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Vascular and Interventional Radiology |
1 From the Department of Vascular and Interventional Radiology, Stanford University Vascular Center, 300 Pasteur Dr, H-3651, Stanford, CA 94305. Received September 11, 2001; revision requested October 29; revision received January 8, 2002; accepted February 26. Address correspondence to M.K.R. (e-mail: mrazavi@stanford.edu).
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTS DISCUSSIONREFERENCES |
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MATERIALS AND METHODS: Angiographic ovarian artery–to–uterine artery anastomoses were studied in 76 consecutive patients undergoing uterine fibroid embolization. Mean patient age was 44.7 years (range, 29–56 years). Clinical follow-up consisted of a standard questionnaire. Procedural failure and complications were compared with the presence of various types of ovarian artery–to–uterine artery connections.
RESULTS: Three types of anastomoses were identified. In type I (33 [21.7%] of 152 arteries), flow from the ovarian artery to the uterus was through anastomoses with the main uterine artery. In type II (six arteries [3.9%]), the ovarian artery supplied the fibroids directly. In type III (10 arteries [6.6%]), the major blood supply to the ovary was from the uterine artery. Seven patients (9%) were considered to have clinical failure, with three of the six women with type II anastomoses being in this group. Three of the five women who experienced menopause after fibroid embolization had bilateral ovarian artery–to–uterine artery anastomoses that were classified as high risk.
CONCLUSION: Delineation of ovarian artery–to–uterine artery anastomosis is of practical relevance in avoiding nontarget ovarian embolization, in identification of those who would be at risk of uterine artery embolization or ovarian failure, and in those in whom the ovarian artery can be embolized safely.
© RSNA, 2002
Index terms: Angiography, 989.1222 • Arteries, ovarian, 986.1222, 986.1264 • Arteries, therapeutic embolization, 989.1264 • Arteries, uterine, 989.1222, 989.1264 • Leiomyoma, 854.315 • Uterine neoplasms, 854.315
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTS DISCUSSIONREFERENCES |
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Although anastomoses between the ovarian and uterine arteries have been studied extensively in cadavers and postmortem specimens (10,11), the frequency and importance of such anastomoses in this patient population and under physiologic conditions are not well described. We prospectively studied the frequency of angiographically detectable anastomoses between the ovarian and uterine arteries. We compared the presence of such arterial communications with procedural failure and premature menopause.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTS DISCUSSIONREFERENCES |
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Embolization and Angiographic Procedures
All patients were extensively counseled as to the known risks, benefits, and alternatives of uterine fibroid embolization, and written informed consent was obtained. Institutional review board approval was obtained. The women in the study cohort underwent initial abdominal aortography after placement of a standard 5-F introducer sheath and a pigtail catheter at the level of the renal arteries. Selective uterine angiography was then performed by injecting 1–3 mL of contrast material (various agents) per second for a total of 5 seconds by using either a 4-F catheter (Berenstein Glide; Meditech/B.C., Natick, Mass) or another uterine catheter (Roberts Uterine Curve Catheter; Cook, Bloomington, Ind). The operator determined the rate and volume of injection according to the size of the uterine artery. If the catheter was judged to induce vasospasm, a microcatheter (Masstransit; Cordis Endovascular, Miami, Fla) was introduced into the uterine artery in a coaxial fashion and the angiographic catheter was pulled back into the internal iliac artery. The uterine artery was embolized to complete stasis of flow in the main uterine artery by using either 355–500-µm polyvinyl alcohol particles (Truefill, Cordis Endovascular; and Contour, Meditech/B.C.) or 500–700-µm trisacryl gelatin microspheres (Embosphere; BioSphere Medical, Rockland, Mass). Repeat pelvic angiography with the pigtail catheter at the level of the renal arteries was then performed. If the ovarian artery was seen on the completion angiogram, it was investigated further with selective angiography. The catheters and sheath were then removed.
In four patients with severe menorrhagia who demonstrated ovarian artery–to-fibroid connections, bilateral (n = 1) and unilateral (n = 3) ovarian arteries were also embolized with polyvinyl alcohol particles after written informed consent for ovarian artery embolization was obtained. One such patient underwent unilateral microcatheter embolization of the anastomoses between the ovarian and uterine arteries distal to the ovary to avoid its devascularization. The flow to the ovary was left intact. The ages of these four women were 40, 45, 46, and 56 years. The latter patient was postmenopausal and the only woman in this series who underwent bilateral ovarian artery embolization.
