“…Based on specific anatomic deformities, CHD has been clinically classified into over 25 distinctive entities, including tetralogy of Fallot (TOF), Ebstein’s anomaly, atrial septal defect (ASD), truncus arteriosus, ventricular septal defect (VSD), coarctation of the aorta, interrupted aortic arch, double outlet right ventricle (DORV), endocardial cushion defect (ECD), atrioventricular septal defect (AVSD), hypoplasia of the left ventricle, aortic stenosis, transposition of the great arteries, anomalous pulmonary venous connection, and patent ductus arteriosus [ 2 ]. Although slight lesions may resolve spontaneously [ 2 ], severe CHD, which accounts for almost one-third of all types of CHD [ 1 ], requires timely medical intervention or surgery, and otherwise may lead to diminished exercise performance and degraded health-associated quality of life [ 3 , 4 , 5 , 6 , 7 ], delayed central nervous development and brain damage [ 8 , 9 , 10 ], ischemic cerebral stroke [ 11 , 12 ], pulmonary arterial hypertension and impaired pulmonary function [ 13 , 14 , 15 , 16 ], chronic kidney disease and acute renal injury [ 17 , 18 , 19 , 20 ], infective endocarditis [ 21 , 22 , 23 , 24 ], aortic dissection and rupture [ 25 ], chronic heart failure [ 26 , 27 ], cardiac dysrhythmias [ 28 , 29 , 30 ], and cardiac premature demise [ 31 , 32 , 33 , 34 ]. Over the past several decades, significant improvement in drug therapy and surgical treatment of CHD has been achieved, which remarkably changes the natural history of severe CHD, allowing over 90% of CHD newborns to survive into adulthood [ 1 ].…”