4-2702/2019
6 · The paper itself

Abstract

BACKGROUND AND

aimsA variety of maternal heart conditions are associated with abnormal placentation and reduced foetal growth. However, their impact on offspring's long-term cardiovascular health is poorly studied. This study aims to investigate the association between intrauterine exposure to pre-existing maternal cardiovascular disease (CVD) and offspring CVD occurring from infancy to early adulthood, using paternal CVD as a negative control.

methodsThis nationwide cohort study used register data of live singletons without major malformations or congenital heart disease born between 1992 and 2019 in Sweden. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using Cox proportional hazards models, adjusted for essential maternal characteristics. Paternal CVD served as a negative control for assessment of unmeasured genetic and environmental confounding.

resultsOf the 2 597 786 offspring analysed (49.1% female), 26 471 (1.0%) were born to mothers with pre-existing CVD. During a median follow-up of 14 years (range 1-29 years), 17 382 offspring were diagnosed with CVD. Offspring of mothers with CVD had 2.09 times higher adjusted HR of CVD (95% CI 1.83, 2.39) compared with offspring of mothers without CVD. Compared with maternal CVD, paternal CVD showed an association of smaller magnitude (HR 1.49, 95% CI 1.32, 1.68). Increased hazards of offspring CVD were also found when stratifying maternal CVD into maternal arrhythmia (HR 2.94, 95% CI 2.41, 3.58), vascular (HR 1.59, 95% CI 1.21, 2.10), and structural heart diseases (HR 1.48, 95% CI 1.08, 2.02).

conclusionsMaternal CVD was associated with an increased risk of CVD in offspring during childhood and young adulthood. Paternal comparison suggests that genetic or shared familial factors may not fully explain this association.

Indexed as

Cardiovascular DiseasesPrenatal Exposure Delayed EffectsAdolescentAdultChildChild, PreschoolCohort StudiesFemaleHumansInfantInfant, NewbornMalePregnancyPregnancy Complications, CardiovascularProportional Hazards ModelsRegistriesDevelopmental programmingMaternal cardiovascular diseaseNegative-control exposureOffspring cardiovascular diseasePaternal cardiovascular diseasePregnancy

Identifiers

PMID39228375
PMCPMC11458151

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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.