The intent of this research was to identify if the degenerative changes within arteries in the endometrium (endometrial angiopathies) correlate with degenerative changes in the uterine arteries and can be used as a predictor of increased risk for uterine artery rupture (UAR). With this objective specimens from 20 mares that died from uterine artery rupture and 21 control mares that died from unrelated causes were obtained from cases submitted to the University of Kentucky Veterinary Diagnostic Laboratory (UKVDL) over a two-year period. Postmortem specimens of each mare were collected from the left and right uterine arteries at the origin, bifurcation, and distal to the bifurcation as well as full thickness uterine wall sections at five different sites. An additional sample was taken from the uterine artery at the site of rupture in the affected mares. Tissue samples were immersed in 10% neutral buffered formalin, routinely processed, and stained with hematoxylin and eosin, Masson’s Trichrome, and Verhoeff´s Van Gieson histochemical stains as well as a smooth muscle-actin immunohistochemical marker. Elastosis, fibrosis, and vascular smooth muscle cell degeneration were identified in this study as potential contributors of vascular degeneration and a scoring system was developed to differentiate the degrees of severity of these specific degenerative changes within the intima and media of the vascular wall. Based on the scoring system, sections of uterine arteries and endometrial arterioles were blindly examined and the scored changes recorded for statistical analysis. Although the degenerative changes in endometrial and uterine arteries were similar within each group, the results could not not be used to predict an increased risk for UAR. Furthermore, we determined the major changes in vascular pathology of the affected uterine arteries and show there is a significant difference in degenerative changes between specific layers of the vascular wall.

Os métodos minimamente invasivos têm sido cada vez mais utilizados para o tratamento do leiomioma e, a embolização da artéria uterina, tem se destacado como método seguro e efetivo. O objetivo deste estudo foi avaliar, pela ressonância magnética da pelve, os fatores preditores da diminuição dos leiomiomas de pacientes submetidos a embolização da artéria uterina. Métodos: Estudaram-se 50 mulheres sintomáticas com leiomioma uterino, na menacme, que foram submetidas a embolização da artéria uterina. Acompanhou-se, por meio da ressonância magnética o volume do útero e dos leiomiomas. Foram examinados 179 leiomiomas nestas pacientes, um mês antes e seis meses depois do procedimento. Resultados: Seis meses após o tratamento, a redução média do volume uterino foi de 38,91%, enquanto os leiomiomas tiveram redução de 55,23%. Nos leiomiomas submucosos e/ou com a relação nódulo/músculo em T2 mais elevada, a redução do volume foi ainda maior (maior que 50,00%). Conclusões: As pacientes portadoras de leiomiomas e submetidas à embolização da artéria uterina apresentaram redução de volume dos nódulos superior a 50,00%, à ressonância magnética, quando eram submucosos e/ou tinham uma relação nódulo/músculo em T2 mais elevada / Objective : Minimally invasive methods are being an alternative to treat leiomyomas, including the uterine artery embolization that has emerged as a safe and effective method. The aim of this study was to evaluate the magnetic resonance imaging predictors of decrease in leiomyomas of patients who underwent uterine artery embolization. Methods: This study followed 50 symptomatic premenopausal women with uterine leiomyoma who underwent uterine artery embolization. Treatment was accompanied by magnetic resonance imaging of both the volume of the uterus and the leiomyomas. We examined 179 leiomyomas in that 50 patients, one month before and six months after of the procedure. Results: Six months after treatment, the mean reduction in uterine was 38.91%, while leiomyomas decreased by 55.23%. In submucosal leiomyomas and/or with a higher node/muscle ratio in T2, the volume reduction was even higher (greater than 50.00%). Conclusions: The patients with leiomyomas and underwent uterine artery embolization, showed reductions in the volume of nodes greater than 50,00%, on the magnetic resonance imaging, when they were submucosal and / or had a higher node-to-muscle ratio in T2

