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dc.creatorBouchlariotou, S.en
dc.creatorLiakopoulos, V.en
dc.creatorDovas, S.en
dc.creatorGiannopoulou, M.en
dc.creatorKiropoulos, T.en
dc.creatorZarogiannis, S.en
dc.creatorGatselos, G.en
dc.creatorZachopoulos, T.en
dc.creatorKyriakou, D. S.en
dc.creatorKallitsaris, A.en
dc.creatorMessinis, I.en
dc.creatorStefanidis, I.en
dc.date.accessioned2015-11-23T10:24:04Z
dc.date.available2015-11-23T10:24:04Z
dc.date.issued2008
dc.identifier10.1159/000112807
dc.identifier.issn0250-8095
dc.identifier.urihttp://hdl.handle.net/11615/26389
dc.description.abstractBackground: Non-dipping pattern of circadian blood pressure in preeclampsia is associated with an increased risk of cardiovascular disease. The pathogenetic mechanisms of this relationship are still unclear. We investigated whether non-dipping in preeclampsia could relate to endothelial activation or damage. Methods: Participants, 20 women with normal pregnancy (mean age 29.9 +/- 5.7 years) and 31 women with preeclampsia (mean age 29.1 +/- 5.1 years), underwent 24-hour ambulatory blood pressure monitoring. Plasma levels of von Willebrand factor (vWf), marker of endothelial damage and of soluble adhesion molecules (sVCAM-1, sICAM-1), and markers of endothelial activation were determined using commercially available enzyme-linked immunoassays. Results: Based on whether the nocturnal mean arterial pressure (MAP) relative to the daytime MAP declined by less than 10%, 21 women with preeclampsia were categorized as non-dippers. Compared to healthy pregnant women, patients with preeclampsia showed significantly enhanced levels of vWf (206.9 +/- 40.6 vs. 123 +/- 24 IU/dl; p < 0.01) and sVCAM-1 (2,269 +/- 426 vs. 1,159.+/- 8 340 ng/ml; p < 0.01). In addition, significantly higher levels of vWf (224.5 +/- 34.9 vs. 170 +/- 23 IU/dl; p < 0.01) and sVCAM-1 (2,405 +/- 421.4 vs. 1,983 +/- 276.7 ng/ml; p = 0.007) were determined, when women with preeclampsia and nocturnal hypertension (non-dippers) were compared to dippers. The results were similar even after adjustment for severity of preeclampsia. In contrast, neither preeclampsia nor dipping status had an effect on sICAM-1 levels. Conclusion: Nocturnal hypertension in preeclampsia is associated with elevated levels of molecules related to endothelial damage. Endothelial damage is a recognized pathogenetic factor for atherosclerosis and history of preeclampsia is a risk factor for cardiovascular disease. In this context, possible clinical implications of our findings deserve further investigation. Copyright (C) 2007 S. Karger AG, Basel.en
dc.sourceAmerican Journal of Nephrologyen
dc.source.uri<Go to ISI>://WOS:000253777700009
dc.subjectblood pressureen
dc.subjectcircadian rhythmen
dc.subjectendothelial damageen
dc.subjectpreeclampsiaen
dc.subjectVON-WILLEBRAND-FACTORen
dc.subjectBLOOD-PRESSURE VARIABILITYen
dc.subjectADHESION MOLECULEen
dc.subjectDISEASEen
dc.subjectPREGNANCYen
dc.subjectRISKen
dc.subjectCELLSen
dc.subjectVCAM-1en
dc.subjectUrology & Nephrologyen
dc.titleNocturnal hypertension is associated with an exacerbation of the endothelial damage in preeclampsiaen
dc.typejournalArticleen


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