Association of human chorionic gonadotropin and post‐pregnancy persistent enhanced myometrial vascularity

OBJECTIVE: To explore the role of circulating human chorionic gonadotropin (hCG) in the pathophysiology of enhanced myometrial vascularity (EMV) postpregnancy and the usefulness of determining hCG level in the clinical evaluation and management of this condition. METHODS: This was a retrospective observational case series of patients managed clinically at our centers who had postpregnancy EMV diagnosed using ultrasound by the observation of a dilated vascular web in the myometrium, with or without retained products of conception (RPOC), that persisted beyond 4-6 weeks following a failed or terminated pregnancy. We retrieved serial maternal serum hCG measurements and noted the highest maternal serum hCG level measured, as well as the time for hCG to reach non-pregnancy levels, defined as hCG ≤ 5 mIU/mL. The time to resolution of the EMV was recorded; this was determined by normal ultrasound findings (when imaging was available), or assumed if a procedure had been performed to resolve the EMV or when hCG reached non-pregnancy levels. When available, we retrieved peak systolic velocity (PSV) values measured in the vascular web. A PSV of ≥ 20 cm/s was considered elevated. Representative ultrasound and color Doppler images were evaluated. RESULTS: Sixteen patients with sonographically diagnosed EMV that was still present over 4-6 weeks after failure or termination of a pregnancy (i.e. persistent EMV) were included. The median duration from diagnosis of EMV until resolution was 113 (range, 58-293) days. Persistence of EMV was associated with prolonged detectable levels of hCG, with a time for hCG to reach non-pregnancy levels of 97 (range, 58-271) days. In the 13 cases in which this was measured, Doppler studies revealed elevated PSV, with a median highest PSV of 80.8 (range, 46.7-146.3) cm/s. One patient was managed expectantly from the outset of their presentation. Four additional patients were followed expectantly for the EMV after they underwent surgical procedures at presentation; seven patients required uterine artery embolization and four required dilatation and curettage to remove the residual placental tissue. CONCLUSIONS: Our findings suggest that pathological persistence of EMV is associated with the prolonged presence of circulating hCG, probably produced by residual trophoblastic tissue. Furthermore, we believe that persistent EMV is potentially maintained, in major part, by the vasodilatory and angiogenic effects of circulating hCG. Recognition of this association provides a physiological explanation for the natural history of EMV and supports expectant management in hemodynamically stable patients. Monitoring of maternal serum hCG and Doppler PSV may help to distinguish self-resolving EMV from cases requiring intervention, and high PSV levels can alert the practitioner to the potential for hemorrhage following intervention. These findings highlight the importance of differentiating EMV from congenital arteriovenous malformation and RPOC without EMV, and may inform more tailored, less invasive clinical management strategies. © 2026 International Society of Ultrasound in Obstetrics and Gynecology.