Difference of endothelial function during pregnancies as a method to predict preeclampsia

Brandão, Augusto Henriques Fulgêncio; Félix, Lara Rodrigues; Patrício, Evilane do Carmo; Leite, Henrique Vítor; Cabral, Antônio Carlos Vieira

doi:10.1007/s00404-014-3243-3

Cited by 31 publications

(29 citation statements)

References 24 publications

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“…Most studies observed lower FMD in the first and second trimesters among high-risk women who subsequently developed preeclampsia [50, 49, 64, 51, 63, 54]. These included studies in women with risk factors for preeclampsia [64], studies that combined low and high-risk women [54, 49, 74], and studies that compared low-risk women to high-risk women who subsequently developed preeclampsia [50, 51].…”

Section: Fmd and Preeclampsiamentioning

confidence: 99%

“…Lower FMD may be more apparent closer to diagnosis. FMD did not differ between women who later developed preeclampsia and those who did not at 16-20 weeks gestation, but was lower in women who later developed preeclampsia at 24-28 weeks [63]. Among women with Type 1 diabetes, FMD was not different between those who later developed preeclampsia and those who did not [62].…”

Section: Fmd and Preeclampsiamentioning

confidence: 99%

See 1 more Smart Citation

Flow-Mediated Dilation: Can New Approaches Provide Greater Mechanistic Insight into Vascular Dysfunction in Preeclampsia and Other Diseases?

Weissgerber

2014

Curr Hypertens Rep

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Endothelial dysfunction is a key feature of preeclampsia, and may contribute to increased cardiovascular disease risk years after pregnancy. Flow-mediated dilation (FMD) is a non-invasive endothelial function test that predicts cardiovascular event risk. New protocols allow researchers to measure three components of the FMD response: FMD, low flow-mediated constriction and the shear stimulus. This review encourages researchers to think beyond “low FMD” by examining how these three components may provide additional insights into the mechanisms and location of vascular dysfunction. The review then examines what FMD studies reveal about vascular dysfunction in preeclampsia, while highlighting opportunities to gain greater mechanistic insight from new protocols. Studies using traditional protocols show that FMD is low in mid-pregnancy prior to preeclampsia, at diagnosis, and for three years post-partum. However, FMD returns to normal by ten years post-partum. Studies using new protocols are needed to gain more mechanistic insight.

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Section: Fmd and Preeclampsiamentioning

confidence: 99%

Section: Fmd and Preeclampsiamentioning

confidence: 99%

Flow-Mediated Dilation: Can New Approaches Provide Greater Mechanistic Insight into Vascular Dysfunction in Preeclampsia and Other Diseases?

Weissgerber

2014

Curr Hypertens Rep

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“…PE could develop at early gestational age <34 weeks or late gestational age ≥34 weeks (Jardim et al, 2015). Early PE is generally linked to compromised trophoblast invasion, placental hypoxia and release of bioactive factors that could target the endothelium, while late PE has been linked to preexisting maternal conditions that could affect endothelial integrity (Brandao et al, 2014). Nevertheless, endothelial dysfunction is present in both early and late PE (Brandao et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

“…Early PE is generally linked to compromised trophoblast invasion, placental hypoxia and release of bioactive factors that could target the endothelium, while late PE has been linked to preexisting maternal conditions that could affect endothelial integrity (Brandao et al, 2014). Nevertheless, endothelial dysfunction is present in both early and late PE (Brandao et al, 2014). Interestingly, PE remits after delivery, pointing to the placenta as the main culprit.…”

Section: Introductionmentioning

confidence: 99%

Mechanisms of Endothelial Dysfunction in Hypertensive Pregnancy and Preeclampsia

Possomato-Vieira

Khalil

2016

Advances in Pharmacology

176

117

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Preeclampsia is a pregnancy-related disorder characterized by hypertension, and could lead to maternal and fetal morbidity and mortality. Although the causative factors and pathophysiological mechanisms are unclear, endothelial dysfunction is a major hallmark of preeclampsia. Clinical tests and experimental research have suggested that generalized endotheliosis in the systemic, renal, cerebral and hepatic circulation could decrease endothelium-derived vasodilators such as nitric oxide, prostacyclin and hyperpolarization factor and increase vasoconstrictors such as endothelin-1 and thromboxane A2, leading to increased vasoconstriction, hypertension and other manifestation of preeclampsia. In search for the upstream mechanisms that could cause endothelial dysfunction, certain genetic, demographic and environmental risk factors have been suggested to cause abnormal expression of uteroplacental integrins, cytokines and matrix metalloproteinases, leading to decreased maternal tolerance, apoptosis of invasive trophoblast cells, inadequate spiral arteries remodeling, reduced uterine perfusion pressure (RUPP), and placental ischemia/hypoxia. RUPP may cause imbalance between the anti-angiogenic factors soluble fms-like tyrosine kinase-1 and soluble endoglin and the pro-angiogenic factors vascular endothelial growth factor and placental growth factor, or stimulate the release of other circulating bioactive factors such as inflammatory cytokines, hypoxia-inducible factor-1, reactive oxygen species, and angiotensin AT1 receptor agonistic autoantibodies. These circulating factors could then target endothelial cells and cause generalized endothelial dysfunction. Therapeutic options are currently limited, but understanding the factors involved in endothelial dysfunction could help design new approaches for prediction and management of preeclampsia.

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“…Therefore, to test our hypothesis, we performed immunohistochemical staining with the CD94/NKG2A monoclonal antibody in the deciduae of normal, C/S, and pre-eclamptic parturitions, and counted them using the unbiased physical disector method. Additionally, we performed volumetric analyses on both the placental villi and villous blood vessels could be related with endothelial dysfunction [11].…”

Section: Introductionmentioning

confidence: 99%

Is parturition-timing machinery related to the number of inhibitor CD94/NKG2A positive uterine natural killer cells?

Mazi

Altunkaynak

Aydin

et al. 2015

Arch Gynecol Obstet

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Difference of endothelial function during pregnancies as a method to predict preeclampsia

Abstract: The difference of FMD values between the second trimester of pregnancy can be used for PE prediction for both, early and late forms of PE.

Cited by 31 publications

References 24 publications

Flow-Mediated Dilation: Can New Approaches Provide Greater Mechanistic Insight into Vascular Dysfunction in Preeclampsia and Other Diseases?

Flow-Mediated Dilation: Can New Approaches Provide Greater Mechanistic Insight into Vascular Dysfunction in Preeclampsia and Other Diseases?

Mechanisms of Endothelial Dysfunction in Hypertensive Pregnancy and Preeclampsia

Is parturition-timing machinery related to the number of inhibitor CD94/NKG2A positive uterine natural killer cells?

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