Excessive menstrual bleeding reflects aberrant angiogenesis, generally due to submucosal myomas and endometrial polyps, although it is also frequently observed with long-term progestin-only contraception, impaired haemostasis and hormonal disorders. Surgery (hysterectomy, endometrial ablation) is used too frequently. Uterine artery embolisation is also an option for myomas. Medical treatments include combined oral contraception, progestins and levonorgestrel-releasing Intrauterine System. Gonadotropin-releasing hormone agonists provide significant improvements in bleeding for myomas, but also decrease estrogen secretion (e.g. hot flushes, decreased bone mass). Progestins, although used widely, remain poorly effective as they promote myoma cell growth. Recently, Selective Progesterone Receptor Modulators (SPRMs) have been shown to induce amenorrhea whilst maintaining endogenous estrogen secretion. Phase II studies have also demonstrated decreased fibroid size in SPRM-treated women. Although the mechanism of amenorrhea observed after SPRM treatment is still poorly understood, they may control uterine bleeding via a direct effect on endometrial blood vessels. Suppression of bleeding in women with uterine fibroids receiving SPRMs is associated with moderate reductions in uterine artery blood flow, without major changes in angiogenic factors and extracellular matrix composition; a clear difference to modifications observed with progestins. These data suggest major progress in the treatment of excessive menstrual bleeding.