ABSTRACT
INTRODUCTION Pre-eclampsia, placental abruption, intrauterine growth retardation (IUGR) and intrauterine fetal death (IUFD) greatly contribute to maternal and fetal morbidity and mortality. Their causes are unknown, but all of them may be associated with abnormal placental vasculature and disturbances of hemostasis leading to inadequate maternal-fetal circulation.1-7 Recent dat afrom studies in pre-eclampsia suggest that endothelial dysfunction, vasoconstriction, placental ischemia and enhanced coagulation are associated with abnormal placental development, which may lead to inadequate maternal-fetal circulation and decreased placental perfusion.8 In normal pregnancy, the trophoblasts invade the spiral arteries, which lose their muscular wall and become flaccid vessels that allow maximum blood flow to the placenta. The abnormal interaction between mother and fetal allograft in abnormal pregnancies leads to abnormal trophoblastic invasion of the spiral arteries, resulting in small, narrowed arteries. The subsequent vasculopathy and secondary thrombosis from hypercoagulability may result in inadequate perfusion of the intervillous space, pre-eclampsia, placental infarcts, IUGR, placental abruption and IUFD. In the case of pre-eclampsia, it is thought that, as pregnancy advances, the growing placenta becomes hypoxic and releases unknown substances that affect endothelial cells and begin the cascade of events that ultimately results in the clinically recognizable syndrome. The known thrombotic nature of the placental vascular lesions and the increased thrombotic risk associated with the existence of thrombophilias strongly suggest a cause-effect relationship between inherited and acquired thrombophilias and the above severe obstetric complications.
