Childbirth and myoma treatment by uterine artery occlusion: do they share a common biology?

When the uterine arteries are bilaterally occluded, either by uterine artery embolization or by laparoscopic obstruction, women with myomas experience symptomatic relief. After the uterine arteries are occluded, most blood stops flowing in myometrial arteries and veins, and the uterus becomes ischemic. It is postulated that myomas are killed by the same process that kills trophoblasts: transient uterine ischemia. When the uterine arteries are bilaterally occluded, either by uterine artery embolization (UAE) or by laparoscopic obstruction, women with myomas experience symptomatic relief. After the uterine arteries are occluded, most blood stops flowing in myometrial arteries and veins, and the uterus becomes ischemic. Over time, stagnant blood in these arteries and veins clots. Then, tiny collateral arteries in the broad ligament (including communicating arteries from the ovarian arteries) open, causing clot within myometrium to lyse and the uterus to reperfuse. Myomas, however, do not survive this period of ischemia. This is unique organ response to clot formation and ischemia. What allows the uterus to survive a relatively long period of ischemia while myomas perish? Childbirth appears to be the predicate biology. Following placental separation, the uteroplacental arteries and the draining veins of the placenta are torn apart at their bases in the junctional zone of the myometrium and bleed directly into the uterine cavity. Left unchecked, every woman would bleed to death in less than 10 minutes after placental delivery. Most women do not bleed to death because vessels in the uterus clot after placental delivery. During pregnancy, clotting and lytic factors in blood increase many fold. Following delivery, uterine contractions continue, intermittently, periodically slowing the velocity of flowing blood through myometrium. The combination of slowed blood flow, elevated clotting proteins, and torn placental vessels (known as Virchow's triad) causes blood in myometrial arteries and veins to clot. Fibrinolytic enzymes later lyse clot in arteries and veins not associated with placenta perfusion, and the uterus is reperfused. Remnant placental tissue - primarily uteroplacental arteries and veins - does not survive this period of ischemia. Placental tissue dies and over weeks is sloughed into the uterine cavity. At the same time, residual endometrial tissue grows under the sloughing placental tissue thus re-establishing the endometrial lining. It is postulated that myomas are killed by the same process that kills trophoblasts - transient uterine ischemia.