Ventricular septal defect can cause pulmonary hypertension. If the defect is small, it can close naturally, but if the defect is large, it will cause serious pulmonary hypertension. Therefore, the two are closely related and must be treated carefully. 1. Ventricular septal defect can occur alone or as part of tetralogy of Fallot. The course of the disease is related to the size of the defect. Small defects can close naturally, while large defects can cause severe pulmonary hypertension. The impact on the body is mainly related to the degree of abnormal shunt in the ventricular septal defect. The degree of abnormal shunt is related to the size of the defect and mainly depends on the resistance of the pulmonary circulation. 2. Ventricular septal defect is the most common congenital heart disease in clinical practice, accounting for about 20% of congenital heart diseases. It can usually be successfully corrected through surgical treatment and restored to normal. However, many patients hope for spontaneous healing and do not follow up regularly, which delays the deterioration of the disease, causes irreversible pulmonary hypertension, and ultimately loses the opportunity for surgery. 3. Pulmonary hypertension is caused by a ventricular septal defect with moderate to large left-to-right shunt, which increases the burden on the left ventricle and gradually leads to left ventricular hypertrophy. The shunted blood reaches the right ventricle, causing a significant increase in pulmonary blood flow, which reflexively causes pulmonary vasospasm and increased pulmonary artery pressure. As ventricular septal defect progresses, pulmonary vascular resistance continues to increase and the workload of the right ventricle continues to increase. As time goes by and age increases, if it is not treated in time, it will cause a series of organic lesions in the pulmonary arterioles, slowly evolving into irreversible resistance-type pulmonary hypertension, and thus losing the last chance for surgery. 4. There is a direct causal relationship between the pulmonary vascular resistance of patients with large ventricular septal defect and the degree of pulmonary vascular lesions in pulmonary hypertension. Pulmonary hypertension can be divided into six levels according to pulmonary vascular lesions: Grade 1: The middle layer of the blood vessels is thickened, but there is no hyperplasia of the intima. Grade 2: Hypertrophy of the vascular media accompanied by reaction of intimal cells. Grade 3: Intimal fibrosis with medial hypertrophy and possible early extensive vascular dilatation. Grade 4: Extensive vasodilation, with regional vascular occlusion and plexiform lesions due to intimal fibrosis. Grade 5: Other vascular dilated lesions, such as cavernous and hemangioma-like lesions. Grade 6: Grade 5 lesions plus necrotizing arteritis. |
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