Cardiovascular System in Preeclampsia and Beyond

Thilaganathan, B.; Kalafat, Erkan

doi:10.1161/hypertensionaha.118.11191

Cited by 188 publications

(182 citation statements)

References 126 publications

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“…; Foo et al . ; Thilaganathan & Kalafat, ) and worsening maternal cardiovascular function with the increased volume load of pregnancy (Melchiorre et al . ; Buddeberg et al .…”

Section: Cardiorenal Interactions In the Pathophysiology Of Preeclampsiamentioning

confidence: 99%

“…The precise aetiology of preeclampsia remains to be determined, and because of countless hypotheses postulated over time, preeclampsia has been labelled ‘the disease of theories’ (Jeffcoate ; Schlembach ). 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).…”

Section: Introductionmentioning

confidence: 99%

“…,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, ). The placental origins hypothesis is supported by the evidence for a role of placentally mediated vasoactive factors in the pathophysiology of preeclampsia (Redman, ), whereas the haemodynamic model is supported by evidence for subclinical maternal cardiovascular dysfunction both preconceptually and post‐partum in women who developed preeclampsia (Melchiorre et al .…”

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%

“…The precise aetiology of preeclampsia remains to be determined, and because of countless hypotheses postulated over time, preeclampsia has been labelled 'the disease of theories' (Jeffcoate 1966;Schlembach 2003). Distinct origins of preeclampsia have been discussed (Ness & Roberts, 1996), but the epidemiological and genetic associations, as well as the inflammatory, vasoactive, endocrine and metabolic perturbations, all support the key involvement of placenta and cardio-vascular system in the pathophysiology of preeclampsia (Thilaganathan & Kalafat 2019;Perry et al 2018a,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 2014;Kalafat & Thilaganathan, 2017;Thilaganathan & Kalafat, 2019).…”

Section: Introductionmentioning

confidence: 99%

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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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“…; Foo et al . ; Thilaganathan & Kalafat, ) and worsening maternal cardiovascular function with the increased volume load of pregnancy (Melchiorre et al . ; Buddeberg et al .…”

Section: Cardiorenal Interactions In the Pathophysiology Of Preeclampsiamentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Preeclampsia: a gestational cardiorenal syndrome

Gyselaers

Thilaganathan

2019

The Journal of Physiology

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Preeclampsia: Linking Placental Ischemia with Maternal Endothelial and Vascular Dysfunction

Bakrania

Spradley

Drummond

et al. 2020

Comprehensive Physiology

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Decreased flow‐mediated dilation in gestational diabetes in pregnancy and post‐partum. A systematic review and meta‐analysis

Chatzakis

Koletsos

Tirta

et al. 2022

Diabetes Metabolism Res

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Aims Gestational diabetes mellitus (GDM) is a common medical complication during pregnancy. Endothelial dysfunction is considered an early step in the progression of atherosclerosis that may contribute to subclinical target organ damage. This meta‐analysis aimed to systemically review the existing data regarding endothelial dysfunction between women with and without GDM during pregnancy and post‐partum using flow‐mediated dilation (FMD). Materials and Methods Eligible studies (cohort and observational) published until October 2021 were identified in the MEDLINE, Scopus, Cochrane Library database and grey literature sources were searched. Results The search yielded 2272 studies, of which 17 were fully reviewed and 12 studies (N = 740 pregnant women) were finally included. Pregnant women with GDM exhibited a significantly lower FMD compared to pregnant women without GDM (pooled mean difference −3.12; 95% CI −5.36 to −0.88). Moreover, in the immediate (1–6 months) post‐partum period, women with previous GDM showed lower FMD compared to healthy women without GDM history (pooled mean difference −7.52; 95% CI −9.44 to −5.59), whereas FMD did not differ in the late post‐partum period (more than 4 years). Conclusions Flow‐mediated dilation is decreased in women with GDM during pregnancy and in the immediate post‐partum period, compared to women without GDM, indicating that the endothelial dysfunction noted during the pregnancy in those women persists in the immediate post‐partum period too. Clinical trial registration PROSPERO CRD42021283113 (http://www.ClinicalTrials.gov).

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Cardiovascular System in Preeclampsia and Beyond

Abstract: Supplemental Digital Content is available in the text.

Cited by 188 publications

References 126 publications

Preeclampsia: a gestational cardiorenal syndrome

Preeclampsia: a gestational cardiorenal syndrome

Preeclampsia: Linking Placental Ischemia with Maternal Endothelial and Vascular Dysfunction

Decreased flow‐mediated dilation in gestational diabetes in pregnancy and post‐partum. A systematic review and meta‐analysis

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