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.

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.

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.

UNASSIGNED: Iliac vein compression syndrome (IVCS) is an underlying cause of varicose vein (VV) recurrence after venous surgery. However, the management of recurrent varicose veins (RVVs) combined with IVCS has rarely been reported. This study aimed to investigate the outcomes of a one-stop procedure to correct outflow obstruction and superficial reflux for patients with RVVs and IVCS.
UNASSIGNED: A retrospective analysis was conducted of 102 consecutive patients diagnosed with RVVs. Computed tomography venography (CTV) was performed to confirm IVCS. The cases were divided into 2 groups: the IRVVs group, including patients with RVVs and IVCS (n=48), and the RVVs group, including patients with RVVs only (n=54). The characteristics, vein reflux, and clinical, etiological, anatomical, and pathophysiological (CEAP) distribution were investigated. Then, the IRVVs group patients who underwent endovenous laser ablation (EVLA) (n=39) were divided into a further 2 groups: the EVLA + S group (n=19), who received EVLA and stenting of iliac vein, and the EVLA group (n=20), who received EVLA treatment alone. The great/small saphenous vein (GSV/SSV) trunk occlusion, VV recurrence, visual analogue scale (VAS), and venous clinical severity score (VCSS) were investigated.
UNASSIGNED: The prevalence rate of femoral vein reflux was 81.2% in IRVVs group and 50% in RVVs group (P<0.05). In the IRVVs group, 72.9% of patients manifested as CEAP clinical class >3, which was higher than that in RVVs group (48.1%) (P<0.05). The 12-month GSV/SSV occlusion rate in the EVLA + S and EVLA groups were 94.7% and 90.0%, respectively. Totals of 9 patients in EVLA + S group and 6 patients in EVLA group had active venous ulcers, and the ulcer healing time in EVLA + S group was significantly shorter (27.22±7.12 vs. 46.67±9.83 days, P<0.05). The reductions in the VAS and VCSS values between baseline, 1 month, and 12 months in the EVLA + S group were more obvious than those in EVLA group (P<0.05).
UNASSIGNED: The one-stop combination treatment of iliac venous stenting and EVLA in patients with RVVs and IVCS is safe and effective and provides prominent symptom relief, improved quality of life, and a more satisfactory ulcer healing than EVLA alone.

Description May-Thurner Syndrome (MTS) is an anatomical syndrome characterized by a predisposition to clot formation when there is compression of the left iliac vein by the right iliac artery. In this case, we discuss an atypical presentation of MTS in a young male after rapid weight loss. The patient was admitted for an unprovoked massive proximal deep vein thrombosis (DVT) after a two-hundred-pound weight loss during the preceding six-month period. Treatment involved mechanical thrombectomy by interventional radiology, initiation of apixaban and recommended follow up with vascular surgery for angioplasty instead of immediate stent placement.

BACKGROUND: This study aimed to identify whether iliac vein compression syndrome(IVCS) is associated with deep vein thrombosis(DVT) after total knee arthroplasty(TKA) and whether lower lumbar degenerative changes were risk factors for IVCS.
METHODS: A total of 259 consecutive patients who underwent TKA from January 2019 to March 2022 was retrospectively reviewed. Preoperative plain radiographs of lumbar spines and CT venography (CTV) for DVT diagnosis at postoperative 7 days were performed in all patients. Imaging findings of lower lumbar degenerative changes were analyzed on plain radiograph including lateral osteophytes, scoliosis, lateralolisthesis, retrolisthesis, anterolisthesis, and lower lumbar lordosis angle (LLLA). Percent compression at the left common iliac vein (LCIV) and right common iliac vein (RCIV) as well as DVT were evaluated on CTV. Moreover, IVCS was defined as greater than 50% of compression of the iliac vein on CTV.
RESULTS: DVT occurred in 79 patients (30.5%) after TKA. The overall occurrence of DVT was significantly higher in patients with IVCS of LCIV (52.8%) than those without (18.8%, P < 0.001). When DVT was further subdivided, compared to non-IVCS, IVCS of LCIV was significantly associated with bilateral DVT (P < 0.001, both), especially distal DVT (P < 0.001, both), and IVCS of RCIV was significantly associated with right-side DVT (P = 0.031), especially popliteal (P = 0.008) and distal DVT(P = 0.011). Female patients (OR: 3.945, P = 0.039), presence of left osteophyte (OR: 2.348, P = 0.006), and higher LLLA (OR: 1.082, P < 0.001) were significantly associated with IVCS of LCIV, and presence of right osteophyte (OR: 3.494, P = 0.017) was significantly associated with IVCS of RCIV.
CONCLUSIONS: IVCS was significantly associated with DVT after TKA and lumbar degenerative changes with lateral osteophytes and hyperlordosis were significant risk factors for IVCS.