May-Thurner syndrome (MTS) is an anatomical condition of external luminal compression of common iliac vein due to a partial obstruction of the common iliac vein between common iliac artery and lumbar vertebra causes deep-vein thrombosis, venous hypertension, and chronic venous insufficiencies. In this article, we review present evidence of the clinical diagnosis and management of MTS. Here, we conducted a literature review of studies on MTS. We also reviewed different clinical features, presentation, diagnostic methods, and therapeutic procedure for this condition. Most studies mentioned the diagnosis of this condition is performed by color Doppler, computed tomographic angiography, venography, and problem-solving cases by intravascular ultrasound technique. Nonsurgical methods of management are first line, and vascular surgery is reserved for refractory cases. Multiple modalities are required to reach the diagnosis of MTS, and noninvasive intervention radiology methods are the first line of management. This review highlights the presentations of MTS and outlines diagnostic procedure and management.

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BACKGROUND: Venous thromboembolism significantly contributes to patient deterioration and mortality. Management of its etiology and anticoagulation treatment is intricate, necessitating a comprehensive consideration of various factors, including the bleeding risk, dosage, specific anticoagulant medications, and duration of therapy. Herein, a case of lower extremity thrombosis with multiple primary malignant tumors and high risk of bleeding was reviewed to summarize the shortcomings of treatment and prudent anticoagulation experience.
METHODS: An 83-year-old female patient was admitted to the hospital due to a 2-wk history of left lower extremity edema that had worsened over 2 d. Considering her medical history and relevant post-admission investigations, it was determined that the development of left lower extremity venous thrombosis and pulmonary embolism in this case could be attributed to a combination of factors, including multiple primary malignant tumors, iliac venous compression syndrome, previous novel coronavirus infection, and inadequate treatment for prior thrombotic events. However, the selection of appropriate anticoagulant medications, determination of optimal drug dosages, and establishment of an appropriate duration of anticoagulation therapy were important because of concurrent thrombocytopenia, decreased quantitative fibrinogen levels, and renal insufficiency.
CONCLUSIONS: Anticoagulant prophylaxis should be promptly initiated in cases of high-risk thrombosis. Individualized anticoagulation therapy is required for complex thrombosis.

UNASSIGNED: Stent intimal hyperplasia leads to in stent restenosis and thrombosis. This study determined whether Fibulin-1 activity in smooth muscle cells (SMCs) contributes to stent restenosis or thrombosis.
UNASSIGNED: Stent implantation was conducted in a pig model. Target vessel samples were stained and analyzed by protein mass spectrometry. Cell experiments and Fibulin-1 SMC specific knockout mice (Fbln1SMKO) were used to investigate the mechanism of Fibulin-1 induced SMC proliferation and thrombosis.
UNASSIGNED: SMC proliferation and phenotypic transition are the main pathological changes of intimal hyperplasia in venous stents. Protein mass spectrometry analysis revealed a total of 67 upregulated proteins and 39 downregulated proteins in intimal hyperplasia after stent implantation compared with normal iliac vein tissues. Among them, Fibulin-1 ranked among the top proteins altered. Fibulin-1 overexpressing human SMCs (Fibulin-1-hSMCs) showed increased migration and phenotypic switching from contractile to secretory type and Fibulin-1 inhibition decreased the activity of SMCs. Mechanistically, Fibulin-1-hSMCs displayed increased levels of angiotensin converting enzyme (ACE) expression and angiotensin II signaling. Inhibition of ACE or angiotensin II signaling alleviated the migration of Fibulin-1-hSMCs. Using Fibulin-1 SMC specific knockout mice (Fbln1SMKO) and venous thrombosis model, we demonstrated that Fibulin-1 deletion attenuated intimal SMCs proliferation and thrombosis. Further, Fibulin-1 concentration was high in iliac vein compression syndrome (IVCS) patients treated with stent and was an independent predictor of venous insufficiency.
UNASSIGNED: Fibulin-1 promotes SMC proliferation partially through ACE secretion and angiotensin II signaling after stent implantation. Fibulin-1 plays a role in venous insufficiency syndrome, implicating the protein in the detection and treatment of IVCS.