The postuterine fibroid embolization clinical follow-up consisted of a questionnaire inquiring about each patient's symptoms, the status of their menses, whether or not they developed symptoms of menopause, and if they had received other treatments for their fibroids after uterine fibroid embolization.
Angiographic Evaluation
All angiograms were evaluated jointly by two interventional radiologists (M.K.R. and K.A.W.). The presence or absence of ovarian arteries and ovarian artery–to–uterine artery anastomoses was determined by consensus opinion.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTS DISCUSSIONREFERENCES |
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Five women developed persistent amenorrhea and symptoms of menopause. All were older than 46 years. Thirty-two women were older than 45 years in this cohort. The risk of menopause after uterine fibroid embolization was therefore 6% (five of 76) among all patients and 16% (five of 32) among those older than 45 years. Three of the six women with bilateral type Ib and/or III (mean age, 50 years; median age, 50 years; age range, 48–54 years) became menopausal.
Confirmation of anovulatory status with serum follicle-stimulating hormone was carried out in one patient. Seven additional women experienced temporary prolonged amenorrhea (defined as temporary amenorrhea >3 months for the purposes of this study). The number of patients with clinical failure, amenorrhea, or menopause and the type of anastomosis are listed in the Table.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTS DISCUSSIONREFERENCES |
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To better elucidate the frequency and importance of ovarian artery–to–uterine artery anastomoses, we prospectively studied the patterns of ovarian artery supply to the fibroids and the uterus in 76 consecutive patients. Three main patterns (and one subtype) emerged. In type I anastomosis, the ovarian artery supplies the fibroids by way of connections to the intramural uterine artery. In these cases, uterine artery embolization typically blocks the flow to the fibroid circulation distal to the point of anastomosis (Fig 2c). Thus, the ovarian artery supply is not likely to be a source of procedural failure and is typically not seen on aortograms obtained after uterine artery embolization. Women with subtype Ia have sufficient flow in the tubal artery such that reflux toward the ovary is not seen on the preembolization selective uterine angiogram. In these patients, careful review of the uterine angiogram may reveal contrast material dilution or washout at the point of anastomosis (Fig 6). An increase in the caliber of the intramural uterine artery or its branches may also indicate the presence of an ovarian artery–to–uterine artery anastomosis. This finding can be quite subtle depending on the relative flow from the ovarian artery in proportion to that from the uterine artery.
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With type II anastomosis, the ovarian artery feeds the fibroids directly. Uterine artery embolization is therefore unlikely to cause complete infarction of the fibroid, and the ovarian artery supply can be a cause of clinical failure of the uterine artery embolization. Enlargement of the ovarian artery after uterine artery embolization, as theorized by Nikolic et al (7), and post–uterine artery embolization observation of a previously undetected ovarian artery, as seen by Matson et al (15), would likely occur in this type of anastomosis. This pattern occurred in 8.0% of the patients and in 3.9% of the ovarian arteries in this study. In the report by Binkert et al (16), three of the 51 patients (6% of patients and 3% of arteries) had continued ovarian artery supply after uterine artery embolization, which suggests a type II anastomosis.
Of the six patients in this series with a type II connection, three underwent ovarian artery embolization in addition to uterine artery embolization and two of the remaining three patients reported clinical failure (67%). In our practice, we council all patients of this possibility. Once discovered at aortography, we usually take a "wait and see" approach. If symptoms do not improve 3 months after uterine artery embolization, we give the option of ovarian artery embolization to our perimenopausal patients (>48 years of age) after a full discussion of its alternatives and potential risks and benefits. Medical or surgical therapy is recommended to the remaining patients. Of the four patients who elected to undergo ovarian artery embolization as well as uterine artery embolization, one was postmenopausal and the other three were premenopausal. One of the latter patients underwent superselective embolization of the "fibroidal" branches of the ovarian artery distal to the ovary. None of the three premenopausal patients had ovarian failure after unilateral ovarian artery embolization. Whether these patients will experience anovulation and menopause earlier than they otherwise would is, of course, unknown at this time.
