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= 45) or placebo (n= 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 = 0.31, 95% CI 0.13–0.78) and pre‐eclampsia (4.7%vs 23.3%, RR = 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 = 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.

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Asymmetric dimethylarginine (ADMA) and monomethylarginine (LMMA) are endogenous inhibitors of nitric oxide synthase. A high level of ADMA in plasma has shown to be a significant risk factor for acute coronary syndromes and elevated plasma ADMA levels are prevalent in patients with hypercholesterolemia. It was therefore hypothesized that lowering plasma cholesterol levels with statin treatment would also lower ADMA concentrations. This double-blind study addressed the effect of high-dose statin treatment on plasma levels of ADMA and LMMA. Forty-eight subjects with mild hypercholesterolemia were randomly assigned to receive simvastatin 80 mg/d, atorvastatin 40 mg/d, or placebo for 8 weeks. Both statins decreased low-density lipoprotein cholesterol effectively (simvastatin 54% and atorvastatin 49%). However, concentrations of arginine derivatives remained unchanged during statin treatment and did not correlate with cholesterol levels. This study indicates that statin treatment has no clear influence on plasma ADMA or LMMA concentrations.