Introduction: Iliac vein compression syndrome (IVCS) is present in over 20% of the population and is associated with left leg pain, swelling, and thrombosis. IVCS symptoms are thought to be induced by altered pelvic hemodynamics, however, there currently exists a knowledge gap on the hemodynamic differences between IVCS and healthy patients. To elucidate those differences, we carried out a patient-specific, computational modeling comparative study. Methods: Computed tomography and ultrasound velocity and area data were used to build and validate computational models for a cohort of IVCS (N = 4, Subject group) and control (N = 4, Control group) patients. Flow, cross-sectional area, and shear rate were compared between the right common iliac vein (RCIV) and left common iliac vein (LCIV) for each group and between the Subject and Control groups for the same vessel. Results: For the IVCS patients, LCIV mean shear rate was higher than RCIV mean shear rate (550 ± 103 s-1 vs. 113 ± 48 s-1, p = 0.0009). Furthermore, LCIV mean shear rate was higher in the Subject group than in the Control group (550 ± 103 s-1 vs. 75 ± 37 s-1, p = 0.0001). Lastly, the LCIV/RCIV shear rate ratio was 4.6 times greater in the Subject group than in the Control group (6.56 ± 0.9 vs. 1.43 ± 0.6, p = 0.00008). Discussion: Our analyses revealed that IVCS patients have elevated shear rates which may explain a higher thrombosis risk and suggest that their thrombus initiation process may share aspects of arterial thrombosis. We have identified hemodynamic metrics that revealed profound differences between IVCS patients and Controls, and between RCIV and LCIV in the IVCS patients. Based on these metrics, we propose that non-invasive measurement of shear rate may aid with stratification of patients with moderate compression in which treatment is highly variable. More investigation is needed to assess the prognostic value of shear rate and shear rate ratio as clinical metrics and to understand the mechanisms of thrombus formation in IVCS patients.

OBJECTIVE: Intraluminal anomalies within the left common iliac vein, characteristic of iliac vein compression syndrome, are thought to result from compression by and pulsation of the overlying right common iliac artery. This cadaver study was designed to expand on the existing literature by surveying and photographing these spurs in addition to exploring whether certain factors, inherent to the cadaver, are associated with spur presence.
METHODS: Dissection to expose the aorta, inferior vena cava, and common iliac arteries and veins was performed in 51 cadavers. The spinal level at which the iliac vein confluence occurred was noted. The point at which the right common iliac artery crossed the left common iliac vein was examined for plaque presence. The overlying arterial structures were then transected to expose the venous system. The inferior vena cava was incised to facilitate observation into the mouth and full extent of the left common iliac vein. Spurs were photographed and documented. Statistical analysis was conducted to determine whether sex, body mass index (BMI), plaque presence, or level of the iliac vein confluence are associated with spur presence.
RESULTS: Spurs within the left common iliac vein were observed in 16 of 51 cadavers (31.4%). All spurs were located at the point that the right common iliac artery crossed the left common iliac vein. Using1 the classification system established by McMurrich, 67% of spurs (n = 10) were marginal and triangular; 25% (n = 4) were columnar. One marginal, linear spur (6%) and one partially obstructed spur with multiple synechiae (6%) were observed. Among this population, males were 73% less likely to have a spur (odds ratio, 0.269; P = .041). No significant relationship was found between plaque presence and spur presence (odds ratio, 0.933; P = .824) and no significant differences were noted between BMI and spur presence (χ2 = 1.752, P = .625). Last, a significantly greater percent of spurs was found within cadavers with an iliac vein confluence located at the L5/S1 disc space (χ2 = 9.650; P = .002).
CONCLUSIONS: Study findings show that spurs are more common when the confluence of the common iliac veins occurs at a lower spinal level. The level of the iliac vein confluence may be important in identifying patients at increased risk of venous disease. The findings also suggest that plaque within the right common iliac artery and BMI display no distinct relationship with spur presence. Further investigation is needed to understand exactly what factors lead to spur formation.

UNASSIGNED: In its normal anatomical relationship, the inferior vena cava is located on the right side of the abdominal aorta. Iliac vein compression syndrome (IVCS) is a pathological condition in which a blood clot is formed due to blood flow obstruction when the left common iliac vein is compressed between the right common iliac artery and the vertebral body. Therefore, right-sided IVCS (RIVCS) is rare. The effectiveness of treatment for RIVCS has not been sufficiently investigated.
UNASSIGNED: A 51-year-old man developed deep vein thrombosis in the right lower extremity and non-massive pulmonary embolism during steroid treatment for IgA nephropathy. Magnetic resonance angiography (MRA) suggested iliac compression syndrome. Symptoms improved with the use of direct oral anticoagulants and compression stockings. At the 8-month follow-up, the clinical course was uneventful.
UNASSIGNED: The causes of RIVCS in this case are believed to be the effects of steroids, prolonged sitting, and compression of the right external iliac vein. However, considering that deep vein thrombosis did not form in the left lower limb where there was no venous compression, it can be considered that the compression of the right external iliac vein had a significant impact. This case has been followed up for 8 months with anticoagulants and is progressing well. This is the first case to report the course of RIVCS treated conservatively with anticoagulant therapy for 8 months. This case suggested that conservative treatment is effective for RIVCS.

