title: Nocturnal hypertension is associated with an exacerbation of the endothelial damage in preeclampsia.
abstract: BACKGROUND
  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.
  
  
  CONCLUSIONS
  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.
authors: Department of Nephrology, School of Medicine, University of Thessaly, Larissa, Greece.
authors: Sofia
authors: S
authors: Bouchlariotou
authors: Vassilios
authors: V
authors: Liakopoulos
authors: Spiros
authors: S
authors: Dovas
authors: Myrto
authors: M
authors: Giannopoulou
authors: Theodoros
authors: T
authors: Kiropoulos
authors: Sotirios
authors: S
authors: Zarogiannis
authors: Georgios
authors: G
authors: Gatselos
authors: Thomas
authors: T
authors: Zachopoulos
authors: Despina S
authors: DS
authors: Kyriakou
authors: Athanasios
authors: A
authors: Kallitsaris
authors: Ioannis
authors: I
authors: Messinis
authors: Ioannis
authors: I
authors: Stefanidis
mesh_terms: D000328:Adult; D016022:Case-Control Studies; D002940:Circadian Rhythm / Q000502:physiology*; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D011225:Pre-Eclampsia / Q000097:blood / Q000503:physiopathology*; D011247:Pregnancy; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood; D014841:von Willebrand Factor / Q000378:metabolism
chemical_list: D019010:Vascular Cell Adhesion Molecule-1; D014841:von Willebrand Factor; D018799:Intercellular Adhesion Molecule-1