The basic effect of vascular interventions is to embolize the blood vessels and block the blood flow to the lesion. Through relevant studies, it was found that: 1. All ectopic endometrium of adenomyosis is located in the myometrium. The ectopic endometrium of adenomyosis is shown to be rich in blood flow under ultrasound, and the hyperechoic lesion area is surrounded by speckled and short rod-like low velocity arteriovenous blood flow, and the ectopic endometrium is shown to be high-signal under MRI, which is surrounded by hyperplastic muscle fibers forming a miniature uterine structure, showing that its blood supply is a small branch of the uterine artery, i.e., the ectopic endometrial lesions of adenomyosis are supplied with blood through the uterine artery, which provides a vascular This provides an anatomical basis for interventional treatment. 2. The ectopic endometrium of adenomyosis originates from the basal layer of endometrium and is mostly in the proliferative stage, which is sensitive to ischemia and hypoxia, which provides the pathological basis for interventional treatment. 3. In uterine artery DSA angiography, it was found that the contrast agent was relatively concentrated in the adenomyosis lesion, indicating that the blood in this lesion was richer than in the normal myometrium, which provided an imaging basis for the assessment of the efficacy and safety of interventional treatment. The mechanism of interventional treatment for adenomyosis is to achieve the purpose of treatment by embolizing the blood supplying arteries of the uterus to cause necrosis and absorption and atrophy of the lesions in the uterus, which is the basic principle and starting point of interventional treatment for adenomyosis. The blockage of blood flow causes necrosis of ectopic endometrium and hyperplastic connective tissue due to ischemia and hypoxia, and the appearance of non-inflammatory edema, followed by gradual dissolution and absorption, resulting in the shrinkage or even disappearance of lesions. 2, The reduction of lesions causes the uterus to become softer and the volume and cavity area to be reduced, effectively reducing menstrual flow. 3. Partial necrosis of the ectopic endometrium and the encapsulated myometrium causes the uterus to shrink and the volume to shrink to close the tiny channels, or the necrosis of the channels themselves closes so that the normal endometrial basal layer can no longer enter the myometrium, which greatly reduces the recurrence rate. 4. The necrosis of ectopic endometrium decreases the local estrogen level and the number of estrogen receptors, etc., interrupting the vicious circle of adenomyosis spreading and eliminating the possible causes of adenomyosis, thus preventing recurrence and also improving the situation of excessive endometrial hyperplasia with reduced menstrual flow. 5. Although the normal endometrial functional layer also appears mild necrosis, it can gradually migrate and grow from the basal layer to restore normal function after the vascular recanalization or the establishment of collateral circulation, while the necrosis of ectopic endometrium is irreversible due to the lack of support from the basal layer, so when the embolized vascular recanalization or collateral circulation is established and the ischemic and hypoxic state is improved, the necrotic lesions cannot grow again, which ensures the This ensures the stability of the therapeutic effect after treatment.