flow alone through our current means of traditional Doppler echocardiography FIG 11.2 Placental weight to birthweight ratio at term gestation (37 to 40 weeks’ gestation) The normal data are displayed in red as mean and dotted lines as 95% confidence intervals In blue are the values for 120 fetuses with complex congenital heart disease The blue line reflects the mean regression for the group with congenital heart disease (Modified from Almog B, Shehata F, Aljabri S, et al Placenta weight percentile curves for singleton and twins deliveries Placenta 2011;32:58–62.) FIG 11.3 Gross pathology specimen of placenta from a full-term newborn with hypoplastic left heart syndrome The arrow points to an area of infarction in the peripheral vascular watershed region of the placenta (From Rychik J, Goff D, McKay E, et al Characterization of the placenta in the newborn with congenital heart disease: distinctions based on type of cardiac malformation Pediatr Cardiol 2018 Epub ahead of print.) In utero, in vivo assessment of the living, functioning placenta would be of tremendous value but it is quite challenging Various groups are in the process of developing tools for imaging-based assessments This approach has great potential to contribute to our understanding of placental dysfunction and its influence on fetal development in those with CHD For example, recent investigation using magnetic resonance imaging techniques has allowed for characterization of placental size using three-dimensional techniques.20 Unique magnetic resonance imaging sequences looking at oxygen saturation, show a significant decrease in the oxygen content of umbilical venous blood in fetuses with CHD.21 Umbilical venous blood should be the most highly oxygenated in the normal fetal circulation However, in CHD, placental vascular dysfunction likely contributes to the relative deoxygenation seen in what should otherwise be highly oxygenated blood content (see also Chapter 7) Moreover, the complex interplay between the altered fetal circulation in CHD and placental blood flow is not well understood In the normal fetal circulation, the right heart ejects the majority of its volume across the ductus arteriosus, which joins the output of the left ventricle in the descending aorta Together, the flow from the right and left ventricle is termed the combined cardiac output (CCO), which can be assessed by established fetal Doppler echocardiography techniques Placental blood flow normally comprises about one-third of fetal CCO in the latter half of pregnancy, decreasing to one-fifth by term gestation This proportion has been shown to be decreased in placental insufficiency, while overall CCO is maintained.22 How placental blood flow and its relationship to CCO is altered in the setting of possible placental abnormalities and diseasespecific changes to the fetal circulation is yet unknown Summary Further study of the postnatal placenta and the placenta in utero are needed Beyond the immediate impact on fetus and mother, the placenta plays a role in programming long-term health.21 The placenta acts as the fetus's sole window to the outside world This picture is filtered through the health and metabolism of the mother Maternal factors, such as nutritional history, blood pressure, and even asthma, affect the morphologic structure of the placenta, and in turn, program the fetus’ organs and systems for life.23 In normally developing fetuses, variations in placental morphology at birth are associated with a range of disorders such as hypertension, coronary artery disease, type 2 diabetes, and colorectal cancer.23 It is not known how abnormalities of the placenta in fetuses with CHD affect fetal programming and long-term outcomes; however, it is highly plausible that many of these factors influence outcomes in our patients with CHD Development of tools that will allow us to study placental structure and function to a higher degree of accuracy will allow for better understanding of factors influencing postnatal outcomes in CHD The presence of placental abnormalities detected after birth suggests that structural and functional abnormalities are present during gestation, many of which may be modifiable For example, the findings of thrombosis and infarction indicate the presence of a placental thrombotic vasculopathy in CHD If confirmed in utero, this finding may ultimately lead to the development of treatment strategies for placental dysfunction in CHD similar to that offered for other fetal conditions.24 What is now clear is that life before birth plays a critical role in outcomes after birth Simply stratifying patients based on the presence or absence of an altered maternal-fetal environment defined as the presence of (1) preeclampsia, (2) a small for gestational age newborn, or (3) prematurity, was recently shown to have an important influence on surgical survival for CHD (Fig 11.4).25 We can no longer ignore this important and potentially modifiable variable Altering the substrate of life through fetal therapy for placental dysfunction in CHD may be a way to improve outcomes in this fragile population