Usefulness of a placental profile in high-risk pregnancies

Toal, Meghana; Chan, Cynthia; Fallah, Shafagh; Alkazaleh, Fawaz; Chaddha, Vandana; Windrim, Rory; Kingdom, John

doi:10.1016/j.ajog.2006.10.897

Cited by 102 publications

(78 citation statements)

References 21 publications

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“…[59][60][61] In women with risk factors for intrauterine growth restriction, uterine artery doppler screening at 19 to 23 weeks may identify pregnancies at risk of antepartum stillbirth and preterm delivery due to intrauterine growth restriction and placental disease. 62 In pregnancies in which intrauterine growth restriction due to uteroplacental vascular insufficiency is diagnosed, maternal surveillance for the development of severe preeclampsia with adverse features is warranted. 63,64 Evaluation of placental function by umbilical artery doppler is a clinical standard to distinguish between SGA and FGR.…”

Section: Screening and Diagnosismentioning

confidence: 99%

Fetal growth restriction: aetiology, screening, diagnosis and management

Augusthy

2015

Int J Reprod Contracept Obstet Gynecol

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Foetal growth restriction (FGR) is a pathological condition that refers to a foetus that fails to reach his/her genetically predetermined growth potential. FGR remains a leading contributor to perinatal mortality and morbidity and metabolic syndrome in later life. The purpose of this review is to provide the summary statements of the aetiology of FGR and to establish a framework for screening, diagnosis, and management of pregnancies affected with foetal growth restriction. For this study, published literature was retrieved through searches of PubMed (Medline), Highwire, Google Scholar, Scopus, Cochrane Database of Systematic Reviews. Conference/Seminar proceedings, textbooks, previously published systematic reviews, controlled clinical trials, high quality prospective and retrospective observational studies, research articles and unpublished studies were also used for this study. The identification of FGR begins with assessment of maternal, foetal, placental and environmental risk factors and the diagnosis is made by Ultrasound biometry examination. Functional assessment of placental and foetal circulation by Doppler velocimetry and blood flow volume, together with computerized assessment of foetal heart rate variability, are key examinations in early and late FGR to assess severity of the disease and monitor foetal wellbeing. Appropriate timing of delivery in early FGR might change the outcome, and appropriate monitoring in late and term FGR might avoid unnecessary interventions.

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Section: Screening and Diagnosismentioning

confidence: 99%

Fetal growth restriction: aetiology, screening, diagnosis and management

Augusthy

2015

Int J Reprod Contracept Obstet Gynecol

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“…Because Ͼ 70% of infarcted placentas are small-for-dates 59 and small dysmorphic placentas on ultrasound scanning (Ͻ 10 cm long at 19-22 weeks' gestation), 58 increase the risk of severe PE and IUGR, 105 we have combined these tests in high-risk clinical practice routinely since 2007, when we demonstrated that normal tests substantially reduce the risk extreme preterm birth from severe PE/HELLP syndrome (odds ratio, 0.2; 95% CI, 0.1-0.4) and severe early-onset IUGR (odds ratio, 0). 106 With the use of this concept we subsequently screened our high-risk population for multiparameter placental dysfunction to recruit to our pilot HEPRIN (HEparin for the PRevention of placental INsufficiency) trial that was recently reported. 107 Of ϳ 250 women screened, we randomly assigned 32 of 41 eligible women to either 7500 IU of UFH twice daily or no drug.…”

Section: Implications For the Design Of Future Heparin Trialsmentioning

confidence: 99%

Is heparin a placental anticoagulant in high-risk pregnancies?

Kingdom

Drewlo

2011

Blood

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Randomized control trials show beneficial effects of heparin in high-risk pregnancies to prevent preeclampsia and intrauterine growth restriction. However, the lack of placental pathology data in these trials challenges the assumption that heparin is a placental anticoagulant. Recent data show that placental infarction is probably associated with abnormalities in development of the placenta, characterized by poor maternal perfusion and an abnormal villous trophoblast compartment in contact with maternal blood, than with maternal thrombophilia. At-risk pregnancies may therefore be predicted by noninvasive prenatal testing of placental function in mid-pregnancy. Heparin has diverse cellular functions that include direct actions on the trophoblast. Dissecting the non-anticoagulant actions of heparin may indicate novel and safer therapeutic targets to prevent the major placental complications of pregnancy. IntroductionA small subset of reproductive-aged women require anticoagulation in the context of a mechanical heart valve 1 or to prevent recurrent venous thromboembolism as in women with antiphospholipid syndrome. 2 When planning pregnancy, they mostly convert from an oral anticoagulant such as Coumadin to subcutaneous injections of heparin to avoid the potential embryopathy induced by transplacental passage of Coumadin. 3 By doing so, they expose themselves to relatively minor side effects such as skin bruising and, because heparin promotes bone loss, to the rare possibility of vertebral bone compression fractures and neurologic complications. 4 In this context heparin is a success story for women whose predecessors were counseled to avoid attempts at motherhood. More than 35 years ago the concept of placental anticoagulation was proposed for women in subsequent pregnancies after recurrent placental infarction. 5 Since then we have witnessed an exponential increase in the prescription of heparin to pregnant women for a wide variety of indications, based on a common theme that superior placental function can be attained via its anticoagulant properties. The fashion has spread widely according to claims that heparin promotes successful implantation after in vitro fertilization, 6,7 prevents recurrent miscarriages, 8 promotes better outcomes in the perinatal period, 9 and, finally, may be used vaginally to induce labor in full-term pregnancies. 10 A common aspect of these studies is the use of safer low molecular weight heparins (LMWHs) in prophylactic regimes that have a low risk of serious side effects when used over a relatively short duration of time in pregnancy. However, the current cost per pregnancy to prescribe prophylactic LMWH is ϳ $3000, a significant burden to uninsured women in countries, such as Canada, with variable employer-based drug plans. Ongoing use of such drugs for these indications in pregnancy therefore deserves more rigorous evidence. Recent impressive but negative trials are making progress by limiting the scope of use in women with recurrent miscarriage. Heparins are complex macromol...

