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• W2589809462 abstract "HomeHypertensionVol. 69, No. 4Offspring Cardiovascular Disease in Preeclampsia Free AccessEditorialPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessEditorialPDF/EPUBOffspring Cardiovascular Disease in PreeclampsiaNature Versus Nurture? Alice M. Wang and S. Ananth Karumanchi Alice M. WangAlice M. Wang From the Boston University Medical Center, MA (A.M.W.); and Beth Israel Deaconess Medical Center, Boston, MA (S.A.K.). Search for more papers by this author and S. Ananth KarumanchiS. Ananth Karumanchi From the Boston University Medical Center, MA (A.M.W.); and Beth Israel Deaconess Medical Center, Boston, MA (S.A.K.). Search for more papers by this author Originally published1 Apr 2017https://doi.org/10.1161/HYPERTENSIONAHA.117.08957Hypertension. 2017;69:589–590Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: January 1, 2017: Previous Version 1 See related article, pp 591–598Several epidemiological studies have suggested that the offspring of mothers with preeclampsia and gestation hypertension have increased risk for long-term hypertension and cardiovascular disease (CVD).1–3 In a study reported in this issue of Hypertension, Alsnes et al,4 using a prospective cohort analysis on offspring cardiovascular risk in young adulthood after hypertensive disorders in pregnancy, confirm that offspring exposed to maternal hypertension during pregnancy had a worse cardiovascular risk profile in adulthood compared with those of normal pregnancies.4 Consistent with previous studies,5,6 differences in systolic blood pressure, diastolic blood pressure, body mass index, and waist circumference were found in the adult offspring with exposure to any maternal hypertensive disorder of pregnancy. Intriguingly, the authors also found that the siblings born after a normotensive pregnancy had similar changes as their exposed siblings. These data suggest that the pregnancy milieu of maternal hypertension may be unlikely to play a role in the pathogenesis of offspring hypertension.Preeclampsia is a pregnancy-specific vascular disease characterized by maternal hypertension and proteinuria and resolves after delivery of the placenta. Mothers with a history of preeclampsia eventually develop salt-sensitive hypertension and CVD.7 Vascular toxins that mediate the maternal syndrome of preeclampsia7 have also been demonstrated to contribute to long-term maternal CVD in animal models.8 Infants born to preeclamptic mothers do not have hypertension and proteinuria, suggesting that the vascular toxins mediating preeclamptic signs/symptoms are likely restricted to maternal compartment. However, offspring born to preeclamptic mothers are often growth restricted, have evidence of systemic and pulmonary vascular dysfunction,9 and are at increased long-term risk for hypertension and CVD.5,6 These observations support the general idea of Barker’s Developmental Origins of Health and Disease hypothesis that adverse pregnancy-related factors can result in adult disease because the exposure is experienced during a sensitive period of developmental plasticity.10 Proof for the Barker hypothesis comes from animal experiments that identify periconceptional maternal factors, such as undernutrition and placental ischemia, are important determinants of offspring’s adult health.11 However, other observations support the concept that familial aggregation of genetic and epigenetic factors may explain a proportion of the offspring CVD. For example, birth weight of the infant is also inversely associated with the CVD in the mothers and in the mother’s parents.12The study by Alsnes et al4 had many strengths. Their study population was the large well-phenotyped HUNT study (Nord–Trondelag Health Study) in Norway with 15 778 participants. Out of 15 778 participants, 706 participants were noted to have exposure to a hypertensive disorder of pregnancy, including gestational hypertension, term preeclampsia, and preterm preeclampsia. Comparing cardiovascular risk factors among siblings discordant for the exposure of maternal hypertension