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• W2568331569 abstract "HomeCirculationVol. 128, No. 20Linking Intrauterine Growth Restriction and Blood Pressure Free AccessEditorialPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessEditorialPDF/EPUBLinking Intrauterine Growth Restriction and Blood PressureInsight Into the Human Origins of Cardiovascular Disease Bettye Sue Hennington, PhD and Barbara T. Alexander, PhD Bettye Sue HenningtonBettye Sue Hennington From the Department of Biology, Tougaloo College, Tougaloo, MS (B.S.H.); and Department of Physiology and Biophysics (B.S.H., B.T.A.) and the Women’s Health Research Center (B.S.H., B.T.A.), University of Mississippi Medical Center, Jackson. Search for more papers by this author and Barbara T. AlexanderBarbara T. Alexander From the Department of Biology, Tougaloo College, Tougaloo, MS (B.S.H.); and Department of Physiology and Biophysics (B.S.H., B.T.A.) and the Women’s Health Research Center (B.S.H., B.T.A.), University of Mississippi Medical Center, Jackson. Search for more papers by this author Originally published17 Oct 2013https://doi.org/10.1161/CIRCULATIONAHA.113.006323Circulation. 2013;128:2179–2180Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: November 15, 2013: Previous Version 1 Abnormal perfusion to the fetus can slow fetal growth and result in intrauterine growth restriction (IUGR).1 IUGR, or failure to reach one’s birth potential, is one of the most common complications during pregnancy and generally results from placental insufficiency.1 IUGR is generally not recognized before delivery, and treatment options for IUGR are limited, with early delivery being the most common.1 Preeclampsia is often a contributory cause of IUGR, and numerous studies indicate that individuals exposed to a preeclamptic pregnancy exhibit a higher body mass index and blood pressure during childhood and adult life.2 Individuals born with IUGR also demonstrate an increase in blood pressure later in life.3 This association forms the basis for the developmental origins of health and disease and indicates that adverse influences during fetal life that slow fetal growth program an individual for greater cardiovascular risk in later life.4,5Article see p 2202Experimental models of placental insufficiency provide proof of principle that IUGR induced by reduced uterine perfusion programs an increase in blood pressure and cardiovascular risk in later life.5 However, in this issue of Circulation, Gaillard et al6 provide a direct link between reduced uterine perfusion and IUGR with increased cardiovascular risk. Using a large, prospective, longitudinal cohort, Gaillard and colleagues report that an increase in third-trimester fetoplacental vascular resistance indicative of reduced perfusion was associated with a decrease in size at birth and a later increase in total fat mass and systolic blood pressure at 6 years of age.6 Thus, this study indicates that assessment of fetal growth characteristics via Doppler flow velocity waveforms in the umbilical artery not only may be indicative of IUGR but also may identify an individual at greater risk for cardiovascular disease in later life.IUGR in this study occurred in a relatively low-risk population of age-appropriate mothers who were in good health, of European descent, and from a middle-class to an upper-middle-class socioeconomic background.6 The socioeconomic background and health of the mother suggest that the mothers in this cohort had adequate access to proper nutrition. IUGR in this cohort was associated with higher umbilical artery vascular resistance.6 Thus, these findings suggest that the causative factors contributing to IUGR in this cohort were most likely not due to maternal undernutrition per se but rather improper remodeling of the uteroplacental circulation. The original hypothesis for the developmental origins of health and disease was based on a geographical association correlating high rates of infant mortality with high rates of death caused by coronary heart disease.4 However, the original observation noted by Barker and Osmond4 was from an area of depressed socioeconomic status, leading them to hypothesize that fetal undernutrition caused by poor living conditions was a causative factor in the fetal programming of cardiovascular risk. Since that original observation and formulation of what is now referred to as the developmental origins of health and disease, numerous population-based studies have noted an inverse relationship between birth weight as a crude marker of slow fetal growth and blood pressure as an indicator of increased cardiovascular risk that is present regardless of socioeconomic status.7 Therefore, significant evidence exists that poor nutrition to the fetus regardless of the reason, poverty or placental insufficiency, contributes to the developmental origins of chronic disease. Notably, this study by Galliard et al clearly demonstrates that the origins of increased programmed cardiovascular risk that arises from IUGR may require more than adequate nutrition to reverse the slow fetal growth that originates from improper remodeling of the maternal/uteroplacental vasculature.Currently, it is not possible to reverse IUGR that results from uteroplacental insufficiency.8 Pregnancies complicated by IUGR are associated with an increased