Effect of antihypertensive therapy with α‐methyldopa on uterine artery Doppler in pregnancies with hypertensive disorders

Abstract Objectives Antihypertensive drugs lower blood pressure by direct vascular effects or central vasodilatory mechanisms. Their effect on uterine artery Doppler resistance indices in hypertensive disorders of pregnancy is uncertain. This study aimed to evaluate the impact of antihypertensive therapy with α‐methyldopa on maternal uterine artery Doppler pulsatility index (PI) and resistance index (RI) in women presenting with hypertensive disorders of pregnancy. Methods This was a cross‐sectional study of 51 women with pre‐eclampsia, 29 with gestational hypertension and 80 matched normotensive controls. Uterine artery PI and RI were measured at recruitment (between 24 and 40 weeks' gestation) and, in the hypertensive groups, 24–48 h after starting α‐methyldopa. Differences between mild and severe, and between early‐ and late‐onset pre‐eclampsia were compared using the Mann–Whitney test. The Wilcoxon rank sum test was used to compare measurements before and after treatment. Results Prior to treatment, uterine artery PI and RI were significantly higher in women with pre‐eclampsia compared with those with gestational hypertension and controls ( P < 0.0001). The median uterine artery PI multiple of the median (MoM) was significantly higher ( P < 0.0001) in early‐onset than in late‐onset pre‐eclampsia (1.83 (range, 0.88–3.65) vs. 1.19 (range, 0.91–1.72)) and in severe compared with mild disease (2.26 (range, 2.02–3.65) vs. 1.29 (range, 0.88–2.9)). Uterine artery PI‐ and RI‐MoMs in both pre‐eclampsia and gestational hypertension, before and after 34 weeks' gestation, were not affected by α‐methyldopa treatment. Conclusions Antihypertensive therapy using α‐methyldopa in women presenting with hypertensive disorders of pregnancy has no significant effect on uterine artery resistance to blood flow, suggesting that it does not impair uteroplacental circulation in these cases. Copyright © 2010 ISUOG. Published by John Wiley & Sons, Ltd.