Os métodos minimamente invasivos têm sido cada vez mais utilizados para o tratamento do leiomioma e, a embolização da artéria uterina, tem se destacado como método seguro e efetivo. O objetivo deste estudo foi avaliar, pela ressonância magnética da pelve, os fatores preditores da diminuição dos leiomiomas de pacientes submetidos a embolização da artéria uterina. Métodos: Estudaram-se 50 mulheres sintomáticas com leiomioma uterino, na menacme, que foram submetidas a embolização da artéria uterina. Acompanhou-se, por meio da ressonância magnética o volume do útero e dos leiomiomas. Foram examinados 179 leiomiomas nestas pacientes, um mês antes e seis meses depois do procedimento. Resultados: Seis meses após o tratamento, a redução média do volume uterino foi de 38,91%, enquanto os leiomiomas tiveram redução de 55,23%. Nos leiomiomas submucosos e/ou com a relação nódulo/músculo em T2 mais elevada, a redução do volume foi ainda maior (maior que 50,00%). Conclusões: As pacientes portadoras de leiomiomas e submetidas à embolização da artéria uterina apresentaram redução de volume dos nódulos superior a 50,00%, à ressonância magnética, quando eram submucosos e/ou tinham uma relação nódulo/músculo em T2 mais elevada / Objective : Minimally invasive methods are being an alternative to treat leiomyomas, including the uterine artery embolization that has emerged as a safe and effective method. The aim of this study was to evaluate the magnetic resonance imaging predictors of decrease in leiomyomas of patients who underwent uterine artery embolization. Methods: This study followed 50 symptomatic premenopausal women with uterine leiomyoma who underwent uterine artery embolization. Treatment was accompanied by magnetic resonance imaging of both the volume of the uterus and the leiomyomas. We examined 179 leiomyomas in that 50 patients, one month before and six months after of the procedure. Results: Six months after treatment, the mean reduction in uterine was 38.91%, while leiomyomas decreased by 55.23%. In submucosal leiomyomas and/or with a higher node/muscle ratio in T2, the volume reduction was even higher (greater than 50.00%). Conclusions: The patients with leiomyomas and underwent uterine artery embolization, showed reductions in the volume of nodes greater than 50,00%, on the magnetic resonance imaging, when they were submucosal and / or had a higher node-to-muscle ratio in T2

No description available.

No description available.

Introdução: As malformações arteriovenosas são lesões congênitas caracterizadas por uma rede capilar malformada (nidus) que comunica o sistema arterial e venoso em um mecanismo de shunt arteriovenoso não irrigando tecido normal. Devido ao shunt arteriovenoso as MAVs apresentam alto fluxo sanguíneo, podem ser assintomáticas ou sintomáticas dependendo de sua localização. O tratamento das MAV busca a exclusão circulatória completa do nidus o que pode ser alcançado por meio de ressecção cirúrgica, radiocirurgia ou embolização endovascular. Objetivo: descrição técnica de uma série de dois casos de MAVs de localização periférica (fora do sistema nervoso central), que foram tratadas através da embolização com uso de cateter-balão de duplo lúmen. Materiais e métodos: Trata-se de estudo retrospectivo que avaliou os pacientes submetidos a embolização com cateter-balão de duplo lúmen para o tratamento das MAVs periféricas pelo Setor de Radiologia Intervencionista do HCFMRP-USP. Resultados: Os achados encontrados foram consistentes com a literatura atual demonstrando altas taxas de sucesso técnico e clínico, sem complicações inerentes ao procedimento. Conclusão: O uso destes dispositivos se mostrou mais eficaz em obliterar completamente o nidus deste tipo de lesão, além de reduzir o tempo de procedimento, a exposição à fluoroscopia. Neste estudo foi obtida a exclusão angiográfica completa das MAV em uma única sessão de embolização e não foram descritas complicações relacionadas ao tratamento. / Introduction: Arteriovenous malformations are congenital lesions characterized by a malformed capillary network (nidus) that communicates the arterial and venous system in an arteriovenous shunt mechanism and does not irrigate normal tissue. Due to the arteriovenous shunt AVMs present high blood flow, they may be asymptomatic or symptomatic depending on their location. The AVM treatment seeks the complete circulatory exclusion of the nidus which can be achieved by means of surgical resection, radiosurgery or endovascular embolization. Objectives: A technical description of a series of two cases of peripheral AVMs that were treated through embolization using a dual-lumen balloon catheter. Materials and methods: This is a retrospective study that evaluated patients undergoing embolization with a double-lumen balloon catheter for the treatment of peripheral AVMs by the Interventional Radiology Sector of HCFMRP-USP. Results: The findings were consistent with the current literature demonstrating high rates of technical and clinical success, without complications inherent to the procedure. Conclusion: The use of these devices has been shown to be more effective in completely obliterating the nidus of this type of lesion, in addition to reducing the procedure time, exposure to fluoroscopy. In this study complete angiographic exclusion of AVM was obtained in a single embolization session and no complications related to treatment were described.

