Hemodynamically-directed atenolol therapy is associated with a blunted rise in maternal sFLT-1 levels during pregnancy.

Objective: Cardiac output and sFlt-1 are elevated prior to clinical evidence of preeclampsia. Early treatment of high cardiac output with atenolol decreases the risk for preeclampsia. We hypothesized that atenolol would impact circulating sFlt-1.
Methods: Cardiac output and plasma sFlt-1 were measured <or=24 weeks' gestation and every 6 to 8 weeks in a longitudinal pilot study of: 1) women with risk factors for preeclampsia (high-risk group; n=46) who were treated with atenolol, and 2) low-risk group (control, n=25) who were not treated.
Results: The groups were similar in maternal age (mean+/-SD: high-risk 28.3+/-5.4 versus control 30.3+/-5.5 years) and enrollment gestational age (17.3+/-4.3 versus 16.1+/-4.2 weeks). The high-risk group had higher cardiac output (9.7+/-1.7 versus 7.3+/-1.7 L/min; p<0.001) and mean arterial pressure (91.8+/-10.6 versus 79.6+/-7.3 mm Hg; p<0.001). Cardiac output and mean arterial pressure decreased while sFlt-1 levels rose less in the high-risk group compared with controls (p=0.001 for all using GEE) even after adjusting for preeclampsia risk factors (age, weight, and primigravida status).
Conclusion: Atenolol in high-risk women was associated with a lower rise in sFlt-1, suggesting an effect of hemodynamically directed treatment on the anti-angiogenic state.