title: The relationship between hemodynamics and inflammatory activation in women at risk for preeclampsia.
abstract: OBJECTIVE
  This study evaluated: 1) whether women with risk factors for preeclampsia had a hyperdynamic circulation and increased markers of endothelial and inflammatory activation; and 2) whether hemodynamically directed therapy was associated with a change in markers.
  
  
  METHODS
  A controlled experimental study was performed for two groups: 1) women at risk for preeclampsia (high risk); and 2) women at low risk (controls). Tumor necrosis factor-alpha (TNF-alpha), TNF-alpha receptors 1 and 2, vascular cell adhesion molecule-1, cellular fibronectin, and cardiac output were measured at or before 24 weeks' gestation and at 6-8 week intervals. High-risk subjects with cardiac output greater than 7.4 L/minute were treated with atenolol. Atenolol therapy was not randomized. Therefore, the longitudinal data were descriptive. Data were analyzed by the t test, Wilcoxon rank sum test, chi(2) test, multivariable linear regression, and the standard two-stage test.
  
  
  RESULTS
  There were 46 high-risk subjects and 25 controls. Maternal age, gestational age, and parity did not differ between the groups. Cardiac output (P <.001) and vascular cell adhesion molecule-1 (P =.02) at baseline were significantly increased in the high-risk group. A total of 42 women in the high-risk group received atenolol for high cardiac output. There was a slower rise in TNF-alpha receptor 1 in the treated group compared with the controls (P <.001).
  
  
  CONCLUSIONS
  Women with risk factors for preeclampsia had a hyperdynamic circulation and endothelial activation. Hemodynamically directed therapy in women at risk was associated with a slower rise in TNF-alpha receptor 1 compared with low-risk women who were not treated, suggesting a relationship between hemodynamics and inflammatory activation.
authors.affiliation: Department of Obstetrics and Gynecology, University of Washington School of Medicine, Seattle, Washington 98195-6460, USA. darcarr@u.washington.edu
authors.forename: D B
authors.initials: DB
authors.lastname: Carr
authors.forename: G B
authors.initials: GB
authors.lastname: McDonald
authors.forename: D
authors.initials: D
authors.lastname: Brateng
authors.forename: M
authors.initials: M
authors.lastname: Desai
authors.forename: C T
authors.initials: CT
authors.lastname: Thach
authors.forename: T R
authors.initials: TR
authors.lastname: Easterling
mesh_terms: D000328:Adult; D015703:Antigens, CD / Q000097:blood; D000959:Antihypertensive Agents / Q000627:therapeutic use*; D001262:Atenolol / Q000627:therapeutic use*; D016534:Cardiac Output, High / Q000503:physiopathology; D005260:Female; D005353:Fibronectins / Q000097:blood; D005865:Gestational Age; D006439:Hemodynamics / Q000502:physiology*; D006801:Humans; D007249:Inflammation / Q000097:blood*; D011225:Pre-Eclampsia / Q000188:drug therapy* / Q000276:immunology / Q000503:physiopathology*; D011247:Pregnancy; D018124:Receptors, Tumor Necrosis Factor / Q000097:blood; D047888:Receptors, Tumor Necrosis Factor, Type I; D012307:Risk Factors; D016896:Treatment Outcome; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood
chemical_list: D015703:Antigens, CD; D000959:Antihypertensive Agents; D005353:Fibronectins; D018124:Receptors, Tumor Necrosis Factor; D047888:Receptors, Tumor Necrosis Factor, Type I; D019010:Vascular Cell Adhesion Molecule-1; D001262:Atenolol