**3. Genetics**

The molecular mechanisms underpinning the failed delamination of the tricuspid valve in Ebstein's anomaly are unknown [12]. Genetic factors resulting in Ebstein's anomaly may be related to the mutations *in myosin heavy chain 7 (MYH7)* and *NKX2.5*. One study reports heterozygous mutations in MYH7 were noted in eight of 141 (6%) patients with Ebstein's anomaly. Ebstein's anomaly with left ventricular noncompaction (LVNC) had a higher frequency of MYH7 mutations (6 out of 8) than Ebstein's anomaly without LVNC [13]. A heterozygous missense mutation in MYH7 was identified in two siblings with familial Ebstein's anomaly and LVNC [14]. Ebstein's anomaly is noted to be the cardiac phenotypes for mutations involving NKX2.5 [15]. Genetic anomalies or syndromes were detected in 19 of 243 fetuses (11%) in a multi-center study. Eleven patients were confirmed with Trisomy 21, two patients were noted to have CHARGE syndrome, and two patients were noted to have a 1p36 deletion [16]. There was no association between Ebstein's anomaly with genetic abnormalities and mortality [16].
