The Role of Cardiovascular Risk Factors in Maternal Cardiovascular Disease according to Offspring Birth Characteristics in the HUNT study

Eirin Haug*, Amanda R Markovitz, Abigail Fraser, Håvard Dalen, Pål R. Romundstad, Bjørn O Åsvold, Janet Wilson Rich-Edwards, Julie Horn

*Corresponding author for this work

Research output: Contribution to journalArticle (Academic Journal)peer-review

5 Citations (Scopus)
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Abstract

A history of preterm or small (SGA) or large (LGA) for gestational age offspring is associated with smoking and unfavorable levels of BMI, blood pressure, glucose and lipids. However, the relative contribution of these conventional cardiovascular risk factors (CVRFs) to the observed excess cardiovascular risk in women with a history of these pregnancy complications is unknown. We examined the association between a history of SGA, LGA or preterm birth and cardiovascular disease among 23,284 parous women and quantified the contribution of individual CVRFs to the excess cardiovascular risk using an inverse odds weighting approach. The hazard ratios (HR) between SGA and LGA offspring and CVD were 1.30 (95% confidence interval (CI): 1.15, 1.48) and 0.89 (95% CI: 0.76, 1.03). Smoking explained 49% and blood pressure may have explained ≈12% of the excess cardiovascular risk in women with SGA offspring. Women with preterm birth had a 24% increased risk of CVD (HR 1.24, 95% CI: 1.06, 1.45), but we found no evidence for CVRF explaining any of this excess cardiovascular risk. While smoking explains a substantial proportion of excess cardiovascular risk in women with SGA offspring and blood pressure may explain a small proportion in these women, we found no evidence that conventional CVRFs explain any of the excess
cardiovascular risk in women with preterm birth
Original languageEnglish
Article number22981
JournalScientific Reports
Volume11
Issue number1
Early online date26 Nov 2021
DOIs
Publication statusPublished - Dec 2021

Bibliographical note

Funding Information:
This work was supported by the Research Council of Norway (Grant Number 231149/F20) to BOÅ, JH, and EBH. Additionally, EBH holds a postdoctoral fellowship from the Kristian Gerhard Jebsen Foundation. JH and BOÅ were also supported by the Liaison Committee for education, research and innovation in Central Norway. BOÅ was additionally supported by St. Olavs Hospital and the Faculty of Medicine and Health Sciences, NTNU; and by the Fulbright Program. AF is supported by a personal fellowship from the UK Medical Research Council (MRC) (Grant Number MR/M009351/1). AF works in a Unit that receives core funding from Medical Research Council in the UK (Grant Number MC_UU_12013/5). AM was supported by the American Heart Association [Grant Number 16PRE29690006] and by Training Grant T32HD060454 in Reproductive, Perinatal and Pediatric Epidemiology from the National Institute of Child Health and Human Development, National Institutes of Health. The funders had no role in study design and analysis, preparation of the manuscript or decision to submit the article for publication. Patients were not involved in the development of this study.

Publisher Copyright:
© 2021, The Author(s).

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