At our institution, 2 of the initial 7 pregnant patients with confirmed coronavirus disease 2019 severe infection (28.6%; 95% CI, 8.2% e64.1%) developed cardiac dysfunction with moderately reduced left ventricular ejection fractions of 40%e45% and hypokinesis. Viral myocarditis and cardiomyopathy have also been reported in nonpregnant coronavirus disease 2019 patients. A case series of nonpregnant patients with coronavirus disease 2019 found that 33% of those in intensive care developed cardiomyopathy. More data are needed to ascertain the incidence of cardiomyopathy from coronavirus disease 2019 in pregnancy, in all pregnant women with coronavirus disease 2019, and those with severe disease (eg, pneumonia). We suggest an echocardiogram in pregnant women with coronavirus disease 2019 pneumonia, in particular those necessitating oxygen, or those who are critically ill, and we recommend the use of handheld, point-of-care devices where possible to minimize contamination of staff and traditional large echocardiogram machines.

Initial ultrasound of a fetus in the third trimester demonstrated shortened and bent fetal extremities with a narrow and misshapen thorax. These findings were suggestive of a fetus affected with a possible lethal skeletal dysplasia. Decisions regarding antepartum, intrapartum and neonatal care were made in this context. A newborn with campomelic dysplasia was delivered and suffered a rapid downhill course.

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Prenatal diagnosis of a posterior nuchal cystic hygroma was made at 13 weeks of gestation in a fetus diagnosed at birth with Noonan syndrome. Through serial sonographic evaluation during pregnancy, the embryologic evolution of cystic hygroma into nuchal skin thickening was appreciated and later correlated with postnatal findings of nuchal skin fold redundancy and pterygium colli in a patient with Noonan syndrome. These observations support the concept of the jugular lymphatic disruption sequence as pathogenesis of the nuchal findings in severely affected Noonan syndrome patients.

To assess the possibility that atrial natriuretic peptide plays a role in salt and water balance during early mammalian development, we examined hearts from fetal and neonatal rates for the presence of this peptide and presumed target tissues for their ability to bind the hormone. Immunohistochemistry was used to localize and radioimmunoassay to quantify this peptide in heart. Immunoreactive atrial natriuretic peptide was visualized in the fetal heart on day 17.5 post-conception. It was distributed throughout the atrial appendages and free wall and, in ventricle, in the trabeculae carnae and chordae tendineae. The concentrations of immunoreactive atrial natriuretic peptide in atria of rats on day 19.5 post-conception were one-tenth of those in the adult. Levels of this peptide in fetal ventricle were low and virtually absent from the adult tissue. Specific binding of radiolabelled atrial natriuretic peptide measured by whole organ counting occurred in several organs from 19.5-day fetal and neonatal rats. A number of these tissues, including the kidney, ileum, adrenal, lung and liver, are targets for and/or bind the peptide in adult rats. Specific binding in these tissues was localized using autoradiography at anatomical sites similar to those in adult organs. Specific binding was also seen in fetal but not neonatal skin. In the kidney, binding was associated with immature as well as mature glomeruli. These findings support the proposition that atrial natriuretic peptide may function in the perinatal rat as it does in the adult and, in addition, may play a unique role during fetal life.