Normotensive preterm delivery and maternal cardiovascular risk factor trajectories across the life course: The HUNT Study, Norway

Markovitz, Amanda R; Haug, E; Horn, Julie; Fraser, Abigail; Tilling, Kate; Rimm, Eric B.; Missmer, Stacey A.; Williams, Paige L.; Romundstad, Pål Richard; Åsvold, Bjørn Olav; Rich‐Edwards, Janet W.

doi:10.1111/aogs.14016

Cited by 6 publications

(6 citation statements)

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“…Although we did not find evidence for cardiovascular risk factors accounting for any of the excess cardiovascular risk in women with history of preterm birth, it is possible that this was due to insufficient statistical power or that the cardiovascular risk factors in our study were continuously measured while those of Tanz et al 22 were dichotomous. Our results are, however, consistent with our previous findings that life course trajectories of cardiovascular risk factors in women with a history of normotensive preterm birth do not differ from those of women with history of normotensive term birth 31 .…”

Section: Discussionsupporting

confidence: 92%

The role of cardiovascular risk factors in maternal cardiovascular disease according to offspring birth characteristics in the HUNT study

Haug

Markovitz

Fraser

et al. 2021

Sci Rep

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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. Whether and to what extent the excess cardiovascular risk observed in women with these pregnancy complications is explained by conventional cardiovascular risk factors (CVRFs) is not known. 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), respectively. 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 CVRFs 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.

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Section: Discussionsupporting

confidence: 92%

The role of cardiovascular risk factors in maternal cardiovascular disease according to offspring birth characteristics in the HUNT study

Haug

Markovitz

Fraser

et al. 2021

Sci Rep

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“…To our knowledge, it is the first to investigate the role of genetic liability for CHD in APOs, conducted in a large, well-characterized, and genetically homogeneous population. This complements previous studies that have shown associations of cardiovascular risk factors (e.g., high blood pressure, dyslipidemia, impaired glucose tolerance) with APOs [ 2 – 7 ], by using a GRS that captures environmental (i.e., genetic risk of higher body mass, smoking, education) as well as likely biological risk for CHD. Unlike those previous studies, interpretation of the magnitude of one SD difference in a genetic risk score for CHD is unclear.…”

Section: Discussionsupporting

confidence: 53%

“…Adverse pregnancy outcomes (APO), such as miscarriage, stillbirth, hypertensive disorders of pregnancy (HDP), gestational diabetes (GD), small for gestational age (SGA), large for gestational age (LGA), and spontaneous preterm birth (sPTB), may unmask a woman’s underlying liability for cardiovascular disease, identifying women who “fail” the cardiometabolic stress test of pregnancy [ 1 ]. Preconception cardiovascular risk factors are associated with APOs [ 2 – 7 ] and the extent of physiological changes of pregnancy including vasodilation, decreases in glucose, and changes in lipoprotein subclasses and biomarkers of low-grade inflammation [ 8 ]. Moreover, adjustment for preconception cardiovascular risk factors attenuates the relationship between APOs and maternal post-partum risk of cardiovascular disease [ 9 – 11 ].…”

Section: Introductionmentioning

confidence: 99%

Parental genetically predicted liability for coronary heart disease and risk of adverse pregnancy outcomes: a cohort study