Type III anastomosis occurred in a small number of arteries (6.6% of the ovarian arteries in this study). In such cases, the ovarian supply appears to be from the uterine artery. Washout of the contrast material toward the uterus, as would be seen in type Ib, is not visualized. This pattern of ovarian supply has been described in dissected specimens. Lippert and Papst (17) indicated that 4% of ovaries draw their blood exclusively from the uterine artery. Dependence of the ovary on the uterine artery may be due to congenital absence of the ovarian artery, occlusive lesions affecting the ovarian artery or the aorta, or ovarian abnormalities such as tumor or inflammatory conditions causing recruitment of additional blood supply. In the study by Karlsson and Persson (12), unilateral tubo-ovarian arteries were seen in 15 of the 32 patients with benign ovarian lesions at selective internal iliac angiography. In these patients, the flow in the tubo-ovarian arteries was demonstrated to be toward the adnexa. Therefore, coexistent ovarian abnormality must be ruled out in patients with this pattern of flow.
The other practical importance of a type III anastomosis is the high likelihood of ovarian artery embolization on the affected side. Similarly, those who exhibit a type Ib connection are also at a higher risk of nontarget ovarian embolization, as described above. In this study, the six patients with bilateral types Ib and/or III anastomoses were considered to be the high-risk group for ovarian artery embolization. They constituted 8% of the 76 women in this study and 19% of the 32 women older than 45 years. Three of these six women became menopausal after uterine artery embolization, and another had prolonged temporary amenorrhea that lasted for 6 months. This observation lends validity to the notion of nontarget ovarian embolization as the cause of premature menopause in this patient population. Careful attention to redistribution of flow during embolization is, therefore, prudent to avoid reflux into the ovarian artery in this group.
On the basis of our observations, presence of bilateral types Ib and/or III anastomoses and age older than 46 years appear to be two risk factors for the development of persistent amenorrhea after uterine artery embolization. There were 32 women older than 45 years in this cohort, five (16%) of whom developed symptoms of menopause. No one younger than 45 years became menopausal in this study. This observation is similar to that of Chrisman et al (8): No one younger than 45 years experienced menopause as a result of uterine fibroid embolization. Although we agree with Chrisman et al on the potential reasons for menopause after uterine fibroid embolization, it appears that a higher frequency of nontarget ovarian embolization is a more plausible explanation. The resultant disturbance in ovarian flow in older patients with presumably diminished ovarian reserve may compromise the organ to a larger extent as compared with that in patients younger than 45 years. An increased prevalence of bilateral ovarian dependence on uterine artery flow in older women may be a reflection of reduced or nonexistent flow in the main ovarian arteries. The small number of patients in the study and in the high-risk group did not allow for a meaningful independent analysis of each risk factor (eg, age and presence of bilateral types Ib and/or III anastomoses).
It should be noted, however, that nonvisualization of an ovarian artery–to–uterine artery anastomosis at selective angiography does not indicate absence of such a connection. Two of the five patients with persistent amenorrhea and presumed premature menopause had no angiographically identifiable anastomosis. This statement is obviously based on our belief that premature menopause after uterine artery embolization is due to interruption of the ovarian blood supply.
There were several limitations to this observational study. First, we did not attempt to correlate the occurrence of these types of anastomoses to anatomic or physiologic factors such as absolute dimensions or the rate of growth of the uterus or fibroids, duration of or recent change in symptoms, location of fibroids, patient's gynecologic history, or risk factors for atherosclerosis. Formation of extrauterine collateral supply to the uterus can be promoted by pelvic adhesions from prior surgeries and possibly by the rapid growth of fibroids. Furthermore, ovarian artery–to–uterine artery connections may enlarge with adnexal abnormalities or atherosclerotic lesions of the aorta and thus promote retrograde flow in the tubo-ovarian segments.
A second limitation of this study is that the described patterns of anastomosis are based on findings of angiography performed with the technique described herein. Anatomic dissections or use of different angiographic techniques, such as performing selective ovarian angiography or hand injection of the uterine arteries, may yield different observations. The former may reveal an increased frequency of types I and II, and the latter is likely to underestimate the occurrence of types Ib and III. Finally, the conclusions of this study regarding the clinical importance of types II and III anastomoses are based on a small number of observations and should be interpreted with caution.
The value of the identification of ovarian artery–to–uterine artery anastomoses should be weighed against the risks of the small increase in radiation dose. Binkert et al (16) estimated this dose to be around 2.1 mSv and concluded that screening aortography is warranted in this patient population. Our observations led us to concur with their conclusion. Delineation of such anastomoses is of practical relevance for avoiding nontarget ovarian embolization, for identifying those who would be at risk of clinical uterine artery embolization or ovarian failure, and for those in whom the ovarian artery can be embolized with little risk to the ovary.
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FOOTNOTES |
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REFERENCES |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTS DISCUSSIONREFERENCES |
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