Reliability of Early Fetal Echocardiography for Congenital Heart Disease Detection: A Preliminary Experience and Outcome Analysis of 102 Fetuses to Demonstrate the Value of a Clinical Flow-Chart Designed for At-Risk Pregnancy Management

Early fetal echocardiography (EFEC) is a fetal cardiac ultrasound analysis performed between the 12th and 16th week of pregnancy (compared with the usual 18-22 weeks). In the last 10 years, the introduction of “aneuploidy sonographic markers” in screening for cardiac defects has led to a shift from late second to end of the first trimester or beginning of the second trimester of pregnancy for specialist fetal echocardiography. In this prospective study, early obstetric screening was performed between January 2014 and October 2015, using “aneuploidy sonographic markers” following SIEOG Guidelines 2014. These parameters were then collected and strategically combined in an evaluation score to select the group of pregnancies for performing EFEC, in accordance with the American Society of Echocardiography guidelines for fetal Echocardiography. All second-level examinations were performed transabdominally using a 3D convex volumetric probe with frequency range of 4-8 MHz (Accuvix – Samsung). The outcome data included transabdominal fetal echocardiography from 18 weeks to term and after birth. Overall, 99 pregnant women in the first trimester underwent EFEC (95 singleton and 4 twin pregnancies). Specifically, 30 fetuses were evaluated for extra-cardiac anomalies evidenced by obstetric screening (30%), 25 for family history of congenital heart diseases (25%), 8 for family history of genetic-linked diseases (8%), 4 for heart diseases suspected by obstetric screening (4%) and 19 by normal screening (19%). Was detected 11 (10.7%) CHD, when EFEC detected CHD, were compared to those performed later in pregnancy (18 weeks GA-term), a high degree of diagnosis correspondence was evidenced. The higher sensitivity value of EFEC vs late-FE, in comparison with the post-natal value, coupled with the high EFEC specificity shown vs both the end points, enabled us to consider it as a really reliable diagnostic technology, at least in perienced hands. The introduction of a key combination of the more sensitive obstetric and cardiologic variables should facilitate the formulation of a possible flow-chart as a guide for CHD at-risk pregnancies

An exploration of the potential utility of fetal cardiovascular MRI as an adjunct to fetal echocardiography

Objectives: Fetal cardiovascular magnetic resonance imaging (MRI) offers a potential alternative to echocardiography, although in practice, its use has been limited. We sought to explore the need for additional imaging in a tertiary fetal cardiology unit and the usefulness of standard MRI sequences. Methods: Cases where the diagnosis was not fully resolved using echocardiography were referred for MRI. Following a three‐plane localiser, fetal movement was assessed with a balanced steady‐state free precession (bSSFP) cine. Single‐shot fast spin echo and bSSFP sequences were used for diagnostic imaging. Results: Twenty‐two fetal cardiac MRIs were performed over 12 months, at mean gestation of 32 weeks (26–38 weeks). The majority of referrals were for suspected vascular abnormalities (17/22), particularly involving the aortic arch (n = 10) and pulmonary vessels (n = 4). Single‐shot fast spin echo sequences produced ‘black‐blood’ images, useful for examining the extracardiac vasculature in these cases. BSSFP sequences were more useful for intracardiac structures. Real‐time SSFP allowed for dynamic assessment of structures such as cardiac masses, with enhancement patterns also allowing for tissue characterisation in these cases. Conclusions: Fetal vascular abnormalities such as coarctation can be difficult to diagnose by using ultrasound. Fetal MRI may have an adjunctive role in the evaluation of the extracardiac vascular anatomy and tissue characterisation. © 2016 The Authors. Prenatal Diagnosis published by John Wiley & Sons, Ltd