<p>This study was undertaken to investigate the involutional changes of the uterus and uterine cavity by ultrasound (US), gray-scale and Doppler, after normal delivery, and to compare with the corresponding findings from women with puerperal complications, particularly retained placental tissue (RPT). The overall design was exploratory and prospective, with the use of descriptive statistics for analysis. </p><p>Forty-two women with uncomplicated vaginal term delivery were examined on post-partum days 1, 3, 7, 14, 28 and 56. The AP diameters of the uterus and uterine cavity and morphological findings were recorded. The maximum AP diameters of the uterus and uterine cavity diminished from 92.0 mm on day 1 to 38.9 mm at day 56 and from 15.8 mm at day 1 to 4.0 mm at day 56, respectively. The uterus was most often empty in the early and late puerperium while a mixed echo pattern over the whole cavity was found during mid puerperium (I).</p><p>Seventy-nine women with secondary post partum hemorrhage (SPH) were examined on the day they presented with clinical symptoms. US revealed an echogenic mass in the uterine cavity in 17 of 18 patients treated surgically and histology confirmed placental tissue in 14 of these. Sixty-one patients with either an empty cavity or mixed echo pattern had an uneventful puerperal course after conservative treatment (II).</p><p>AP diameters and morphological findings for 55 women with endometritis, 28 after caesarean section and 20 after manual evacuation of the placenta overlapped extensively with normal references (III).</p><p>The physiological vascular involution studied in 45 women after normal delivery showed that PI and RI indices did not change significantly until day 28 postpartum. The presence of at least one uterine artery notch was found in 13.3% of the women at day 1 and in 90.6% at day 56 postpartum (IV).</p><p>PI and RI values were measured and compared with reference values in 20 women with clinical suspicion of RPT who were to undergo surgical evacuation. Mean resistance indices were below the 10th percentile for eight of these 20 women, but overlapping was considerable. Doppler US has limited value as a diagnostic tool for RPT. The absence of a hyper-vascular area in the myometrium does not exclude RPT but an echogenic mass in the cavity is a sign of RPT (V).</p>

This study was undertaken to investigate the involutional changes of the uterus and uterine cavity by ultrasound (US), gray-scale and Doppler, after normal delivery, and to compare with the corresponding findings from women with puerperal complications, particularly retained placental tissue (RPT). The overall design was exploratory and prospective, with the use of descriptive statistics for analysis. Forty-two women with uncomplicated vaginal term delivery were examined on post-partum days 1, 3, 7, 14, 28 and 56. The AP diameters of the uterus and uterine cavity and morphological findings were recorded. The maximum AP diameters of the uterus and uterine cavity diminished from 92.0 mm on day 1 to 38.9 mm at day 56 and from 15.8 mm at day 1 to 4.0 mm at day 56, respectively. The uterus was most often empty in the early and late puerperium while a mixed echo pattern over the whole cavity was found during mid puerperium (I). Seventy-nine women with secondary post partum hemorrhage (SPH) were examined on the day they presented with clinical symptoms. US revealed an echogenic mass in the uterine cavity in 17 of 18 patients treated surgically and histology confirmed placental tissue in 14 of these. Sixty-one patients with either an empty cavity or mixed echo pattern had an uneventful puerperal course after conservative treatment (II). AP diameters and morphological findings for 55 women with endometritis, 28 after caesarean section and 20 after manual evacuation of the placenta overlapped extensively with normal references (III). The physiological vascular involution studied in 45 women after normal delivery showed that PI and RI indices did not change significantly until day 28 postpartum. The presence of at least one uterine artery notch was found in 13.3% of the women at day 1 and in 90.6% at day 56 postpartum (IV). PI and RI values were measured and compared with reference values in 20 women with clinical suspicion of RPT who were to undergo surgical evacuation. Mean resistance indices were below the 10th percentile for eight of these 20 women, but overlapping was considerable. Doppler US has limited value as a diagnostic tool for RPT. The absence of a hyper-vascular area in the myometrium does not exclude RPT but an echogenic mass in the cavity is a sign of RPT (V).

