Low dose acetylsalicylic acid in prevention of pregnancy-induced hypertension and intrauterine growth retardation in women with bilateral uterine artery notches

Abstract

Objective To evaluate the efficacy of low-dose acetylsalicylic acid in the prevention of pregnancy-induced hypertension and intrauterine growth retardation in high-risk pregnancies as determined by transvaginal Doppler ultrasound study of the uterine arteries at 12 to 14 weeks of gestation. Design Randomised, double blind and placebo-controlled trial.Setting The Department of Obstetrics and Gynaecology, Tampere University Hospital, Finland.Population One hundred and twenty pregnant women considered to be at high risk of pre-eclampsia or intrauterine growth retardation were screened by transvaginal Doppler ultrasound at 12 to 14 weeks of gestation. Methods Ninety pregnant women with bilateral notches in the uterine arteries were randomised to receive acetylsalicyclic acid 0.5mg/kg/day (n ¼ 45) or placebo (n ¼ 45) from 12 to 14 weeks of gestation. Main outcome measures Hypertensive disorders of pregnancy and intrauterine growth retardation.Results Forty-three women on acetylsalicyclic acid and 43 on placebo were successfully followed up. The use of acetylsalicyclic acid was associated with a statistically significant reduction in the incidence of pregnancy-induced hypertension (11.6% vs 37.2%, RR ¼ 0.31, 95% CI 0.13 -0.78) and pre-eclampsia (4.7% vs 23.3%, RR ¼ 0.2, 95% CI 0.05 -0.86). The incidence of hypertension before 37 weeks of pregnancy was also significantly reduced (2.3% vs 20.9%, RR ¼ 0.22, 95% CI 0.05 -0.97). The reduction in the incidence of intrauterine growth retardation (2.3% vs 7%) was not statistically significant. Acetylsalicyclic acid was not associated with excess risk of maternal or fetal bleeding. Conclusion In women rated in Doppler velocimetry waveform analysis to be at high risk of pre-eclampsia, low-dose acetylsalicyclic acid reduces the incidence of pregnancy-induced hypertension and especially proteinuric pre-eclampsia.

Aspirin and Preeclampsia Prevention in Patients With Abnormal Uterine Artery Blood Flow

“…These findings were consistent with some recent studies regarding ASA therapy for prevention of preeclampsia, following uterine artery Doppler studies, which showed tendency towards benefit (29). In a study on 86 high-risk women with abnormal Doppler findings in 12-14 weeks of pregnancy, aspirin treatment resulted in lowering the risk of preeclampsia from 37.2% in the placebo group comparing to 11.6% in the aspirin group (34). In another study by Bower et al on women with abnormal uterine artery flow velocity waveforms, there was 29% incidence of preeclampsia in the ASA group and 41% in the placebo group, showing a significant difference (25).…”

Prevention of gravidic endothelial hypertension by aspirin treatment administered from the 8th week of gestation

“…19 The study of Bujold and et al 18 confirms this hypothesis, because the papers dealing with early aspirin treatment consistently show a positive effect, with a relative risk ranging from 0.07 to 0.63 for pre-eclampsia and from 0.20 to 1 for IUGR. [20][21][22][23][24][25][26][27] The present study is the largest to date with respect to the number of patients and the only one to administer aspirin at such an early point of gestation. In accordance with previous observations, we show that aspirin diminishes the risk of developing a hypertensive gravidic disease by threefold and delays the time of delivery by almost 2 weeks, thus increasing the birth weight by more than 150 g. The risk of maternal complications was also reduced, and the risk of fetal complications was reduced by B10-fold.…”

Molecular Mechanisms Regulating the Vascular Prostacyclin Pathways and Their Adaptation during Pregnancy and in the Newborn

“…Third, factors other than PGI 2 / TXA 2 imbalance contribute to the pathogenesis of PE (Reslan and Khalil, 2010). Other causes of the negative or partially positive results with aspirin in PE may be related to the timing and dosage of aspirin (Vainio et al, 2002;Walsh, 2004). Late initiation of treatment with aspirin may not prevent the development of PE, because placental implantation is already established by week 18 of gestation (Vainio et al, 2002).…”

“…Other causes of the negative or partially positive results with aspirin in PE may be related to the timing and dosage of aspirin (Vainio et al, 2002;Walsh, 2004). Late initiation of treatment with aspirin may not prevent the development of PE, because placental implantation is already established by week 18 of gestation (Vainio et al, 2002). In addition, aspirin at 50 to 60 mg/day is effective in inhibiting TXA 2 production by platelets but not that by placental trophoblasts or maternal leukocytes (Walsh, 2004).…”