With the exception of coarctation, in which no shunt (or cyanosis) exists, the anomalies listed cause a shunting of blood between the systemic and lower-pressure pulmonary circulation. Transposition of the great vessels is a right-to-left shunt that leads to cyanosis. Except where there is persistent congenital pulmonary hypertension, patent ductus arteriosus and atrial septal defects cause a shunting of oxygenated blood from the aorta and left atrium, respectively, back into the pulmonary artery and right atrium. These anomalies cause recirculation of oxygenated blood within the cardiopulmonary circuit but not cyanosis. When a VSD is combined with pulmonary artery atresia (tetralogy of Fallot), the resulting undercirculation in the pulmonary system joins transposition as a cause of cyanosis. Other, less common congenital lesions in which the pulmonary arterial blood flow is relatively decreased include tricuspid atresia, Ebstein anomaly, and hypoplastic right ventricle.