risk of perinatal morbidity and mortality, with early delivery considered the main treatment option.8,9 Infants delivered preterm often have serious, long-term health problems, including respiratory distress, problems with vision and hearing, cerebral palsy, developmental delays, and infection.8 In addition, individuals born preterm also exhibit a moderate increase in blood pressure in later life.10 Thus, not only is early delivery to prevent the immediate demise of the IUGR fetus associated with the early morbidities that accompany preterm birth, but also individuals born preterm may have an increased risk for the development of hypertension and cardiovascular disease in later life.There are multiple causes of IUGR, yet most are thought to result from the improper modification of the spiral arteries and resulting increased placental resistance.1 Ultrasound technologies are advancing in their ability to detect resistance within the uterine and umbilical arteries as methods for the identification of IUGR and evaluation of fetal health.1 However, use is generally not indicated for routine screening in low-risk populations.9 Although Doppler evaluation is used for the assessment and management of high-risk pregnancies, detection rates during the first and second trimester remain low.1 Thus, reliable markers that exhibit an adequate positive predictive value for early detection of IUGR are needed. Numerous serum markers of angiogenic factors, growth factors, placental proteins, and hormones have been evaluated.11 However, to date, none of these have exhibited a strong predictive accuracy.11 Additionally, treatment options for IUGR have not been effective.8Proper development of the uteroplacental circulation is critical for adequate transfer of oxygen and nutrients to the fetus and removal of wastes from the fetus.12 Development of the uteroplacental circulation occurs to convert high-resistance vessels to low-resistance vessels to facilitate the growing needs of the developing fetus.12 Pijnenborg et al12 propose that this conversion occurs in 2 stages. The first stage is initiated from 8 to 10 weeks of age and involves endovascular plugging of the spiral arteries, followed by shallow invasion of the spiral arteries by trophoblast cells.12 The second stage occurs from 12 to 14 weeks of age and involves deeper trophoblast invasion of the spiral arteries to complete remodeling of the uteroplacental circulation.12 Therefore, on the basis of the direct link between reduced uterine perfusion and later cardiovascular risk reported by Galliard et al, early detection of pregnancies destined to be complicated by IUGR and the development of viable options to prevent impaired uteroplacental perfusion and subsequent IUGR are crucial not only for the health of the fetus and infant but also for the cardiovascular health of the IUGR individual throughout life.An additional finding of merit in this study by Galliard et al involves the reported sex difference in the association between higher umbilical artery vascular resistance and IUGR, with increased total fat mass and blood pressure in girls at 6 years of age more affected than those in boys.6 Very few studies have examined whether sex affects programmed cardiovascular risk in children. Additionally, studies of children <11 years of age differ in their findings, reporting that the inverse association between birth weight, as a crude marker for slow fetal growth, and systolic blood pressure is stronger in boys than girls13 or is present in girls but not boys.14 Differences in methods for measuring blood pressure and whether birth records or recall were used for birth weights may contribute to these discrepancies. However, further studies clearly are needed to elucidate the impact of sex on programmed cardiovascular risk.In summary, Gaillard et al6 provide a definitive link between impaired placental perfusion and slow fetal growth with programmed cardiovascular risk. Their study also indicates that sex affects cardiovascular outcome at 6 years of age after IUGR during fetal life.6 Findings from this study by Galliard and colleagues in this issue of Circulation clearly demonstrate a need for the development of reliable early markers that can identify pregnancies at risk before the initiation of events leading to IUGR and preventive or treatment options to avert the adverse impact of IUGR on gestational outcome and the long-term health of the individual. Furthermore, this study also provides merit for continued monitoring of this cohort to further investigate how IUGR affects cardiovascular risk with age and how changes in the hormonal milieu via transitions through puberty, middle age, and menopause affect the sex difference in programmed risk. Clearly, additional longitudinal cohort studies are needed to clarify the long-term impact of the developmental origins of cardiovascular disease across the life span.Sources of FundingDr Alexander is supported by National Institutes of Health grants HL074927 and HL51971. Dr Hennington is supported by Mississippi INBRE funded by grants from the National Center for Research Resources (5P20RR016476-11) and the National Institute of General Medical Sciences (8 P20 GM103476-11) from the National Institutes of Health, as well as the National Institute for Minority Health and Health Disparities 5P20MD002725.DisclosuresNone.FootnotesThe opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.Correspondence to Barbara T. Alexander, PhD, Department of Physiology and Biophysics, Women’s Health Research Center, University of Mississippi Medical Center, 2500 N State St, Jackson, MS 39216. E-mail [email protected]References1. Gebb J, Dar P. Colour Doppler ultrasound of spiral artery blood flow in the prediction of pre-eclampsia and intrauterine growth restriction.Best Pract Res Clin Obstet Gynaecol. 