Enhanced myometrial vascularity: what, where and when to treat

Enhanced myometrial vascularity (EMV) is defined as focal myometrial hypervascularity at the former placental implantation site identified after a recent pregnancy. Spectral Doppler imaging shows characteristic high velocity, low resistance flow. Proposed mechanisms underlying prolonged EMV include delayed involution of remodeled uterine arteries and persistent trophoblastic activity with associated neoangiogenesis. EMV may reflect normal involution or subinvolution of the placental site or may be associated with retained products of conception. While often self-limited in asymptomatic patients, EMV in the setting of abnormal uterine bleeding warrants further evaluation and tailored management. Terminological ambiguity persists between EMV and acquired arteriovenous malformation (AVM) or fistula (AVF). Although Doppler findings may suggest arteriovenous shunting, cross-sectional imaging alone cannot reliably distinguish these entities, and catheter angiography remains the reference standard when definitive characterization is required. Importantly, many cases labeled as “acquired AVM” in the postpregnancy setting likely represent EMV related to persistent uteroplacental circulation or subinvolution rather than true vascular malformations. This distinction is clinically important, as true high-flow lesions, though less common, carry a risk of significant hemorrhage and may require uterine artery embolization. EMV may also be seen following intrauterine ectopic pregnancies, most commonly those implanted within a Cesarean scar. Several conditions may mimic EMV, including adenomyosis, pseudoaneurysm, gestational trophoblastic disease, fibroids, polyps, endometrial neoplasm and infection. Management is individualized based on clinical status, imaging findings, and associated conditions. Accurate recognition of EMV and use of this specific terminology as well as differentiation from mimics, is essential to guide appropriate care and avoid unnecessary interventions. Similar content being viewed by others

Enhanced myometrial vascularity (EMV) is an increasingly recognized sonographic finding in the postpregnancy setting, which can be identified following early pregnancy loss, termination of pregnancy, or delivery [1, 2]. It may be detected incidentally in otherwise asymptomatic patients or present clinically with postpregnancy uterine bleeding. EMV can be associated with retained products of conception (RPOC) or subinvolution of placental site vascularity (SIPS) [3, 4]. It can also occur following intrauterine ectopic pregnancies, most commonly those implanted within a Cesarean scar [5]. Importantly, its imaging appearance may overlap with that of uterine arteriovenous malformations (AVMs) and arteriovenous fistulas (AVFs), creating a significant diagnostic challenge [6]. The clinical importance of EMV lies in this overlap, as misdiagnosis may lead to unnecessary uterine artery embolization (UAE) or high-risk surgical intervention, whereas underrecognition may result in delayed treatment and potentially severe hemorrhage. This review aims to summarize the current understanding of EMV, with a focus on its pathophysiology, imaging features, differential diagnosis, and clinical implications, in order to clarify its position within the spectrum of postpregnancy uterine vascular changes and to support more consistent clinical decision-making. Definition EMV is defined as focal myometrial hypervascularity at the former placental implantation site identified after a recent pregnancy, with spectral Doppler imaging demonstrating characteristic high velocity, low resistance flow [7].

and pathophysiology During pregnancy, trophoblastic flow is necessarily present within the myometrium and the placenta and reflects implantation-site vascularity. The uterine component reflects invasion of the placental trophoblast into the myometrium with remodeling of maternal vessels into a high velocity, low resistance circuit. Color Doppler is not routinely used in the evaluation of a normal first-trimester intrauterine pregnancy, as the additional acoustic energy may result in tissue heating and potential bioeffects on the developing embryo. Consequently, radiologists may not be familiar with this finding in routine first-trimester imaging. After a pregnancy, the uteroplacental circulation normally involutes as the previously dilated, low-resistance uterine vessels regress toward their non-gravid state. While it is possible to normally detect this flow transiently after pregnancy, it is the more pronounced/persistent flow in the setting of abnormal uterine bleeding that is considered EMV and which may require further evaluation and treatment. Proposed mechanisms underlying prolonged EMV include delayed involution of the physiologically remodeled, dilated uterine arteries that supply the placenta, resulting in persistence of a high-velocity, low-resistance vascular network. Another contributing factor may be excessive invasion of the myometrium by syncytiotrophoblasts, accompanied by neoangiogenesis and increased endothelial proliferation, further sustaining abnormal vascularity [2, 8, 9]. Diagnostic criteria for EMV on