OBJECTIF: évaluer un modèle prédictif de prééclampsie associant des marqueurs cliniques, biologiques (Inhibine A, PP-13, hCG, ADAM12, PAPP-A et PlGF) et du Doppler des artères utérines (DAU) au 1er trimestre de la grossesse. METHODE : étude prospective de cohorte de 893 nullipares chez qui DAU et prélèvement sanguin étaient réalisés à 11-14 semaines. RESULTATS : 40 grossesses se sont compliquées de prééclampsie (4,5%) dont 9 de prééclampsie précoce (1,0%) et 16 de prééclampsie sévère (1,8%). Le meilleur modèle prédictif de la prééclampsie sévère associait les marqueurs cliniques, PAPP-A et PlGF (taux de détection 87,5% pour 10% de faux positif). Le DAU étant corrélé à la concentration de PAPP-A (r=-0,117 ; p<0,001), il n’améliorait pas la modélisation. CONCLUSION : la combinaison de marqueurs cliniques et biologiques (PlGF et PAPP-A) au 1er trimestre permet un dépistage performant de la prééclampsie sévère. Le DAU n’est pas un instrument efficace de dépistage au 1er trimestre dans cette population. / OBJECTIVE: To determine the value of combined screening for pregnancy hypertensive disorders by maternal characteristics, first trimester uterine artery Doppler (UAD) and serum biomarkers (Inhibine A, PP-13, hCG, ADAM12, PAPP-A et PlGF). STUDY DESIGN: In this prospective cohort study, 893 nulliparous women had UAD evaluation and collection of serum sample at 11-14 weeks. RESULTS: 40 women developed preeclampsia (4.5%) of which 9 early-onset preeclampsia (1.0%), and 16 severe preeclampsia (1.8%). The best model to predict preeclampsia associated maternal charateristics, PAPP-A and PlGF (detection rate 87.5% for 10% of false positive). UAD was correlated to PAPP-A concentration (r=-0.117 ; p<0.001), and so did not add to predictive accuracy. CONCLUSION: Combination of maternal characteristics and first trimester PlGF and PAPP-A provides a useful screening for severe preeclampsia. First trimester UAD was not an efficient screening tool in this population.

