Left-to-right shunt congenital heart disease leads to pulmonary hypertension due to increased pulmonary blood flow, which can eventually cause functional and organic changes in the pulmonary vasculature [1-3]. The correct evaluation of the nature of pulmonary hypertension is important for the correct selection of interventional and surgical indications and timing. 1, the definition of pulmonary hypertension, pathological changes and its mechanism of occurrence The normal systolic pressure (sPAP), diastolic pressure (dPAP) and mean pressure (mPAP) of pulmonary arteries are about 24, 9 and 16 mmHg (1 mmHg = 0.133 kPa). Pulmonary hypertension was diagnosed with sPAP > 30 mmHg, dPAP > 15 mmHg, mPAP > 20 mmHg at rest or mPAP > 30 mmHg during exercise. mPAP between 21 and 30 mmHg, 31 and 50 mmHg and > 50 mmHg were considered mild, moderate and severe pulmonary hypertension, respectively. In the WHO symposium on pulmonary hypertension held in France in September 1998, pulmonary hypertension secondary to congenital heart disease (congenital heart disease) was classified as pulmonary hypertension [4]. Heath and Edwards [5] classified pulmonary arterial hypertension into 6 grades according to the order of occurrence of pulmonary vascular lesions: grade I, hypertrophy of the small pulmonary artery muscles; grade II, hypertrophy of the small pulmonary artery muscles and cellular intimal hyperplasia; grade III, intimal fibrous hyperplasia forming laminar-like changes; grade IV, plexiform lesion formation; grade V, extensive fibrosis of the intima and intima of small pulmonary arteries with iron-containing heme deposits; grade VI, necrotizing arteritis. Grade Ⅰ to Ⅱ are reversible lesions, grade Ⅲ is the critical state, and grade Ⅳ to Ⅵ are irreversible lesions. The mechanism of the occurrence of pulmonary hypertension in precardiac disease has not been fully elucidated. Recent studies have shown that pulmonary revascularization due to abnormal hemodynamics plays an important role in the development and progression of pulmonary hypertension [6]. The mechanical effects of increased pulmonary blood flow and elevated pressure cause damage to the pulmonary vascular endothelium, resulting in changes in endothelial cell function, transmitter release, and increased vascular permeability, followed by information transfer between endothelial cells, pulmonary vascular smooth muscle cells, monocytes, macrophages, and fibroblasts, and the release of growth factors, resulting in increased protein synthesis, active cell proliferation and reduced apoptosis, resulting in abnormal pulmonary vascular growth and remodeling The result is the formation of pulmonary arterial hypertension. 2, non-invasive examination methods to evaluate the nature of pulmonary hypertension Non-invasive examination methods include clinical physical examination, chest X-ray plain film, echocardiography, CT and MRI, etc., but the sensitivity of these techniques for the evaluation of pulmonary hypertension is not ideal [7, 8]. The chest radiographs of pulmonary hypertension show bulging pulmonary hilar segments, dilated hilar arteries with thinning peripheral vessels, and enlarged right ventricles. The values of the bulging pulmonary artery segment, the transverse diameter of the main pulmonary trunk, the area of the main pulmonary trunk, and the wide diameter of the hilar can be measured on telemetry and lateral films. Chest radiographs play a reference role in the evaluation of pulmonary hypertension. Echocardiography relies on the measurement of tricuspid or pulmonary valve blood flow velocity to determine the degree of pulmonary hypertension [9, 10]; pulsed Doppler can also measure pulmonary artery pressure. Echocardiography is very accurate in showing anatomical abnormalities in congenital heart disease, but measuring pulmonary artery pressure is not yet accurate enough and has very limited diagnostic ability for pulmonary vascular lesions. Multi-row CT and electron beam CT are important complementary diagnostic methods to cardiovascular imaging because of their high temporal, spatial and density resolution, large scanning range, no overlap of images, and convenience, safety and speed, combined with 3D reconstruction, which can clearly show various morphological abnormalities of pulmonary vessels during PH, including dilatation of the central pulmonary artery and abnormal perfusion of small pulmonary arteries [11-14], but for flow The measurement of kinetic parameters has yet to be further investigated. The magnetic resonance imaging velocity-encoded cine (VEC MR) technique is an important method for measuring hemodynamic parameters in left-to-right shunt precordial disease.VEC MR imaging can estimate the peak flow velocity in the stenotic segment; the pressure curve can be calculated by the modified Bernoulli equation [15]. The VEC MR can measure not only the left and right pulmonary artery flow velocities separately, but also the ascending and main pulmonary artery flow velocities to estimate the degree of cardiac shunt. In the presence of atrial septal defect, partial pulmonary venous malformation and ventricular septal defect, which are left-to-right shunt lesions, pulmonary artery flow exceeds aortic flow, and the difference is equal to the left-to-right shunt; in the presence of ductus arteriosus, aortic flow exceeds pulmonary artery flow, and the difference is also equal to the shunt; VEC MR can also measure the ratio of pulmonary circulation flow to body circulation flow ( Qp/Qs). 3. Invasive examination methods to evaluate the nature of pulmonary hypertension Although cardiac catheterization is an invasive test, it is still the most commonly used method to examine pulmonary vascular pathology [12]. Through cardiac catheterization, pulmonary artery pressure, pulmonary wedge pressure, and left atrial pressure can be measured; and pulmonary artery oxygenation and left-to-right shunt levels can be measured to clarify the diagnosis; total pulmonary resistance can also be calculated. Total pulmonary resistance is an important parameter for preoperative determination of pulmonary vascular lesions [13]. The vasodilatation test is one of the methods of cardiac catheterization to evaluate the nature of pulmonary hypertension, and there are more methods applied, and the commonly used methods include oxygen inhalation test, prostaglandin E, nitric oxide (NO), and tolazoline (tolazoline) to dilate small pulmonary arteries. Inhaled high concentration of oxygen can cause pulmonary vasodilation, so that the pulmonary artery pressure and resistance drop, the method does not require the use of drugs, side effects are small, widely used; prostaglandin E (PGE) has a strong selective expansion of the pulmonary vascular bed, reduce pulmonary artery pressure and resistance effect, the effect on the body circulation pressure and resistance is small, and the half-life is short, the use of safer; nitric oxide (NO) is vascular endothelial diastolic factor ( EDRF), the main component of vascular endothelial diastolic factor ( EDRF), can selectively dilate the pulmonary artery; Tolazoline is the earliest application of pulmonary vasodilator, due to certain side effects, currently less applied. If the pulmonary artery pressure decreases after oxygenation, those whose pulmonary vascular resistance falls below 6.5-7.0Wood units are more likely to have dynamic PH; pulmonary artery systolic pressure decreases after PGE application to