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“…The primary outcome of these clinical trials has typically consisted of a composite clinical outcome, including preeclampsia, small for gestational age, placental abruption, and maternal or perinatal death. However, the risk of recurrent severe preeclampsia even in these 'high-risk' populations is at most 30%, as most women develop normal placental function in a subsequent pregnancy, and the anticipated effect size was likely significantly underestimated, reducing the power of these trials [48,49].…”

Section: Patient Selectionmentioning

confidence: 99%

“…A potential strategy for improved inclusion criteria to identify pregnant women at the highest risk of developing early-onset preeclampsia with FGF into clinical trials is one that would include the assessment of placental and maternal cardiovascular function in the current pregnancy, in tandem with comprehensive assessment of clinical risk factors [5,48]. The likelihood of placental dysfunction can be assessed using placental ultrasound as early as the first trimester in pregnant women who subsequently develop severe preeclampsia [53].…”

Section: Patient Selectionmentioning

confidence: 99%

Low molecular weight heparin for the prevention of severe preeclampsia: where next?

McLaughlin

Scholten

Parker

et al. 2018

Brit J Clinical Pharma

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Low molecular weight heparin has been extensively evaluated for the prevention of preeclampsia in high-risk pregnant women; however, the results from these trials have been conflicting. This review discusses the potential mechanisms of action of low molecular weight heparin for the prevention of severe preeclampsia, how to optimize the selection of high-risk women for participation in future trials, and the importance of trial standardization. Preeclampsia preventionPreeclampsia is a hypertensive disorder of pregnancy, clinically diagnosed by new-onset hypertension after 20 weeks' gestation with evidence of organ injury [1]. The potential maternal and perinatal complications of preeclampsia are significant, including maternal seizures, fetal growth restriction (FGR) and stillbirth. Approximately 5% of women develop preeclampsia, with the majority of women experiencing mild preeclampsia that occurs near term and is safely managed by delivery [2]. Only 1% of pregnant women develop early-onset preeclampsia, where both the maternal and fetal implications are substantially greater, typically resulting in FGR and the need for iatrogenic preterm delivery before 34 weeks' gestation [2]. Early-onset preeclampsia is hypothesized to be a direct consequence of the interactions between a dysfunctional placenta and maternal cardiovascular system, while late-onset preeclampsia is hypothesized to be largely triggered by maternal constitutional factors [3][4][5]. Typically, women with early-onset preeclampsia present with an acute, severe syndrome that threatens the life of both the mother and her fetus. In contrast, late-onset preeclampsia is a less severe illness with a favourable clinical outcome in countries with well-developed maternity systems. However, in countries with limited medical resources, preeclampsia remains among the most frequent causes of maternal death [6].The early-and late-onset subsets of preeclampsia exhibit different types and severity of placental pathologies and express divergent maternal haemodynamics. Early-onset preeclampsia is strongly associated with placental disease characterized by maternal vascular malperfusion, where the abnormal placental villi secrete excessive amounts of antiangiogenic proteins and reduced levels of pro-angiogenic proteins into the maternal circulation [7][8][9]. Women with early-onset disease, typically associated with FGR, develop hypertension earlier in pregnancy that is characterized by increased systemic vascular resistance, reduced cardiac output and stroke volume along with relative bradycardia [5]. In contrast, late-onset preeclampsia is less commonly associated with severe placental disease, and consequently exhibits less British Journal of Clinical Pharmacology Br J Clin Pharmacol (2018) 84 673-678 673

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Usefulness of a placental profile in high-risk pregnancies

Cited by 102 publications

References 21 publications

Fetal growth restriction: aetiology, screening, diagnosis and management

Fetal growth restriction: aetiology, screening, diagnosis and management

Is heparin a placental anticoagulant in high-risk pregnancies?

Low molecular weight heparin for the prevention of severe preeclampsia: where next?

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