ultrasound On grayscale ultrasound, EMV typically appears as a focal, ill-defined, heterogeneous area within the myometrium, most commonly located near the endometrial-myometrial junction [2]. This region often contains multiple tortuous, serpiginous tubular structures. It may be associated with echogenic endometrial material in cases of RPOC. Color and spectral Doppler ultrasound shows prominent vascularity, low-resistance high-velocity flow with peak systolic velocity (PSV) usually ≥ 20 cm/s [7]. However, accurate angle correction for PSV measurement is frequently limited by vessel tortuosity, and no standardized measurement technique has been established, therefore, absolute PSV values may not be reliable [3, 6]. Although some authors have suggested that higher PSV values may correlate with an increased risk of heavier bleeding, this association has not been consistently validated in large cohort studies [10, 11]. Controversy in terminology There has been longstanding terminological ambiguity in the literature, with the terms EMV and AVM sometimes used interchangeably [6, 12]. However, these entities are not synonymous, and clearer distinctions are increasingly emphasized to avoid overdiagnosis and unnecessary intervention. Congenital AVM is exceedingly rare in the uterus [12]. It arises from a developmental failure of the primitive capillary plexus during fetal angiogenesis, resulting in a complex network of multiple direct communications between arteries and veins without an intervening capillary bed [13]. These lesions are typically extensive, may involve surrounding pelvic structures, and often present outside the immediate postpregnancy setting. Acquired AVM, in contrast, is more relevant in gynecologic practice. It is generally considered a vascular lesion that develops after uterine trauma or iatrogenic injury, such as dilation and curettage (D&C), Cesarean delivery, or other instrumentation. Pathologically, it consists of a disorganized network of arteries and veins connected through a central nidus, again lacking a normal capillary bed [13, 14]. Several authors advocate that the term “AVM” should be reserved exclusively for congenital malformations, recommending against using “acquired AVM” to describe postprocedural or postpregnancy vascular lesions [3, 15]. AVF is also an acquired lesion, most often resulting from similar iatrogenic or traumatic causes. Unlike AVM, an AVF classically represents a single direct communication between an artery and a vein without an intervening nidus [13]. In the postpregnancy or postprocedural setting, when imaging demonstrates a focal area of markedly increased myometrial vascularity, particularly with serpiginous vessels and high-velocity, low-resistance, and sometimes turbulent flow on Doppler, radiologists may use descriptive terms such as “acquired AVM” or “AVF” to indicate suspected arteriovenous shunting. However, an important limitation is that imaging alone (including ultrasound with Doppler, CT, or MRI) often cannot reliably distinguish between an acquired AVM and an AVF, as both can demonstrate overlapping features of arteriovenous shunting [13]. Catheter angiography remains the reference standard for more definitive characterization, though it is typically reserved for cases requiring intervention. In this article, the authors use the term “acquired AVM” to describe cases in which there is suspected arteriovenous communication, while acknowledging that a definitive distinction from an AVF cannot be reliably made based on imaging alone. From a practical standpoint, many cases labeled as “acquired AVM” in the postpregnancy setting likely represent part of the EMV spectrum, reflecting persistent uteroplacental circulation or subinvolution rather than a true structural vascular malformation. Use of the term EMV in this setting is preferred over AVM/AVF since it highlights the pregnancy connection. EMV is a more general term that avoids specifying whether there is truly any arteriovenous shunting, since this is not reliably determined on ultrasound. Prolonged EMV post pregnancy Prolonged EMV may be encountered in the setting of subinvolution of the placental site or incomplete pregnancy loss (RPOC). Normal involution of the placental bed is a gradual process that can take several weeks, during which the previously dilated, low resistance uteroplacental vessels progressively regress [16]. Subinvolution of the placental site vascularity (SIPS) refers to delayed or incomplete regression of uteroplacental vessels. It is a histopathologic diagnosis characterized by persistence of dilated spiral arteries at the implantation site, possibly related to an abnormal immunologic recognition process [17, 18]. On ultrasound, SIPS typically manifests as EMV localized to the placental implantation site, with low-resistance vessels that may range from mild hypervascularity to large, dilated vessels. However, these imaging findings overlap with physiologic involution of EMV. Therefore, when EMV is identified, it often remains unclear whether this represents normal involution in progress or pathologically delayed involution consistent with SIPS. SIPS is not an imaging diagnosis; definitive evaluation should be deferred to