Congenital heart defects are the most common group of congenital malformations, affecting approximately 1% of live births worldwide. Among non-syndromic cases, about 20% are categorized as severe. Since the 1990s, advances in medical and surgical therapy have markedly improved survival, and more than 90% of individuals with CHD now reach adulthood. These survival gains have increased the number of persons with CHD who become parents, prompting renewed attention to how maternal cardiac status and related factors may influence outcomes in their children.
Pregnancy produces substantial hemodynamic changes, and maternal cardiovascular function is a major determinant of perinatal outcomes in women with CHD. Epidemiological studies have associated maternal CHD with higher rates of preterm birth, fetal growth restriction, pre-eclampsia, and fetal loss. Women with complex CHD are also at increased risk of maternal cardiovascular complications such as arrhythmias and heart failure. These maternal complications frequently lead to premature delivery and a greater need for obstetric interventions, including cesarean section. Clinical guidelines therefore emphasize individualized risk stratification and specialized multidisciplinary management throughout pregnancy for women with CHD.
Overall fecundity appears similar between people with CHD and the general population; however, individuals with more severe disease are less likely to have children. Among those who become parents, the number of children is comparable to peers without CHD. Observational data suggest that paternal CHD does not increase the risk of common adverse neonatal outcomes such as preterm birth or small for gestational age, pointing toward prominent maternal contributions—both biological and contextual—to pregnancy and neonatal risk profiles.
Children of parents with CHD have elevated recurrence risk for congenital cardiac defects. A Danish study reported higher recurrence when the mother was affected (4.8%) than when the father was affected (2.7%), indicating roles for genetic transmission as well as maternal or intrauterine influences. Beyond structural anomalies, concern is growing about longer-term offspring outcomes. Infants born preterm or small for gestational age—more common in pregnancies with maternal CHD—are known to carry increased risk for neurodevelopmental, physical, behavioral, and educational challenges during childhood. Whether maternal CHD independently predicts these longer-term developmental vulnerabilities beyond its relation to prematurity and growth restriction has been uncertain.
A recent population-based Canadian study including more than 256,000 children assessed child development at kindergarten (age 5–6 years) using the teacher-rated Early Development Instrument (EDI). The study defined developmental vulnerability as scoring below the 10th percentile in any two of five EDI domains: physical health and wellbeing, social competence, emotional maturity, language and cognitive development, and communication and general knowledge. Children whose mothers had CHD were more likely to show developmental vulnerability at school entry—an overall 28% increased risk compared with unexposed children. The increased risk spanned multiple domains including physical health, social competence, language and cognitive development, and communication. Importantly, the association was strongest for offspring of mothers with severe CHD, where risk was nearly doubled relative to children of mothers without CHD.
The mechanisms are likely multifactorial and remain to be disentangled. Pathways plausibly include the effects of preterm birth and fetal growth restriction, both more frequent in pregnancies complicated by CHD, which can impair neurodevelopment. Other potential contributors are alterations in the intrauterine environment, genetic susceptibility to both CHD and neurodevelopmental traits, and postnatal environmental factors including parental health, caregiving capacity, and socioeconomic context. Existing clinical frameworks and figures emphasize these interacting domains but do not yet resolve causal pathways.
These observations broaden clinical focus from survival and immediate perinatal outcomes to longer-term child development. They imply that maternal CHD—particularly severe CHD—should be considered a marker for potential developmental vulnerability in offspring. Current risk stratification models and most guidelines prioritize maternal cardiovascular outcomes; for example, the European Society of Cardiology lists maternal predictors of adverse offspring outcomes such as low oxygen saturation (<90%), left-sided obstruction, heart failure, and anticoagulant use. However, no validated tool exists to predict which children will experience long-term developmental problems related to maternal CHD.
Clinically, preconception counseling and specialized obstetric management remain essential. In addition, the findings support extending surveillance into the postnatal period: children born to mothers with CHD may benefit from closer developmental monitoring at key early-childhood milestones and from timely referral to early supportive interventions when concerns are identified.
Key unanswered questions include the relative contributions of genetics, intrauterine physiology, perinatal complications (prematurity, growth restriction), and the postnatal social environment to observed developmental risks. There is a need for studies that can separate these pathways and quantify their individual effects. Development of validated risk prediction tools that incorporate maternal cardiac severity, perinatal factors, and social determinants could enable targeted follow-up. Nevertheless, because prematurity and fetal growth restriction are common final pathways across multiple maternal conditions, broader strategies—such as universal developmental screening and systematic follow-up of at-risk children—may yield the largest public health benefits.
Improvements in survival for people with CHD have produced a growing population of mothers with CHD. Evidence from large population-based data indicates that maternal CHD is associated not only with increased maternal and perinatal complications but also with elevated risk of developmental vulnerability in offspring at school entry, particularly when the mother has severe disease. These findings call for expanded clinical attention that spans preconception counseling, specialist obstetric care, and postnatal developmental surveillance and support, while research works to clarify mechanisms and create validated tools for risk stratification.