Pregnancy-induced changes in hemostasis lead to a state of hypercoagulability, so in a woman with AF at risk of stroke/thromboembolism in the non-pregnant state, pregnancy will increase this risk threefold to fourfold.421,422 VKAs cross the placenta and have the potential to cause fetal wastage, bleeding in the fetus, and teratogenicity. The most common fetal anomaly developing as a consequence of fetal exposure to warfarin consists of midfacial hypoplasia and stippled epiphyses and typically occurs after in utero exposure to VKAs during the rst trimester of pregnancy.421 VKAs have also been associated with CNS abnormalities after exposure during any trimester, but these complications are There is general consensus that in order to minimize the risk of warfarin embryopathy, it is reasonable to avoid warfarin between weeks 6 and 12 of gestation because of the high risk of fetal defects, especially if the dose of warfarin is higher than 5 mg per LMWH does not cross the placenta, and there is no evidence that LMWH causes teratogenicity or increases fetal bleeding. Because of accelerated clearance, LMWH has a shorter half-life and lower peak plasma concentration during pregnancy, thus potentially requiring higher doses. For this reason, use of LMWH (such as between weeks 6 and 12) has to be managed with dose adjustment according to weight and target anti-Xa level (4-6 h post-dose 0.8-1.2 U/mL). UFH does not cross the placenta and therefore can be safely used in pregnancy. However, it carries some risk of heparin-induced thrombocytopenia and osteopenia, which may lead to symptomatic vertebral fracture in Moreover, the pharmacokinetic changes of pregnancy result in a shorter half-life and lower peak plasma concentration of heparin compounds, with the need to titrate doses in order to keep the mid-interval aPTT (6 h post dose $ twice control values). 