2018
DOI: 10.1016/j.ejogrb.2018.04.003
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Endothelial dysfunction as a long-term effect of late onset hypertensive pregnancy disorders: High BMI is key

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Cited by 13 publications
(9 citation statements)
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“…Pre-pregnancy obesity has been reported to be an independent risk factor for subsequent hypertension among women who ever experienced preeclampsia [43]. Furthermore, women may have elevated markers of long-term endothelial dysfunction if they were overweight before developing preeclampsia [44]. Although we restricted our analysis to women with complete information on antenatal BMI, we cannot rule out the possibility of unmeasured confounding from dyslipidaemia or recurrent preeclampsia, particularly if women with a first episode of preeclampsia received anti-hypertensive treatment or alternative cardio-protective intervention post partum.…”
Section: Plos Medicinementioning
confidence: 99%
“…Pre-pregnancy obesity has been reported to be an independent risk factor for subsequent hypertension among women who ever experienced preeclampsia [43]. Furthermore, women may have elevated markers of long-term endothelial dysfunction if they were overweight before developing preeclampsia [44]. Although we restricted our analysis to women with complete information on antenatal BMI, we cannot rule out the possibility of unmeasured confounding from dyslipidaemia or recurrent preeclampsia, particularly if women with a first episode of preeclampsia received anti-hypertensive treatment or alternative cardio-protective intervention post partum.…”
Section: Plos Medicinementioning
confidence: 99%
“…It is believed that endothelial cells phagocytose the deported trophoblasts and apoptosis-derived debris to suppress the activation of endothelial cells caused by the low level of necrotic trophoblastic debris during normal pregnancy (Chen et al, 2006; Chen Q. et al, 2012). When this process becomes dysregulated, the apoptotic trophoblastic debris-mediated protection of endothelial cells is lost and excessive necrotic debris of trophoblasts could then activate endothelial cells or prevent them from self-renewal (Kertesz et al, 2000; Gupta et al, 2005c), consistent with endothelial injury being the pathological hallmark of PE (Alma et al, 2018).…”
Section: Sdevs and Pe-associated Endothelial Injurymentioning
confidence: 99%
“…The probable explanation might be that high occurrence of cardiovascular disease such as hypertension, hyperlipidemia and diabetes along with the increasing BMI contributed to the damage of microvascular endothelial structure. 38 …”
Section: Resultsmentioning
confidence: 99%