La grossesse est un état physiologique particulier où de nombreux changements fonctionnels et structuraux surviennent. Chez la rate, pour répondre aux besoins grandissants du fœtus, l’artère utérine se développe pour atteindre le double de son diamètre original avant parturition. Par conséquent, le débit sanguin utérin augmente d’environ vingt fois. Pour ce faire, les vaisseaux utérins sont l’objet d’un remodelage caractérisé par une hypertrophie et une hyperplasie des différentes composantes de la paroi. De plus, ce remodelage est complètement réversible après la parturition, par opposition au remodelage vasculaire « pathologique » qui affecte les artères systémiques, dans l’hypertension chronique, par exemple. La grossesse s’accompagne aussi de modifications hormonales importantes, comme les œstrogènes dont la concentration s’accroît progressivement au cours de cette période. Elle atteindra une concentration trois cents fois plus élevée avant terme que chez une femme non gravide. Cette hormone possède de multiples fonctions, ainsi qu’un mode d’action à la fois génomique et non génomique. Considérant l’ensemble de ces éléments, nous avons formulé l’hypothèse que l’œstradiol serait responsable de modifier la circulation utérine durant la grossesse, par son action vasorelaxante, mais aussi en influençant le remodelage de la vasculature utérine. Nous avons montré que le 17β-Estradiol (17β-E2) produit une relaxation due à un effet non génomique des artères utérines en agissant directement sur le muscle lisse par un mécanisme indépendant du monoxyde d’azote et des récepteurs classiques aux œstrogènes (ERα, ERβ). De plus, la relaxation induite par le 17β-E2 dans l’artère utérine durant la gestation est réduite par rapport à celle des artères des rates non gestantes. Ceci serait attribuable à une diminution de monoxyde d’azote provenant de la synthase de NO neuronale dans les muscles lisses des artères utérines. Nos résultats démontrent que le récepteur à l’œstrogène couplé aux protéines G (GPER), la protéine kinase A (PKA) et la protéine kinase G (PKG) ne sont pas impliqués dans la signalisation intracellulaire associée à l’effet vasorelaxant induit par le 17β-E2. Cependant, nous avons montré une implication probable des canaux potassiques sensibles au voltage, ainsi qu’un rôle possible des canaux potassiques de grande conductance activés par le potentiel et le calcium (BKCa). En effet, le penitrem A, un antagoniste présumé des canaux potassiques à grande conductance, réduit la réponse vasoralaxante du 17β-E2. Toutefois, une autre action du penitrem A n’est pas exclue, car l’ibériotoxine, reconnue pour inhiber les mêmes canaux, n’a pas d’effet sur cette relaxation. Quoi qu’il en soit, d’autres études sont nécessaires pour obtenir une meilleure compréhension des mécanismes impliqués dans la relaxation non génomique sur le muscle lisse des artères utérines. Quant à l’implication de l’œstrogène sur le remodelage des artères utérines durant la gestation, nous avons tenté d’inhiber la synthèse d’œstrogènes durant la gestation en utilisant un inhibiteur de l’aromatase. Plusieurs paramètres ont été évalués (paramètres sanguins, réactivité vasculaire, pression artérielle) sans changements significatifs entre le groupe contrôle et celui traité avec l’inhibiteur. Le même constat a été fait pour le dosage plasmatique de l’œstradiol, ce qui suggère l’inefficacité du blocage de l’aromatase dans ces expériences. Ainsi, notre protocole expérimental n’a pas réussi à inhiber la synthèse d’œstrogène durant la grossesse chez le rat et, ce faisant, nous n’avons pas pu vérifier notre hypothèse. En conclusion, nous avons démontré que le 17β-E2 agit de façon non génomique sur les muscles lisses des artères utérines qui implique une action sur les canaux potassiques de la membrane cellulaire. Toutefois, notre protocole expérimental n’a pas été en mesure d’évaluer les effets génomiques associés au remodelage vasculaire utérin durant la gestation et d’autres études devront être effectuées. / Pregnancy is a peculiar physiological state in which many structural and functional changes occur. In rats, to meet the growing needs of the fetus, uterine artery expands to reach twice its original diameter before parturition. Therefore, uterine blood flow increases by about twenty times. To do this, the uterine vessels undergo substantial remodelling characterized by hypertrophy and hyperplasia of the various components of the wall. Furthermore, this remodelling is completely reversible after parturition, as opposed to “pathological vascular remodelling” that affects systemic arteries in chronic hypertension, for instance. Pregnancy is also accompanied by significant hormonal changes, such as estrogens whose concentration in the blood increases progressively during this period. It reaches concentrations three hundred times higher before term than in non-pregnant women. This hormone has multiple functions and mediates its effects by genomic and non-genomic pathways. Considering these elements, we hypothesized that estradiol would be responsible for remodeling the uterine circulation during pregnancy, by its vasorelaxant action, but also by influencing the remodeling of the uterine vasculature. We have shown that 17β-Estradiol (17β-E2) produced non-genomic relaxation of uterine arteries by acting directly on smooth muscle using a mechanism independent of nitric oxide and classical estrogen receptors (ERα, ERβ). Moreover, the relaxation induced by 17β-E2 in the uterine artery during pregnancy is reduced compared to that of arteries from non-pregnant animals. This is the result of decrease of nitric oxide derived from neuronal NO synthase in smooth muscle of uterine arteries. Our results also show that the estrogen receptor coupled to G proteins (GPER), protein kinase A (PKA) and protein kinase G (PKG) are NOT involved in intracellular signaling associated with the vasorelaxant effect induced by the 17β-E2. Moreover, we have shown a possible involvement of potassium channels sensitive to voltage and a possible involvement of large conductance calcium-activated potassium channels (BKCa). Indeed, the penitrem A, a suspected antagonist of BKCa, reduced the vasoralaxant responses of 17β-E2. However, some other actions of penitrem A are not excluded because iberiotoxin, known to inhibit the same channels, had no effect on this relaxation. However, further studies are needed to obtain a better understanding of the mechanisms involved in the relaxation non-genomics on the smooth muscle of uterine arteries. As for the involvement of estrogen on the remodeling of uterine arteries during pregnancy, we attempted to inhibit the synthesis of estrogen during pregnancy using an aromatase inhibitor. Several parameters were evaluated (plasma values, vascular reactivity, blood pressure) without significant changes between the control group and those treated with the inhibitor. The same observation was made for the determination of plasma estradiol, suggesting the uneffectiveness of aromatase blocking in these experiments. Thus, our experimental protocol failed to inhibit the synthesis of estrogen in rats during pregnancy and, in so doing, we cannot confirm or refute our hypothesis. In conclusion, we demonstrated that 17β-E2 acts on smooth muscle of the uterine arteries by a non-genomic pathway by apparently acting on potassium channels. However, our experimental protocol was not able to assess the genomic effects associated with uterine vascular remodeling during pregnancy and further studies are required to ascertain this aspect of our work.