pathology [3, 15] (Fig. 1A-D). In asymptomatic patients, incidentally detected EMV on ultrasound is typically managed expectantly, as it often resolves spontaneously without intervention [6]. In contrast, patients with EMV who present with abnormal uterine bleeding may require an intervention. Even in cases where RPOC is not clearly visualized, D&C may still be beneficial in selected symptomatic patients through several proposed mechanisms. First, it mechanically disrupts abnormal, persistently dilated vessels at the placental site, which can reduce ongoing bleeding. Second, the procedure induces uterine contractions and stimulates tissue remodeling, promoting hemostasis and facilitating restoration of normal uterine architecture. Finally, uterine evacuation allows for histopathologic examination of the removed tissue, enabling definitive confirmation of SIPS or occult RPOC, thereby guiding further management if needed [19]. However, this approach must be used judiciously. In cases with pronounced vascularity or suspected high-flow arteriovenous shunting, uterine instrumentation carries a significant risk of hemorrhage. In such situations, alternative strategies such as UAE may be safer and more effective for controlling bleeding while minimizing procedural risk. Spectrum of EMV associated with RPOC Retained products of conception refer to gestational tissue, fetal, placental, or both, that remains within the endometrial cavity following delivery, spontaneous or induced early pregnancy loss [3, 4]. On ultrasound, the term RPOC should generally be reserved for cases with visible intracavitary tissue. The sonographic appearance can vary widely, from a discrete echogenic mass to more subtle, heterogeneous endometrial thickening. EMV is usually present, but the degree of vascularity associated with RPOC is variable and not specific, ranging from no detectable associated vascularity to marked EMV [4] (Fig. 1E, F). Endometrial thickness is an important adjunctive finding — a thin endometrium of less than 10 mm has a high negative predictive value for RPOC [20]. Serum beta human chorionic gonadotropin (β-hCG) trends can provide additional diagnostic guidance. However, a positive β-hCG does not necessarily indicate that RPOC is present since serum β-hCG can remain detectable for up to 2 months after pregnancy loss and up to 1 month following delivery [21]. EMV associated with RPOC or persistent trophoblastic tissue is often accompanied by a detectable or slowly declining β-hCG; however, vascularity itself is not dependent on β-hCG positivity. EMV may be present despite a negative β-hCG and can persist after β-hCG normalization, particularly in the setting of residual vascular remodeling or nonviable retained tissue [2, 15]. Acquired AVM EMV and acquired AVM may appear identical on ultrasound. MRI/MR angiography or catheter angiography may aid in differentiation. Catheter angiography is not routinely performed solely for diagnostic purposes. However, it may be indicated when non-invasive imaging is inconclusive and there is ongoing clinical concern for significant vascular pathology, particularly in patients with persistent or heavy uterine bleeding. In these settings, angiography is most often performed in conjunction with planned endovascular treatment, such as UAE, allowing for both definitive diagnosis and immediate therapeutic intervention in the same setting. Acquired AVM is usually a sequela of instrumentation (e.g., D&C) and represents a fistulous communication between artery and vein without intervening capillary network. On ultrasound, AVM is typically centered in the myometrium without an associated vascular endometrial mass and demonstrates early venous drainage on angiography (Fig. 2A-D), which may be sometimes appreciated on MR angiography; however, detection of early venous drainage may be challenging. Although an early draining vein is usually ascribed to AVM (51), high flow due to persistent uteroplacental circulation can also lead to an early enhancement of a draining vein at dynamic MRI or angiography in setting of EMV [22]. In patients with significant uterine bleeding who are likely to require UAE, immediate management may take precedence over definitive distinction between EMV and acquired AVM, as both entities can be effectively treated with endovascular therapy. However, if bleeding is mild or intermittent and hysteroscopy with D&C is considered as a treatment option, the referring gynecologist may need to know if there is an AVM, since a D&C in this scenario can cause significant bleeding. When diagnostic uncertainty persists, following the initial evaluation with transvaginal color Doppler ultrasound, MRI with MR angiography can help differentiate EMV with RPOC from acquired AVM (Fig. 3A-F), guide UAE planning, and evaluate for suspected placenta accreta spectrum disorder. EMV may regress spontaneously or can be treated with D&C when associated with RPOC, whereas acquired AVM typically requires embolization. The comparative features of EMV, SIPS and acquired uterine AVM/AVF are summarized in Table 1. EMV associated with uterine ectopic pregnancy During pregnancy, trophoblastic flow is an expected finding that reflects implantation-site