2011; 25:355–366.CrossrefMedlineGoogle Scholar2. 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.CrossrefMedlineGoogle Scholar3. Spence D, Stewart MC, Alderdice FA, Patterson CC, Halliday HL. Intra-uterine growth restriction and increased risk of hypertension in adult life: a follow-up study of 50-year-olds.Public Health. 2012; 126:561–565.CrossrefMedlineGoogle Scholar4. Barker DJ, Osmond C. Infant mortality, childhood nutrition, and ischaemic heart disease in England and Wales.Lancet. 1986; 1:1077–1081.CrossrefMedlineGoogle Scholar5. Ojeda NB, Grigore D, Alexander BT. Developmental programming of hypertension: insight from animal models of nutritional manipulation.Hypertension. 2008; 52:44–50.LinkGoogle Scholar6. Gaillard R, Steegers EAP, Tiemeier H, Hofman A, Jaddoe VWV. Placental vascular dysfunction, fetal and childhood growth, and cardiovascular development: the Generation R Study.Circulation. 2013; 128;2202–2210.LinkGoogle Scholar7. Mu M, Wang SF, Sheng J, Zhao Y, Li HZ, Hu CL, Tao FB. Birth weight and subsequent blood pressure: a meta-analysis.Arch Cardiovasc Dis. 2012; 105:99–113.CrossrefMedlineGoogle Scholar8. Committee on Practice Bulletins—Obstetrics. Practice Bulletin No. 134: fetal growth restriction.Obstet Gynecol. 2013; 121:1122–1133.CrossrefMedlineGoogle Scholar9. Sciscione AC, Hayes EJ; Society for Maternal-Fetal Medicine. Uterine artery Doppler flow studies in obstetric practice.Am J Obstet Gynecol. 2009; 201:121–126.CrossrefMedlineGoogle Scholar10. de Jong F, Monuteaux MC, van Elburg RM, Gillman MW, Belfort MB. Systematic review and meta-analysis of preterm birth and later systolic blood pressure.Hypertension. 2012; 59:226–234.LinkGoogle Scholar11. Conde-Agudelo A, Papageorghiou AT, Kennedy SH, Villar J. Novel biomarkers for predicting intrauterine growth restriction: a systematic review and meta-analysis.BJOG. 2013; 120:681–694.CrossrefMedlineGoogle Scholar12. Pijnenborg R, Bland JM, Robertson WB, Brosens I. Uteroplacental arterial changes related to interstitial trophoblast migration in early human pregnancy.Placenta. 1983; 4:397–413.CrossrefMedlineGoogle Scholar13. Bowers K, Liu G, Wang P, Ye T, Tian Z, Liu E, Yu Z, Yang X, Klebanoff M, Yeung E, Hu G, Zhang C. Birth weight, postnatal weight change, and risk for high blood pressure among Chinese children.Pediatrics. 2011; 127:e1272–e1279.CrossrefMedlineGoogle Scholar14. O’Sullivan J, Wright C, Pearce MS, Parker L. The influence of age and gender on the relationship between birth weight and blood pressure in childhood: a study using 24-hour and casual blood pressure.Eur J Pediatr. 2002; 161:423–427.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Yang L, Feng L, Huang L, Li X, Qiu W, Yang K, Qiu J and Li H (2023) Maternal Factors for Intrauterine Growth Retardation: Systematic Review and Meta-Analysis of Observational Studies, Reproductive Sciences, 10.1007/s43032-021-00756-3 Gantenbein K and Kanaka-Gantenbein C (2022) Highlighting the trajectory from intrauterine growth restriction to future obesity, Frontiers in Endocrinology, 10.3389/fendo.2022.1041718, 13 Schabel M, Roberts V, Gibbins K, Rincon M, Gaffney J, Streblow A, Wright A, Lo J, Park B, Kroenke C, Szczotka K, Blue N, Page J, Harvey K, Varner M, Silver R, Frias A and Stevenson G (2022) Quantitative longitudinal T2* mapping for assessing placental function and association with adverse pregnancy outcomes across gestation, PLOS ONE, 10.1371/journal.pone.0270360, 17:7, (e0270360) Tinius R, Maples J, Schafer M, Paudel A, Fortner K, Zite N and Nagpal T (2022) To Be Active or to Stop? A Cross-Sectional Retrospective Study Exploring Provider Advice and Patient Fears Surrounding Physical Activity in Pregnancies Complicated by Fetal Growth Restriction, International Journal of Environmental Research and Public Health, 10.3390/ijerph19106076, 19:10, (6076) Konwar R, Basumatary B, Dutta M, Mahanta P and Dunne N (2021) Accuracy of Fetal Weight Estimation by Ultrasonographic Evaluation in a Northeastern Region of India, International Journal of Biomaterials, 10.1155/2021/9090338, 2021, (1-7), Online publication date: 20-Dec-2021. Long J, Zhang M, Wang G, Hong X, Ji Y, Bustamante-Helfrich B, Wang X and Mueller N (2021) Association of Placental Pathology With Childhood Blood Pressure Among Children Born Preterm, American Journal of Hypertension, 10.1093/ajh/hpab097, 34:11, (1154-1162), Online publication date: 20-Nov-2021. 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November 12, 2013Vol 128, Issue 20 Advertisement Article InformationMetrics © 2013 American Heart Association, Inc.https://doi.org/10.1161/CIRCULATIONAHA.113.006323PMID: 24135070 Originally publishedOctober 17, 2013 Keywordspre-eclampsiablood pressurefetal developmentpregnancyEditorialsPDF download Advertisement" @default.
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