Pre‐eclampsia: Contribution of Maternal Constitutional Factors and the Consequences for Cardiovascular Health

Barden, Anne

doi:10.1111/j.1440-1681.2006.04448.x

Cited by 38 publications

(28 citation statements)

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“…In this respect, it has been linked to inflammation in the pathogenesis of hypertension [34] and particularly, in preeclampsia [44]. Furthermore, its impact on the development of longterm cardiovascular disease is being evaluated [45]. Recent publications have also considered chronic subclinical inflammation as a pathophysiological factor causing type 2 diabetes, gestational diabetes, the metabolic syndrome, obesity, atherosclerotic cardiovascular disease and myocardial infarction [46].…”

Section: Discussionmentioning

confidence: 99%

Biochemical Profiling Study in Umbilical Cord Blood as Predictors of Neonatal Damage

Gruccio¹

2014

Int J Clin Pediatr

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Background: During pregnancy inflammatory, metabolic and immunologic disorders that affect differently the fetus, are known. These could be early disorders: abortion, intrauterine growth retardation, low birth weight and neonatal death; or late disorders: cardiovascular and metabolic disease in adults. The objective was to analyze different biochemical parameters in maternal venous blood and newborn's umbilical cord blood (UCB) from healthy and pathological mothers for early detection of future perinatal complications. Methods:Maternal venous blood (283) and UCB (283) were analyzed. The patients were consecutively, prospectively and transversally studied. Delivery: cesarean section. Mothers and newborns were classified: control group (C) (n = 99) and pathological group (P) (n = 184). Glucose, urea, creatinine, uric acid (UA), bilirubin (Bi), proteins (PT), albumin (Alb), transaminases (ALT/AST), alkaline phosphatase, gamma-glutamyl transpeptidase (GGT), creatinkinasa (CK), lactate dehydrogenase (LDH), iron, calcium, phosphorus, magnesium, sodium, potassium (K), chlorine, cholesterol (Chol), triglycerides (TG) and hsCRP were determined by recommended methods. Student's t and Mann-Whitney tests were applied, P < 0.05.Results: P newborns from P mothers showed significant decrease: in gestation weeks (GW) and newborn weight (NW) with respect to C newborns from C mothers (P < 0.001); significant increases in Chol, TG, UA, K, Bi, AST and GGT (P: 0.01, < 0.001, 0.03, < 0.001, 0.04, < 0.001, < 0.001, respectively) and significant decreases in CK, PT and Alb (P < 0.001). P mothers showed significant increase in UA, ALT, AST, GGT (P: 0.04, 0.02, 0.04, < 0.001, respectively) with respect to C mothers. Conclusions:The decrease in GW and NW in P newborns with respect to C would be related to intrauterine growth restriction (IUGR) accompanying these disorders; increases in Chol, TG, UA, K, Bi, AST and GGT would be related to cellular destruction associated to maternal disorders and deficit in pulmonary development by IUGR respectively, whereas decreases in CK, PT and Alb to IUGR. Increase in UA, ALT, AST and GGT from P mothers with respect to C would be associated to inflammatory process with liver alterations. A future study including greater number of samples and analysis of each maternal disorder is proposed to obtain early markers of neonatal damage and to prevent future perinatal complications.

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Section: Discussionmentioning

confidence: 99%

Biochemical Profiling Study in Umbilical Cord Blood as Predictors of Neonatal Damage

Gruccio¹

2014

Int J Clin Pediatr

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“…4 Both pregnant and nonpregnant rats overexpressing sFlt-1 protein have high BP, proteinuria, and endotheliosis, the hallmarks of pre-eclampsia. 5 Although pre-eclampsia is a placenta-related disease, not all pregnant women with low placental perfusion develop preeclampsia, 6 and women who have had pre-eclampsia often develop cardiovascular diseases later in life, 7,8 suggesting that maternal factors can predispose to pre-eclampsia. 8,9 Pregnant women with pre-existing microvascular diseases, such as hypertension, diabetes, and insulin resistance, have an increased risk of pre-eclampsia.…”

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confidence: 99%

“…5 Although pre-eclampsia is a placenta-related disease, not all pregnant women with low placental perfusion develop preeclampsia, 6 and women who have had pre-eclampsia often develop cardiovascular diseases later in life, 7,8 suggesting that maternal factors can predispose to pre-eclampsia. 8,9 Pregnant women with pre-existing microvascular diseases, such as hypertension, diabetes, and insulin resistance, have an increased risk of pre-eclampsia. 8,10,11 Mice lacking eNOS have high BP, insulin resistance, hyperlipidemia, and decreased production of nitric oxide (NO).…”

mentioning

confidence: 99%

“…8,9 Pregnant women with pre-existing microvascular diseases, such as hypertension, diabetes, and insulin resistance, have an increased risk of pre-eclampsia. 8,10,11 Mice lacking eNOS have high BP, insulin resistance, hyperlipidemia, and decreased production of nitric oxide (NO). 12 Some, but not all, investigators report that NOS3 polymorphisms leading to lower NO production are associated with hypertension 13 and/or preeclampsia.…”

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confidence: 99%

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eNOS Deficiency Acts through Endothelin to Aggravate sFlt-1–Induced Pre-Eclampsia–Like Phenotype