during pregnancy, authors identified 210 sibships and elegantly demonstrated that there were no clear differences in blood pressure and body mass index between siblings born by the same mother, where at least 1 sibling was born after a hypertensive pregnancy. This intriguing finding about the siblings suggests that complex genetic and social traits, such as parental obesity, similar diet, and physical activity, may have a greater effect on offspring blood pressure and body mass index/waist circumference than the pregnancy milieu of maternal hypertension. In addition, if offspring born into families with a history of 1 complicated pregnancy have increased cardiovascular risk, it is worthwhile to consider how closely entire families should be followed for diseases like hypertension.The study by Alsnes et al4 also had significant weaknesses. First, for reasons related to sample size for the primary analysis, authors pooled gestational hypertension and preeclampsia into 1 group. It is clear that hypertensive disorders of pregnancy have different mechanisms. Therefore, it is important to study the different subgroups of maternal hypertensive disorders of pregnancy separately to clearly evaluate the long-term cardiovascular risk for the offspring. Certain specific subgroups, such as offspring born to mothers with preterm preeclampsia (usually accompanied by severe fetal growth restriction), may have added CVD risk profile. Lazdam et al13 previously reported that there is increased hypertension in the offspring of mothers with early-onset preeclampsia, but not in offspring of mothers with term preeclampsia or normotensive pregnancy; this suggests that the duration and severity of the fetal exposure to maternal hypertensive disease may be important. In the study by Alsnes et al,4 the duration of intrauterine exposure to maternal hypertension was not defined. Short-lived maternal hypertension in the third trimester, such as in term preeclampsia, typically has minimal effect on fetal growth and would be expected to have minimal long-term cardiovascular effects relative to the complex interplay of genetic factors, as well as lifetime environmental/lifestyle choices. In the small subgroup of mothers with preterm preeclampsia, Alsnes et al4 found that offspring with exposure to maternal preterm preeclampsia had systolic and diastolic blood pressures and body mass index/waist circumference that were no different than offspring of normal pregnancies, despite having a lower gestational age and substantially lower mean birth weight, findings that contradict prior studies.9,13 Whether this is related to small sample size leading to a type II error or presence of other cofounders (such as socioeconomic status) remains to be explored.In summary, the work by Alsnes et al4 suggest that genetic and shared environmental factors may play a critical role in mediating hypertension and CVD in offsprings exposed to maternal hypertension; however, additional studies with larger sample size and sufficient power to study specifically early-onset preeclampsia (subgroup with the greatest risk for fetal growth restriction) are needed to answer the contribution of nature versus nurture debate in the pathogenesis of offspring CVD after maternal preeclampsia.DisclosuresS.A. Karumanchi is a coinventor on patents in preeclampsia biomarkers for the diagnosis and therapy of preeclampsia. S.A. Karumanchi has financial interest in Aggamin Therapeutics and reports serving as a consultant to Thermofisher Scientific. A.M. Wang reports no conflict.FootnotesThe opinions expressed in this article are not necessarily those of the editors or of the American Heart AssociationCorrespondence to Ananth Karumanchi, Beth Israel Deaconess Medical Center, 330 Brookline Avenue, Boston, MA 02215. E-mail [email protected]References1. Fraser A, Nelson SM, Macdonald-Wallis C, Sattar N, Lawlor DA. Hypertensive disorders of pregnancy and cardiometabolic health in adolescent offspring.Hypertension. 