Preeclampsia and the cardiovascular system: An update

Perry, Helen; Khalil, Asma; Thilaganathan, B.

doi:10.1016/j.tcm.2018.04.009

Cited by 48 publications

(41 citation statements)

References 79 publications

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“…We thank Dr Gonser for his appreciation of our systematic review and his support of the hypothesis that the commonality between uterine artery and ophthalmic artery Doppler waveforms is attributed to the fact that both indices reflect maternal cardiovascular function. There are now considerable new data which support the cardiovascular origin of pre‐eclampsia,. Although we agree that ophthalmic artery Doppler assessment may prove superior to uterine artery waveform analysis in screening and diagnosis of pre‐eclampsia, data are currently lacking to support this assertion 3 .…”

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confidence: 76%

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Kalafat

Laoreti

Khalil

et al. 2019

Ultrasound in Obstet & Gyne

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confidence: 76%

“…Although we agree that ophthalmic artery Doppler assessment may prove superior to uterine artery waveform analysis in screening and diagnosis of pre‐eclampsia, data are currently lacking to support this assertion 3 . We believe it is important to explore the potential use of other arterial waveform analysis methods and, indeed, maternal echocardiography–.…”

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confidence: 99%

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Kalafat

Laoreti

Khalil

et al. 2019

Ultrasound in Obstet & Gyne

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“…Preeclampsia refers to a severe complication during pregnancy that is characterized of hypertension and proteinuria after 20 weeks of gestation in pregnant women with no evidence of previous hypertension [1][2][3]. Women with preeclampsia are at higher risk for the development of cardiovascular diseases during pregnancy and after delivery [4][5][6]. Moreover, preeclampsia has been identified as a risk factor of maternal and perinatal morbidity and mortality worldwide [1].…”

Section: Introductionmentioning

confidence: 99%

Circulating endocan and preeclampsia: a meta-analysis

Lan

Liu

2020

Bioscience Reports

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Background: Endocan, a novel protein involved in inflammation and endothelial dysfunction, has been suggested to be related to preeclampsia, although the results of previous studies were not consistent. The aim of the study was to evaluate the potential difference of circulating endocan in women with preeclampsia and those with normal pregnancy. Methods: Matched case–control studies evaluating the difference of circulating endocan between women with preeclampsia and those with normal pregnancy were identified via systematic search of PubMed and Embase databases. A random-effect model or a fixed-effect model was used to pool the results according to the heterogeneity. Subgroup analysis was performed to evaluate whether the timing of preeclampsia onset affected the outcome. Results: Overall, eight matched case–control studies, including 451 women with preeclampsia and 442 women with normal pregnancy were included. Significant heterogeneity was detected among the included studies (P for Cochrane’s Q test = 0.006, I2 = 65%). Meta-analysis with a random-effect model showed that women with preeclampsia had significantly higher circulating level of endocan compared with women with normal pregnancy (standardized mean difference = 0.37, 95% confidence interval: 0.13–0.62, P = 0.003). Subsequent subgroup analyses showed that the difference of circulating endocan between women with early onset preeclampsia and those with normal pregnancy was not statistically different from that between women with late-onset preeclampsia and those with normal pregnancy (P for subgroup difference = 0.81). Conclusions: Women with preeclampsia have higher circulating endocan than those with normal pregnancy.

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“…Distinct origins of preeclampsia have been discussed (Ness & Roberts, ), but the epidemiological and genetic associations, as well as the inflammatory, vasoactive, endocrine and metabolic perturbations, all support the key involvement of placenta and cardiovascular system in the pathophysiology of preeclampsia (Thilaganathan & Kalafat ; Perry et al . ,b). Currently, a vivid debate is ongoing as to whether the initiating process of placental dysfunction in preeclampsia is the cause or the consequence of maternal cardiovascular dysfunction (Redman ; Kalafat & Thilaganathan, ; Thilaganathan & Kalafat, ).…”

Section: Introductionmentioning

confidence: 99%

“…Irrespective of the outcome of the ongoing debate on the aetiology of preeclampsia, it is generally accepted today that the eventual clinical syndrome of preeclampsia is triggered by placental dysfunction – predominantly associated with abnormal placentation in early preeclampsia and with uteroplacental malperfusion in later disease (Redman, ; Perry et al . ,b; Thilaganathan & Kalafat, ). Despite the lack of experimentally measurable reduced oxygen concentrations in placentas of hypertensive pregnancies (Huppertz et al .…”

Section: Introductionmentioning

confidence: 99%

Preeclampsia: a gestational cardiorenal syndrome

Gyselaers

Thilaganathan

2019

The Journal of Physiology

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It is generally accepted today that there are two different types of preeclampsia: an early‐onset or placental type and a late‐onset or maternal type. In the latent phase, the first one presents with a low output/high resistance circulation eventually leading in the late second or early third trimester to an intense and acutely aggravating systemic disorder with an important impact on maternal and neonatal mortality and morbidity; the other type presents initially as a high volume/low resistance circulation, gradually evolving to a state of circulatory decompensation usually in the later stages of pregnancy, with a less severe impact on maternal and neonatal outcome. For both processes, numerous dysfunctions of the heart, kidneys, arteries, veins and interconnecting systems are reported, most of them presenting earlier and more severely in early‐ than in late‐onset preeclampsia; however, some very specific dysfunctions exist for either type. Experimental, clinical and epidemiological observations before, during and after pregnancy are consistent with gestation‐induced worsening of subclinical pre‐existing chronic cardiovascular dysfunction in early‐onset preeclampsia, and thus sharing the pathophysiology of cardiorenal syndrome type II, and with acute volume overload decompensation of the maternal circulation in late‐onset preeclampsia, thus sharing the pathophysiology of cardiorenal syndrome type 1. Cardiorenal syndrome type V is consistent with the process of preeclampsia superimposed upon clinical cardiovascular and/or renal disease, alone or as part of a systemic disorder. This review focuses on the specific differences in haemodynamic dysfunctions between the two types of preeclampsia, with special emphasis on the interorgan interactions between heart and kidneys, introducing the theoretical concept that the pathophysiological processes of preeclampsia can be regarded as the gestational manifestations of cardiorenal syndromes.

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Preeclampsia and the cardiovascular system: An update

Cited by 48 publications

References 79 publications

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Circulating endocan and preeclampsia: a meta-analysis

Preeclampsia: a gestational cardiorenal syndrome

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