Hagaman

Kim

et al. 2012

Journal of the American Society of Nephrology

109

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Excess soluble fms-like tyrosine kinase 1 (sFlt-1) of vascular endothelial growth factor receptor 1 secreted from the placenta causes pre-eclampsia-like features by antagonizing vascular endothelial growth factor signaling, which can lead to reduced endothelial nitric oxide synthase (eNOS) activity; the effect of this concomitant decrease in eNOS activity is unknown. We tested whether the decrease in nitric oxide occurring in female mice lacking eNOS aggravates the pre-eclampsia-like phenotype induced by increased sFlt-1. Untreated eNOS-deficient female mice had higher BP than wild-type mice. Adenovirus-mediated overexpression of sFlt-1 increased systolic BP by approximately 27 mmHg and led to severe loss of fenestration of glomerular capillary endothelial cells in both eNOS-deficient and wild-type mice. However, only the eNOS-deficient sFlt-1 mice exhibited severe foot process effacement. Compared with wild-type sFlt-1 mice, eNOS-deficient sFlt-1 mice also showed markedly higher urinary albumin excretion (467674 versus 174623 mg/d), lower creatinine clearance (126629 versus 452663 ml/min), and more severe endotheliosis. Expression of preproendothelin-1 (ET-1) and its ET A receptor in the kidney was higher in eNOS-deficient sFlt-1 mice than in wild-type sFlt-1 mice. Furthermore, the selective ET A receptor antagonist ambrisentan attenuated the increases in BP and urinary albumin excretion and ameliorated endotheliosis in both wild-type and eNOS-deficient sFlt-1 mice. Ambrisentan improved creatinine clearance and podocyte effacement in eNOS-deficient sFlt-1 mice. In conclusion, reduced maternal eNOS/nitric oxide exacerbates the sFlt1-related pre-eclampsia-like phenotype through activation of the endothelin system. Pre-eclampsia is a pregnancy-related disease characterized by high BP and proteinuria, and affects 3%-5% of all pregnancies. 1,2 Although the etiology of pre-eclampsia is not fully understood, it is widely accepted that placental hypoxia/ischemia increases the production by the placenta of soluble fms-like tyrosine kinase 1 (sFlt-1) and soluble endoglin, and likely other factors. 1 Increased sFlt-1 is recognized as one of the most important causal factors for maternal symptoms of pre-eclampsia. 1 sFlt-1 is a splice variant of vascular endothelial growth factor (VEGF) receptor-1 that lacks the cytoplasmic and transmembrane domains, but retains the ligandbinding domain. sFlt-1 decreases the chance of VEGF binding to its signaling receptor, and reduces the phosphorylation of Ser 1177 of endothelial nitric oxide synthase (eNOS) by VEGF and the activity of eNOS. 3 Plasma concentration of sFlt-1 is

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“…45,46 It has been proposed that maternal constitutional factors, including the metabolic syndrome, may be a possible underlying mechanism common to cardiovascular disease and preeclampsia. 47,48 Also, the offspring of women from a preeclamptic pregnancy have a greater cardiovascular risk, and intrauterine exposure to preeclampsia is associated with increased risk of hypertension in the adolescent offspring. 49,50 The mechanisms remain unknown.…”

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confidence: 99%

Learning From the Placenta

2010

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Abstract-Preeclampsia is a common and potentially lethal pregnancy complication for women and offspring. Women who develop preeclampsia also run a long-term augmented risk of cardiovascular disease and premature death, and two theories are discussed. Women developing preeclampsia and persons developing cardiovascular disease may have common risk factors, which are unmasked by the "stress" of pregnancy. Alternatively, a new risk factor might occur de novo during the preeclamptic pregnancy. In preeclampsia, lipid deposition in walls of the maternal uterine arteries leading to the placenta, named spiral arteries, regularly occurs. These vascular lesions resemble early stages of atherosclerosis and are named "acute atherosis" and is thought to regress after delivery. The mechanisms that contribute to acute atherosis in preeclampsia are largely unknown, but are related to the impaired vascular remodeling of the spiral arteries in the first half of pregnancy. One striking feature is that the development of these "atherosclerosis-like" lesions requires a few months in pregnancy and may be partly linked to invasion of trophoblasts (specialized fetally derived placenta cells). We summarize normal and pathological vessel remodeling in pregnancy and discuss similarities and differences between preeclampsia and arteriosclerosis. The transient appearance of acute atherosis of uterine wall spiral arteries seen in pregnancy complications and the molecular interaction between trophoblast, smooth muscle and vascular cells could add important elements to explain arteriosclerosis and stenosis in cardiovascular disease. Preeclampsia affects 5% to 7% of all pregnancies and is a major health problem, 1 being responsible for Ϸ50 000 maternal deaths annually. 2 Children and mothers who have undergone a preeclamptic pregnancy experience an increased long-term cardiovascular risk. 3 The diagnosis is based on increased blood pressure in normally normotensive women and the development of proteinuria at Ͼ20 weeks of pregnancy. 4 Although the pathogenesis is still unclear, factors such as oxidative stress, circulating placenta-derived factors, immunologic defects, and genetic variance may all be important.

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Pre‐eclampsia: Contribution of Maternal Constitutional Factors and the Consequences for Cardiovascular Health

Cited by 38 publications

References 63 publications

Biochemical Profiling Study in Umbilical Cord Blood as Predictors of Neonatal Damage

Biochemical Profiling Study in Umbilical Cord Blood as Predictors of Neonatal Damage

eNOS Deficiency Acts through Endothelin to Aggravate sFlt-1–Induced Pre-Eclampsia–Like Phenotype

Learning From the Placenta

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