Iliac vein stenting for the treatment of iliac vein compression syndrome (IVCS) has been gradually developed. This article investigated the long-term patency and improvement of clinical symptoms after endovascular stenting for iliac vein obstruction patients. From 2020 to 2022, 83 patients at a single institution with IVCS underwent venous stent implantation and were divided into two groups: non-thrombotic IVCS (n = 55) and thrombotic IVCS (n = 28). The main stent-related outcomes include technical success, long-term patency, and thrombotic events. The technical success rate of all stent implantation was 100%. The mean length of hospital stay and cost were higher in the thrombotic IVCS group than in the non-thrombotic ICVS group, as well as the length of diseased vessel segment and the number of stents implanted were higher than in the control non-thrombotic group. The 1-, 2-, and 3-year patency rates were 85.4%, 80% and 66.7% in the thrombosis group, which were lower than 93.6%, 88.7%, and 87.5% in the control group (P = .0135, hazard ratio = 2.644). In addition, patients in both groups had a foreign body sensation after stent implantation, which resolved spontaneously within 1 year after surgery. Overall, there were statistically significant differences in long-term patency rate outcome between patients with thrombotic and non-thrombotic IVCS, the 1-, 2-, and 3-year patency rates in non-thrombotic IVCS patients were higher than those in thrombotic IVCS patients.

Abdominal vascular compression syndrome (AVCS) is caused by the compression of abdominal blood vessels by adjacent structures or the compression of abdominal organs by neighboring blood vessels. Such compressions can result in a variety of clinical symptoms. They are not commonly seen in ultrasound practices, and their presence may have been underrecognized and underdiagnosed. This article reviews the clinical features, ultrasound characteristics, and diagnostic criteria of four types of AVCS, namely, celiac artery compression syndrome, renal vein compression syndrome, iliac vein compression syndrome, and superior mesenteric artery syndrome to increase awareness of these conditions among ultrasound practitioners. The ultrasound criteria for AVCS are primarily based on studies with small sample sizes, and therefore, it is important to exercise caution if these criteria are used.

To evaluate 4D Flow magnetic resonance imaging (MRI) sequences for quantitative flow measurements of the pelvic venous vasculature.
A prospective study of healthy volunteers was performed. After informed consent all subjects underwent 4D flow sequences at a 3 T MRI scanner with different isotropic resolution and different velocity encoding (Venc) settings: (sequence #1) voxel size (VS) 1.63 mm3, Venc 50 cm/s; (sequence #2) VS 1.63 mm3, Venc 100 cm/s and (sequence #3) VS 2.03 mm3, Venc 50 cm/s. Perfusion parameters were calculated for all venous vessel segments starting at the level of the inferior vena cava and extending caudally to the level of the common femoral vein. For reference, arterial flow was calculated using 1.63 mm3 isotropic resolution with a Venc of 100 cm/s.
Ten healthy subjects (median age 28 years, interquartile range [IQR]: 26.25-28 years) were enrolled in this study. Median scanning time was 12:12 minutes (IQR 10:22-13:32 minutes) for sequence #1, 11:02 minutes (IQR 9:57-11:19 minutes) for sequence #2 and 6:10 minutes (IQR 5:44-6:47 minutes) for sequence #3. Flow measurements were derived from all sequences. The venous pelvic vasculature showed similar perfusion parameters compared to its arterial counterpart, for example the right common iliac arterial segment showed a perfusion of 8.32 ml/s (IQR: 6.94-10.68 ml/s) versus 7.29 ml/s (IQR: 4.70-8.90 ml/s) in the corresponding venous segment (P = 0.218). The venous flow measurements obtained from the three investigated sequences did not reveal significant differences.
4D Flow MRI is suitable for quantitative flow measurement of the venous pelvic vasculature. To reduce the scanning time without compromising quantitative results, the resolution can be decreased while increasing the Venc. This technique may be utilized in the future for the diagnosis and treatment response assessment of iliac vein compression syndromes.