Relation of nocturnal blood pressure dipping to cellular adhesion, inflammation and hemostasis
BACKGROUNDSubjects 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 acti...
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Published in: | Journal of hypertension Vol. 22; no. 11; pp. 2087 - 2093 |
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Main Authors: | , , , , , , , |
Format: | Journal Article |
Language: | English |
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Hagerstown, MD
Lippincott Williams & Wilkins, Inc
01-11-2004
Lippincott Williams & Wilkins |
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Abstract | BACKGROUNDSubjects 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.
DESIGNStudy 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.
RESULTSMultivariate 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.
CONCLUSIONNocturnal 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. |
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AbstractList | BACKGROUNDSubjects 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.DESIGNStudy 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.RESULTSMultivariate 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.CONCLUSIONNocturnal 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. 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. 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. 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. 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. BACKGROUNDSubjects 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. DESIGNStudy 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. RESULTSMultivariate 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. CONCLUSIONNocturnal 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. |
Author | Perez, Christy J Nelesen, Richard A Hong, Suzi von Känel, Roland Jain, Shamini Mills, Paul J Adler, Karen A Dimsdale, Joel E |
AuthorAffiliation | aDepartment of Psychiatry, University of California San Diego, California, USA, bDepartment of General Internal Medicine, University Hospital, Bern, cInstitute for Behavioral Sciences, Federal Institute of Technology, Zurich, Switzerland and dDepartment of Psychology, San Diego State University, California, USA |
AuthorAffiliation_xml | – name: aDepartment of Psychiatry, University of California San Diego, California, USA, bDepartment of General Internal Medicine, University Hospital, Bern, cInstitute for Behavioral Sciences, Federal Institute of Technology, Zurich, Switzerland and dDepartment of Psychology, San Diego State University, California, USA |
Author_xml | – sequence: 1 givenname: Roland surname: von Känel fullname: von Känel, Roland organization: aDepartment of Psychiatry, University of California San Diego, California, USA, bDepartment of General Internal Medicine, University Hospital, Bern, cInstitute for Behavioral Sciences, Federal Institute of Technology, Zurich, Switzerland and dDepartment of Psychology, San Diego State University, California, USA – sequence: 2 givenname: Shamini surname: Jain fullname: Jain, Shamini – sequence: 3 givenname: Paul surname: Mills middlename: J fullname: Mills, Paul J – sequence: 4 givenname: Richard surname: Nelesen middlename: A fullname: Nelesen, Richard A – sequence: 5 givenname: Karen surname: Adler middlename: A fullname: Adler, Karen A – sequence: 6 givenname: Suzi surname: Hong fullname: Hong, Suzi – sequence: 7 givenname: Christy surname: Perez middlename: J fullname: Perez, Christy J – sequence: 8 givenname: Joel surname: Dimsdale middlename: E fullname: Dimsdale, Joel E |
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Keywords | Hypertension coronary artery disease cell adhesion molecules Interleukin Cell adhesion molecule Cardiovascular disease Inflammation cardiovascular diseases Coronary heart disease Endothelium interleukins Hemostasis Arterial pressure Blood pressure Ambulatory Monitoring blood pressure monitoring |
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Snippet | BACKGROUNDSubjects who fail to dip their nocturnal blood pressure (BP) are at substantially increased risk for cardiovascular diseases. The pathogenetic... Subjects who fail to dip their nocturnal blood pressure (BP) are at substantially increased risk for cardiovascular diseases. The pathogenetic mechanisms of... |
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SubjectTerms | Adult Arterial hypertension. Arterial hypotension Arteriosclerosis - epidemiology Arteriosclerosis - physiopathology Biological and medical sciences Biomarkers Blood and lymphatic vessels Blood Pressure - physiology Cardiology. Vascular system Cell Adhesion - physiology Circadian Rhythm - physiology Clinical manifestations. Epidemiology. Investigative techniques. Etiology Endothelium, Vascular - physiopathology Female Fundamental and applied biological sciences. Psychology Hemodynamics. Rheology Hemostasis - physiology Humans Hypertension - epidemiology Hypertension - immunology Hypertension - physiopathology Male Medical sciences Multivariate Analysis Risk Factors Vasculitis - epidemiology Vasculitis - physiopathology Vertebrates: cardiovascular system |
Title | Relation of nocturnal blood pressure dipping to cellular adhesion, inflammation and hemostasis |
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