vascularity that is present in both normal intrauterine pregnancies and uterine ectopic pregnancies (EPs). Uterine EPs are uncommon and include Cesarean scar EP (~6%), interstitial EP (2–4%), and cervical EP (< 1%), listed in order of prevalence with approximate proportions among all ectopic pregnancies [23, 24]. EMV may be seen following uterine EP, most commonly those implanted within a Cesarean scar. In a Cesarean scar EP, EMV at the implantation site may persist for several weeks following methotrexate treatment, whether administered locally or systemically [5]. If β-hCG levels downtrend and the patient is asymptomatic, presence of low-level EMV does not necessarily indicate treatment failure. The mean time to β-hCG normalization is generally longer with local treatment compared to systemic therapy [25]. In rare instances, Cesarean scar EP can expel spontaneously. This may happen if the Cesarean scar EP is partially endophytic, growing toward the endometrial cavity [26]. For patients who present with bleeding and/or rising β-hCG levels after treatment or presumed passage of a Cesarean scar EP, color Doppler evaluation of the prior implantation site is recommended. If EMV is detected in conjunction with symptoms and/or increasing β-hCG levels, retreatment is often required [27]. Recent literature suggests that Cesarean scar EP may represent a precursor to placenta accreta spectrum (PAS) (Fig. 4A, B). The presence of a residual mass at the Cesarean scar site demonstrating both increased vascular flow and avascular lacunae should raise concern for PAS rather than isolated EMV. Emerging evidence indicates that UAE alone is likely insufficient for the treatment of PAS [26, 27]. Mimics Pseudoaneurysm (PSA) is a blood-filled collection that communicates with the arterial lumen as a result of a defect in the arterial wall. Uterine artery PSA may occur following procedures such as D&C, myomectomy, Cesarean section, or hysterectomy, and has also been reported after uncomplicated vaginal delivery [28, 29]. On color Doppler imaging, PSA demonstrates a characteristic “yin–yang” appearance, reflecting turbulent swirling flow within the sac, which helps distinguish it from pregnancy-related EMV. Spectral Doppler evaluation of the neck reveals a classic bidirectional “to-and-fro” waveform, with systolic inflow into the sac and diastolic outflow back into the feeding artery [30] (Fig. 5A, B). If unrecognized, a PSA may enlarge and eventually rupture, leading to significant hemorrhage. Therefore, it is essential to include PSA in the differential diagnosis of vaginal bleeding, particularly in the postoperative or postpartum setting. Endometritis and myometritis can mimic EMV on imaging. However, vascularity is usually diffusely increased throughout the endometrium and myometrium (Fig. 5C). Ultrasound may also reveal intraluminal air, though a small amount of air is normal in the early postpartum period [31]. Recognition of clinical signs such as fever, uterine tenderness, and leukocytosis along with careful imaging assessment, is essential to differentiate infection from true EMV. Potential complications of endometritis/myometritis include pyometra, abscess formation, and thrombophlebitis [3, 31]. Vascular adenomyosis. Adenomyosis is characterized by endometrial glands and stroma within the myometrium. This ectopic tissue behaves like endometrium, may respond to hormones and proliferate. This stimulates angiogenesis in the surrounding myometrium. Spectrum of vascularity can be variable. In early pregnancy in setting of marked vascular adenomyosis, sonographic findings may be mistaken for gestational trophoblastic disease or a neoplasm [14]. Follow up ultrasound should be considered to ensure normal pregnancy development. Gestational trophoblastic disease (GTD) comprises a spectrum of disorders characterized by abnormal proliferation of trophoblastic tissue, ranging from benign molar pregnancies to malignant gestational trophoblastic neoplasia. Serum β-hCG levels are typically markedly elevated and often exceed expected values for gestational age [32]. Molar pregnancies represent benign or premalignant end of the spectrum and include complete and partial hydatidiform moles. A complete hydatidiform mole is the most common form. Approximately 90% have a 46,XX karyotype and 10% are 46,XY; in both cases, the genetic material is entirely paternal in origin, usually resulting from fertilization of an empty ovum by a single sperm that duplicates its genome or, less commonly, by two sperm [32]. On ultrasound, a complete mole classically appears as an intrauterine mass with numerous small cystic spaces (“snowstorm” or “cluster of grapes” appearance) and no identifiable fetal tissue [33, 34]. Partial moles are typically triploid, most often arising from fertilization of a normal ovum by two sperm. Their sonographic appearance is variable, ranging from findings similar to a complete mole to those resembling early pregnancy loss. Unlike complete moles, fetal tissue may be present [32]. Both complete and partial molar pregnancies typically demonstrate little to no significant myometrial vascularity, as the abnormal chorionic villi contain minimal functional vasculature [35]. However, if