Why the study?
Does hemodynamically directed therapy with atenolol reduce inflammatory activation markers in women at risk for preeclampsia?
Does hemodynamically directed therapy with atenolol reduce inflammatory activation markers in women at risk for preeclampsia?
Hemodynamically directed therapy with atenolol in women at risk for preeclampsia may attenuate the rise in inflammatory markers such as TNF-α receptor 1, suggesting a link between hemodynamics and inflammation.
May attenuate inflammatory rise in high-risk pregnancies; hypothesis-generating and requires randomized confirmation before practice change.
In Brief 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-α (TNF-α), TNF-α 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, χ2 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-α 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-α receptor 1 compared with low-risk women who were not treated, suggesting a relationship between hemodynamics and inflammatory activation. Hemodynamically directed therapy in women at risk for preeclampsia is associated with a slower rise in tumor necrosis factor-a receptor 1 compared with low-risk women who are not treated.
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Carr et al. (2001) studied this question.
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