The majority of<unk> S cases are sporadic meaning they arise in patients with no family history of<unk> S. Some cases may have a genetic component, as<unk> S has been shown to be heritable and associated with specific gene mutations. Possible contributing factors may include intrauterine infarction, infectious changes, and a selective<unk>  ventricular cardiomyopathy. Genetics Genetic loci associated with<unk> S include GJA1 (connexin 43), HAND1, NKX2.5, 10q22, and 6q23. There is a slight risk of recurrence in future pregnancies, estimated to be 2-4%, which increases to 25% in families with two affected children. This is thought to be mediated by genetic mutations with incomplete penetrance.<unk> S is also associated with several genetic syndromes, including trisomy 13 (Patau syndrome), trisomy 18 (Edwards syndrome), partial trisomy 9, Turner's syndrome (XO), Jacobsen syndrome (11q deletion syndrome), Holt-Oram syndrome, and Smith-Lemli-Opitz syndrome. Altered Blood Flow A popular theory termed the "no flow, no grow" hypothesis suggest that primary anatomic defects of the aortic and mitral valves lead to malformations of the<unk>  ventricle and its outflow tract. These primary defects can be divided into those that lead to outflow tract obstruction or reduced<unk>  ventricular filling. Outflow tract obstruction leads to<unk>  ventricular hypertrophy and reduction in the<unk>  ventricular lumen. One example of this would be in the case of aortic stenosis. Aortic stenosis that occurs during fetal development results in added stress on the<unk>  ventricle in utero. This can eventually lead to decreased perfusion through the<unk>  ventricle which is believed to inhibit ventricular growth.
Hypoplastic left heart syndrome
Hypoplastic right heart syndrome
Asphyxiating thoracic dysplasia
Double aortic arch
Pulmonary atresia
Double outlet right ventricle
Pulmonary hypoplasia
Congenital diaphragmatic hernia