a molar pregnancy progresses to an invasive mole or choriocarcinoma, trophoblastic tissue penetrates the myometrium and induces neovascularization. In these cases, color Doppler imaging reveals marked hypervascularity, often with low-resistance, high-velocity flow [36] (Fig. 5D). Neovascularization associated with endometrial malignancy may produce tortuous, high-velocity, low-resistance vessels within the myometrium and resemble EMV (Fig. 5E, F). Fibroids, particularly intracavitary or submucosal types, can sometimes mimic EMV on imaging [37]. While typical fibroids usually show predominantly peripheral vascularity, atypical fibroids may exhibit heterogeneous internal flow and ill-defined margins. Endometrial polyps, particularly when large or heterogeneous with prominent internal vascularity and an irregular contour may resemble the sonographic patterns seen with RPOC or EMV. In the postpregnancy setting, this overlap can complicate interpretation, emphasizing the need to correlate imaging with clinical history, β-hCG levels, and, when necessary, follow-up or hysteroscopic evaluation. Management Management of EMV should be individualized, considering the presence and severity of bleeding, suspicion for RPOC, the degree and pattern of vascularity on imaging, and the patient’s hemodynamic stability. The following discussion provides an integrated overview of the main management strategies, while detailed, condition-specific treatment considerations are addressed in the respective sections of this review. In cases of prolonged EMV and suspected SIPS, expectant management is appropriate for patients with minimal or no bleeding; if bleeding persists, D&C may be performed [3, 38]. Patients with significant bleeding, pronounced EMV, or acquired AVM typically require UAE to control hemorrhage safely. If bleeding remains uncontrolled despite conservative or minimally invasive measures, hysterectomy may be indicated. When vascular RPOC is identified, management is generally directed at removal, although uterotonic medications may also be considered [4]. In suspected PAS disorder associated with Cesarean scar EP, UAE alone is likely insufficient for the treatment of PAS, and surgical intervention may be required [27]. Summary Enhanced myometrial vascularity is focal myometrial hypervascularity at the placental implantation site, characterized by high-velocity, low-resistance flow on spectral Doppler imaging in the postpregnancy setting. EMV reflects persistent uteroplacental circulation or subinvolution of the placental site. In contrast, acquired AVM or AVF is abnormal structural arteriovenous shunting with direct communication between arteries and veins, typically related to prior uterine trauma or instrumentation. Although the imaging appearances may overlap, EMV should not be used interchangeably with acquired AVM/AVF, as the underlying pathophysiology, natural history, and management strategies may differ. From a practical standpoint, many cases labeled as “acquired AVM” in the postpregnancy setting likely represent part of the EMV spectrum rather than a true structural vascular malformation. In patients with bleeding, a history of prior uterine intervention, or a focal area of markedly increased vascularity on ultrasound, further evaluation with MRI/MR angiography, or catheter angiography may be warranted to assess vascular anatomy and guide management. A variety of conditions can mimic EMV. Accurate diagnosis requires correlation of imaging findings with clinical history, β-hCG trends, and, when necessary, follow-up imaging or hysteroscopic evaluation. Management of EMV is individualized and depends on the severity of bleeding, presence of associated RPOC or uterine ectopic pregnancy, and the patient’s hemodynamic stability. Data availability No datasets were generated or analysed during the current study.

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Dewilde K, Groszmann Y, Van Schoubroeck D, Grewal K, Huirne J, de Leeuw R, Bourne T, Timmerman D, Van den Bosch T. Enhanced myometrial vascularity secondary to retained pregnancy tissue: time to stop misusing the term arteriovenous malformation. Ultrasound in Obstetrics and Gynecology. 2024;63(1):5–8. doi:https://doi.org/10.1002/uog.27476 PubMed PMID: 37676250. Author information Authors and Affiliations Contributions M.G. drafted the manuscript. M.G. and M.M.H. contributed equally to the preparation of figures. M.M.H. critically reviewed the manuscript. Both authors approved the final manuscript. Corresponding author Ethics declarations Competing interests The authors declare no competing interests. Additional information Publisher’s note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Supplementary Information Below is the link to the electronic supplementary material. 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To view a copy of this licence, visit http://creativecommons.org/licenses/by-nc-nd/4.0/. About this article Cite this article Grigovich, M., Horrow, M.M. Enhanced myometrial vascularity: what, where and when to treat. Abdom Radiol (2026). https://doi.org/10.1007/s00261-026-05597-9 Received: Accepted: Published: Version of record: DOI: https://doi.org/10.1007/s00261-026-05597-9