Fetal Tachyarrhythmia - Part I: Diagnosis

Fetal tachycardia, first recognized in 1930 by Hyman et al1, is a condition occurring in approximately 0.4-0.6% of all pregnancies2. A subset of these cases with more sustained periods of tachycardia is clinically relevant. The necessity of therapeutic intervention in this condition is still a matter of discussion focused on the natural history of the disease. The spectrum of opinions varies from non-intervention3,4,5 based on a number of cases in which the tachycardia subsided spontaneously6, to aggressive pharmacotherapeutic intervention7,8 based on reports of deterioration of the fetal condition ultimately ending in significant neurological morbidity9,10,11, or fetal demise12,13,14. Prenatal treatment through indirect, maternally administered drug therapy seems to be the preference of most centers15,16,17,18,19,20,21. This matter will be discussed further in Fetal Tachyarrhythmia, Part II, Treatment

Maternal Cardiovascular Impairment in Pregnancies Complicated by Severe Fetal Growth Restriction

Abstract—Fetal growth restriction and preeclampsia are both conditions of placental etiology and associated to increased risk for the long-term development of cardiovascular disease in the mother. At presentation, preeclampsia is associated with maternal global diastolic dysfunction, which is determined, at least in part, by increased afterload and myocardial stiffness. The aim of this study is to test the hypothesis that women with normotensive fetal growth-restricted pregnancies also exhibit global diastolic dysfunction. This was a prospective case-control study conducted over a 3-year period involving 29 preterm fetal growth-restricted pregnancies, 25 preeclamptic with fetal growth restriction pregnancies, and 58 matched control pregnancies. Women were assessed by conventional echocardiography and tissue Doppler imaging at diagnosis of the complication and followed-up at 12 weeks postpartum. Fetal growth-restricted pregnancies are characterized by a lower cardiac index and higher total vascular resistance index than expected for gestation. Compared with controls, fetal growth-restricted pregnancy was associated with significantly increased prevalence (P�0.001) of asymptomatic left ventricular diastolic dysfunction (28% versus 4%) and widespread impaired myocardial relaxation (59% versus 21%). Unlike preeclampsia, cardiac geometry and intrinsic myocardial contractility were preserved in fetal growth-restricted pregnancy. Fetal growth-restricted pregnancies are characterized by a low output, high resistance circulatory state, as well as a higher prevalence of asymptomatic global diastolic dysfunction and poor cardiac reserve. These findings may explain the increased long-term cardiovascular risk in these women who have had fetal growth-restricted pregnancies. Further studies are needed to clarify the postnatal natural history of cardiac dysfunction in these women

Fetal echocardiography

Summary available; p. 7-10

Hypoxia induces dilated cardiomyopathy in the chick embryo: mechanism, intervention, and long-term consequences

Background: Intrauterine growth restriction is associated with an increased future risk for developing cardiovascular diseases. Hypoxia in utero is a common clinical cause of fetal growth restriction. We have previously shown that chronic hypoxia alters cardiovascular development in chick embryos. The aim of this study was to further characterize cardiac disease in hypoxic chick embryos. Methods: Chick embryos were exposed to hypoxia and cardiac structure was examined by histological methods one day prior to hatching (E20) and at adulthood. Cardiac function was assessed in vivo by echocardiography and ex vivo by contractility measurements in isolated heart muscle bundles and isolated cardiomyocytes. Chick embryos were exposed to vascular endothelial growth factor (VEGF) and its scavenger soluble VEGF receptor-1 (sFlt-1) to investigate the potential role of this hypoxia-regulated cytokine. Principal Findings: Growth restricted hypoxic chick embryos showed cardiomyopathy as evidenced by left ventricular (LV) dilatation, reduced ventricular wall mass and increased apoptosis. Hypoxic hearts displayed pump dysfunction with decreased LV ejection fractions, accompanied by signs of diastolic dysfunction. Cardiomyopathy caused by hypoxia persisted into adulthood. Hypoxic embryonic hearts showed increases in VEGF expression. Systemic administration of rhVEGF165 to normoxic chick embryos resulted in LV dilatation and a dose-dependent loss of LV wall mass. Lowering VEGF levels in hypoxic embryonic chick hearts by systemic administration of sFlt-1 yielded an almost complete normalization of the phenotype. Conclusions/Significance: Our data show that hypoxia causes a decreased cardiac performance and cardiomyopathy in chick embryos, involving a significant VEGF-mediated component. This cardiomyopathy persists into adulthood