The objective of this report is to provide an update of our current knowledge about the impact of maternal age on pregnancy outcome. Pregnancy in women > or =35 years old is associated with a higher maternal and perinatal mortality. The older gravida also has a higher chance of being delivered by Caesarean section. Most of the complications associated with older age are caused by age-related confounders such as leiomyomas, type II diabetes, hypertension and multiparity. Diabetes and hypertension increase almost linearly with age. Pregnant women with diabetes or hypertension are at increased risk of adverse pregnancy outcome irrespective of age. The currently available literature indicates that premenopausal pregnant women of advanced age who are in good health do not need special care besides the normal obstetric practice. At present, establishing pregnancy in postmenopausal women is more an ethical than a medical issue, partly because the information reported on pregnancy in postmenopausal women is insufficient to determine a reliable risk profile. In these women cardiovascular ageing accelerates. Therefore, until proven otherwise, postmenopausal women should be considered particularly at increased risk for vascular complications during pregnancy. This risk is likely to increase progressively with the number of years elapsed since the onset of postmenopause.

The venous compartment has an important function in

The effects on fetal cerebral blood flow (Qc) of changes in the carotid arterial and sagittal sinus venous PO2, PCO2, and oxygen content were studied in the chronically catheterized ovine fetus in utero at 130-140 days of gestation. Forty-seven measurements of Qc were made in 20 fetuses with radioactive microspheres. In 11 of these animals, 84 measurements of cerebral arteriovenous differences of oxygen content were performed, permitting an indirect measurement of cerebral blood flow (Qc*), assuming a constant cerebral metabolic rate. Arterial and, in 11 animals, sagittal sinus blood was withdrawn for analysis of PO2, PCO2, oxygen content, and pH at the time of the flow measurements. Preliminary analysis showed the best predictor of Qc and Qc* to be the reciprocal of the arterial oxygen content (1/CaO2). Multiple linear regression analysis combining the effects of 1/CaO2 with arterial PCO2 (PaCO2) gave the following equations: Qc = 458.8 (1/CaO2) + 2.68 PaCO2 - 107.93 (R2 = 0.68); Qc* = 435.54 (1CaO2) + 2.20 PaCO2 - 75.03 (R2 = 0.86). As a result of the hyperbolic relationship between Qc (and Qc*) and CaO2, changes in CaO2 at the low levels found during intrauterine life exert an important influence on the fetal cerebral circulation.

Objectives Left-ventricular

The objective of this review was to provide a comprehensive and practical concept on the pathogenesis of preeclampsia on the basis of the currently available scientific evidence. A MEDLINE search was performed of English-language articles published between 1966 and 1997, supplemented with references cited in relevant research articles. Using our data sources, we developed a scheme describing the sequence of events between implantation and the time of manifest clinical disease characterized by generalized endothelial cell dysfunction. A yet unidentified toxic circulating factor released by the ischemic placenta, is held responsible for the impaired endothelial cell function. Particularly, epidemiological studies point to a concept in which immune maladaptation to the fetal allograft plays a key role in causing defective placentation leading to placental ischaemia. The incidence of preeclampsia in sisters and daughters of women who had had preeclampsia is raised. Disease states with vascular involvement, like chronic hypertension and diabetes mellites, are associated with an increased risk for preeclampsia. Recently subclinical abnormalities in hemostasis, metabolism and volume homeostasis have been described in patients with a history of preeclampsia. Placental ischemia secondary to defective placentation, a prerequisite for the development of preeclampsia, has a multifactorial origin consisting of three major components: immune maladaptation, genetic predisposition, and vascular mediated factors. Probably, a summation of these factors will determine whether a pregnant woman is to develop the syndrome. The recently described subclinical abnormalities in hemostasis, metabolism, and vascular function in patients with a history of preeclampsia might give the clinician the opportunity to reduce the recurrence risk by pharmacotherapeutic intervention.