Hernáez,

Skåra,

Page

et al. 2024

BMC Med

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Background Adverse pregnancy outcomes (APO) may unmask or exacerbate a woman’s underlying risk for coronary heart disease (CHD). We estimated associations of maternal and paternal genetically predicted liability for CHD with lifelong risk of APOs. We hypothesized that associations would be found for women, but not their male partners (negative controls). Methods We studied up to 83,969‬ women (and up to 55,568‬ male partners) from the Norwegian Mother, Father and Child Cohort Study or the Trøndelag Health Study with genotyping data and lifetime history of any APO in their pregnancies (1967–2019) in the Medical Birth Registry of Norway (miscarriage, stillbirth, hypertensive disorders of pregnancy, gestational diabetes, small for gestational age, large for gestational age, and spontaneous preterm birth). Maternal and paternal genetic risk scores (GRS) for CHD were generated using 148 gene variants (p-value < 5 × 10−8, not in linkage disequilibrium). Associations between GRS for CHD and each APO were determined using logistic regression, adjusting for genomic principal components, in each cohort separately, and combined using fixed effects meta-analysis. Results One standard deviation higher GRS for CHD in women was related to increased risk of any hypertensive disorders of pregnancy (odds ratio [OR] 1.08, 95% confidence interval [CI] 1.05–1.10), pre-eclampsia (OR 1.08, 95% CI 1.05–1.11), and small for gestational age (OR 1.04, 95% CI 1.01–1.06). Imprecise associations with lower odds of large for gestational age (OR 0.98, 95% CI 0.96–1.00) and higher odds of stillbirth (OR 1.04, 95% CI 0.98–1.11) were suggested. These findings remained consistent after adjusting for number of total pregnancies and the male partners’ GRS and restricting analyses to stable couples. Associations for other APOs were close to the null. There was weak evidence of an association of paternal genetically predicted liability for CHD with spontaneous preterm birth in female partners (OR 1.02, 95% CI 0.99–1.05), but not with other APOs. Conclusions Hypertensive disorders of pregnancy, small for gestational age, and stillbirth may unmask women with a genetically predicted propensity for CHD. The association of paternal genetically predicted CHD risk with spontaneous preterm birth in female partners needs further exploration.

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“…[39][40][41][42][43][44] Similarly, much-though not all-of the risk of CVD associated with preeclampsia history is accounted for by the emergence of traditional cardiovascular risk factors, such as hypertension, after pregnancy. 34,45 Both the existence and variability in prepregnancy and postpregnancy cardiometabolic risk factors may suggest useful preeclampsia subtypes.…”

Section: Different Long-range Outcomes Of Preeclampsia As Indicators ...mentioning

confidence: 99%

Subtypes of Preeclampsia: Recognition and Determining Clinical Usefulness

et al. 2021

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The concept that preeclampsia is a multisystemic syndrome is appreciated in both research and clinical care. Our understanding of pathophysiology recognizes the role of inflammation, oxidative and endoplasm reticulum stress, and angiogenic dysfunction. Yet, we have not progressed greatly toward clinically useful prediction nor had substantial success in prevention or treatment. One possibility is that the maternal syndrome may be reached through different pathophysiological pathways, that is, subtypes of preeclampsia, that in their specificity yield more clinical utility. For example, early and late onset preeclampsia are increasingly acknowledged as different pathophysiological processes leading to a common presentation. Other subtypes of preeclampsia are supported by disparate clinical outcomes, long-range prognosis, organ systems involved, and risk factors. These insights have been supplemented by discovery-driven methods, which cluster preeclampsia cases into groups indicating different pathophysiologies. In this presentation, we review likely subtypes based on current knowledge and suggest others. We present a consideration of the requirements for a clinically meaningful preeclampsia subtype. A useful subtype should (1) identify a specific pathophysiological pathway or (2) specifically indicate maternal or fetal outcome, (3) be recognizable in a clinically useful time frame, and (4) these results should be reproducible and generalizable (but at varying frequency) including in low resource settings. We recommend that the default consideration be that preeclampsia includes several subtypes rather than trying to force all cases into a single pathophysiological pathway. The recognition of subtypes and deciphering their different pathophysiologies will provide specific targets for prevention, prediction, and treatment directing personalized care.

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Normotensive preterm delivery and maternal cardiovascular risk factor trajectories across the life course: The HUNT Study, Norway

Abstract: This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Cited by 6 publications

References 32 publications

The role of cardiovascular risk factors in maternal cardiovascular disease according to offspring birth characteristics in the HUNT study

The role of cardiovascular risk factors in maternal cardiovascular disease according to offspring birth characteristics in the HUNT study

Parental genetically predicted liability for coronary heart disease and risk of adverse pregnancy outcomes: a cohort study

Subtypes of Preeclampsia: Recognition and Determining Clinical Usefulness

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