2013; 62:614–620. doi: 10.1161/HYPERTENSIONAHA.113.01513.LinkGoogle Scholar2. Geelhoed JJ, Fraser A, Tilling K, Benfield L, Davey Smith G, Sattar N, Nelson SM, Lawlor DA. Preeclampsia and gestational hypertension are associated with childhood blood pressure independently of family adiposity measures: the Avon Longitudinal Study of Parents and Children.Circulation. 2010; 122:1192–1199. doi: 10.1161/CIRCULATIONAHA.110.936674.LinkGoogle Scholar3. Kajantie E, Eriksson JG, Osmond C, Thornburg K, Barker DJ. Pre-eclampsia is associated with increased risk of stroke in the adult offspring: the Helsinki birth cohort study.Stroke. 2009; 40:1176–1180. doi: 10.1161/STROKEAHA.108.538025.LinkGoogle Scholar4. Alsnes IV, Vatten LJ, Fraser A, Bjørngaard JH, Rich-Edwards J, Romundstad PR, Åsvold BO. Hypertension in pregnancy and offspring cardiovascular risk in young adulthood: prospective and sibling studies in the HUNT study (Nord–Trondelag Health Study) in Norway.Hypertension. 2017; 69:591–598. doi: 10.1161/HYPERTENSIONAHA.116.08414.LinkGoogle Scholar5. Davis EF, Lazdam M, Lewandowski AJ, Worton SA, Kelly B, Kenworthy Y, Adwani S, Wilkinson AR, McCormick K, Sargent I, Redman C, Leeson P. Cardiovascular risk factors in children and young adults born to preeclamptic pregnancies: a systematic review.Pediatrics. 2012; 129:e1552–e1561. doi: 10.1542/peds.2011-3093.CrossrefMedlineGoogle Scholar6. Davis EF, Lewandowski AJ, Aye C, Williamson W, Boardman H, Huang RC, Mori TA, Newnham J, Beilin LJ, Leeson P. Clinical cardiovascular risk during young adulthood in offspring of hypertensive pregnancies: insights from a 20-year prospective follow-up birth cohort.BMJ Open. 2015; 5:e008136. doi: 10.1136/bmjopen-2015-008136.CrossrefMedlineGoogle Scholar7. Powe CE, Levine RJ, Karumanchi SA. Preeclampsia, a disease of the maternal endothelium: the role of antiangiogenic factors and implications for later cardiovascular disease.Circulation. 2011; 123:2856–2869. doi: 10.1161/CIRCULATIONAHA.109.853127.LinkGoogle Scholar8. Pruthi D, Khankin EV, Blanton RM, Aronovitz M, Burke SD, McCurley A, Karumanchi SA, Jaffe IZ. Exposure to experimental preeclampsia in mice enhances the vascular response to future injury.Hypertension. 2015; 65:863–870. doi: 10.1161/HYPERTENSIONAHA.114.04971.LinkGoogle Scholar9. Jayet PY, Rimoldi SF, Stuber T, Salmòn CS, Hutter D, Rexhaj E, Thalmann S, Schwab M, Turini P, Sartori-Cucchia C, Nicod P, Villena M, Allemann Y, Scherrer U, Sartori C. Pulmonary and systemic vascular dysfunction in young offspring of mothers with preeclampsia.Circulation. 2010; 122:488–494. doi: 10.1161/CIRCULATIONAHA.110.941203.LinkGoogle Scholar10. Barker DJ, Osmond C. Low birth weight and hypertension.BMJ. 1988; 297:134–135.CrossrefMedlineGoogle Scholar11. Alexander BT, Dasinger JH, Intapad S. Fetal programming and cardiovascular pathology.Compr Physiol. 2015; 5:997–1025. doi: 10.1002/cphy.c140036.CrossrefMedlineGoogle Scholar12. Smith GC, Wood AM, White IR, Pell JP, Hattie J. Birth weight and the risk of cardiovascular disease in the maternal grandparents.Am J Epidemiol. 2010; 171:736–744. doi: 10.1093/aje/kwp448.CrossrefMedlineGoogle Scholar13. Lazdam M, de la Horra A, Diesch J, Kenworthy Y, Davis E, Lewandowski AJ, Szmigielski C, Shore A, Mackillop L, Kharbanda R, Alp N, Redman C, Kelly B, Leeson P. Unique blood pressure characteristics in mother and offspring after early onset preeclampsia.Hypertension. 2012; 60:1338–1345. doi: 10.1161/HYPERTENSIONAHA.112.198366.LinkGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited ByNair A, Silva S, Agbor L, Wu J, Nakagawa P, Mukohda M, Lu K, Sandgren J, Pierce G, Santillan M, Grobe J and Sigmund C (2019) Endothelial PPARγ (Peroxisome Proliferator–Activated Receptor-γ) Protects From Angiotensin II–Induced Endothelial Dysfunction in Adult Offspring Born From Pregnancies Complicated by Hypertension, Hypertension, 74:1, (173-183), Online publication date: 1-Jul-2019. April 2017Vol 69, Issue 4 Advertisement Article InformationMetrics © 2017 American Heart Association, Inc.https://doi.org/10.1161/HYPERTENSIONAHA.117.08957PMID: 28223476 Originally publishedApril 1, 2017 PDF download Advertisement SubjectsHypertension" @default.
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