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The Relationship Between Hemodynamics and Inflammatory Activation in Women at Risk for Preeclampsia

From the Departments of Obstetrics and Gynecology and Medicine, University of Washington School of Medicine, Seattle, Washington; Department of Biostatistics, Columbia University, New York, New York; and Department of Biostatistics, Merck & Co., Inc., Rahway, New Jersey.

Address reprint requests to: Darcy B. Carr, MD, Department of Obstetrics and Gynecology, University of Washington School of Medicine, Box 356460, Seattle, WA 98195-6460; E-mail: darcarr{at}u.washington.edu.

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- (TNF-), TNF- 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, 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- receptor 1 in the treated group compared with the controls (P < .001).

CONCLUSION: 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- receptor 1 compared with low-risk women who were not treated, suggesting a relationship between hemodynamics and inflammatory activation.

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