Relation of nocturnal blood pressure dipping to cellular adhesion, inflammation and hemostasis.

Background: Subjects who fail to dip their nocturnal blood pressure (BP) are at substantially increased risk for cardiovascular diseases. The pathogenetic mechanisms of this relationship have not been elucidated. We investigated whether non-dipping would relate to procoagulant and proinflammatory activity.
Design: Study participants were 76 unmedicated normotensive and hypertensive subjects (44 male, 32 female; 41 white, 35 black; mean age, 36 +/- 8 years) who underwent 24-h outpatient ambulatory BP monitoring. Based on whether their average nocturnal systolic BP relative to their average daytime systolic BP declined by less than 10%, 34 subjects were categorized as non-dippers. D-dimer, plasminogen activator inhibitor-1, von Willebrand factor, soluble intercellular adhesion molecule-1, and interleukin-6 were measured in plasma.
Results: Multivariate analyses showed that D-dimer (median/interquartile range, 242/162-419 ng/ml versus 175/132-254 ng/ml; P=0.041), plasminogen activator inhibitor-1 (36/19-61 ng/ml versus 17/6-44 ng/ml; P=0.010), von Willebrand factor (122/91-179% versus 92/66-110%; P=0.001), and soluble intercellular adhesion molecule-1(227/187-291 ng/ml versus 206/185-247 ng/ml; P=0.044) were all higher in non-dippers than in dippers. Adjustment for gender, ethnicity, age, body mass index, smoking status, hypertension status, and social class revealed independent effects of non-dipping. Non-dippers continued to have higher D-dimer (P=0.030) and von Willebrand factor (P=0.034) than dippers. A similar trend not reaching statistical significance emerged for soluble intercellular adhesion molecule-1 (P=0.055). In contrast, dipping status had no effect on interleukin-6.
Conclusion: Nocturnal BP non-dipping is associated with elevated levels of molecules related to endothelial dysfunction and atherosclerosis. The finding provides one possible mechanism linking non-dipping with cardiovascular disease.