Nocturnal Hypertension Is Associated with an Exacerbation of the Endothelial Damage in Preeclampsia

• Published in: American journal of nephrology Vol. 28; no. 3; pp. 424 - 430
• Main Authors: Bouchlariotou, Sofia, Liakopoulos, Vassilios, Dovas, Spiros, Giannopoulou, Myrto, Kiropoulos, Theodoros, Zarogiannis, Sotirios, Gatselos, Georgios, Zachopoulos, Thomas, Kyriakou, Despina S., Kallitsaris, Athanasios, Messinis, Ioannis, Stefanidis, Ioannis
• Format: Journal Article
• Language: English
• Published: Basel, Switzerland S. Karger AG 01.01.2008
• Subjects: Adult; Case-Control Studies; Circadian Rhythm - physiology; Endothelium, Vascular - physiopathology; Female; Humans; Intercellular Adhesion Molecule-1 - blood; Original Report: Laboratory Investigation; Pre-Eclampsia - blood; Pre-Eclampsia - physiopathology; Pregnancy; Vascular Cell Adhesion Molecule-1 - blood; von Willebrand Factor - metabolism; Endothelial damage; Blood pressure; Circadian rhythm; Preeclampsia
• ISSN: 0250-8095; 1421-9670
• DOI: 10.1159/000112807

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), un- derwent 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 im-plications of our findings deserve further investigation.