Authors

• Andrea Crkvenac Gregorek — Medicinski fakultet Sveučilišta u Zagrebu, Klinički bolnički centar Zagreb, Zagreb, Hrvatska — ORCID: 0000-0002-7790-1347
• Dražen Perkov — Medicinski fakultet Sveučilišta u Zagrebu, Klinički bolnički centar Zagreb, Zagreb, Hrvatska — ORCID: 0000-0001-5398-059X
• Ljiljana Banfić — Medicinski fakultet Sveučilišta u Zagrebu, Klinički bolnički centar Zagreb, Zagreb, Hrvatska — ORCID: 0000-0002-4538-8980
• Zoran Miovski — Medicinski fakultet Sveučilišta u Zagrebu, Klinički bolnički centar Zagreb, Zagreb, Hrvatska — ORCID: 0000-0002-3850-8905
• Krešimir Putarek — Medicinski fakultet Sveučilišta u Zagrebu, Klinički bolnički centar Zagreb, Zagreb, Hrvatska — ORCID: 0000-0003-0361-5740
• Majda Vrkić Kirhmajer — Medicinski fakultet Sveučilišta u Zagrebu, Klinički bolnički centar Zagreb, Zagreb, Hrvatska — ORCID: 0000-0002-1340-1917

Abstract

**Introduction:** Symptomatic chronic iliac venous compression caused by May-Thurner syndrome (MTS) can occur at advanced age. May-Thurner syndrome results from a frequent anatomic variant in which left common iliac vein (VIC) is compressed by right common iliac artery. MTS usually presents with acute iliofemoral deep venous thrombosis (DVT), but clinical course can also develop gradually. Endovascular intervention with venous stenting can provide resolution of the symptoms. (1-3) **Case report:** 78-year-old woman presented with chronic, painful, sever edema of the left leg. Two years before, she noticed gradual swelling of her left leg and progression of her symptoms with time. In that period several Duplex ultrasound (DUS) excluded DVT, native CT of abdomen and pelvis did not reveal abnormalities and she was treated as lymphedema of unknown origin. At presentation, she complained of venous claudication, her proximal thigh volume was 66 cm on the left side and 54 cm on the right side. Besides antihypertensive drugs, she was taking rivaroxaban due to permanent atrial fibrillation (AF). DUS of the left leg showed clear signs of pelvic veins compression (attenuated respiratory flow variation, dilated deep veins, limitation of full compression), but without DVT. CT venography revealed MTS with filiform lumen of VIC. A venography was performed, followed by angioplasty and stent implantation. Control venography showed unlimited blood flow through stented vein. Significant regression of left leg edema was evident shortly after the procedure. Volume difference between left and right tight changed from 12 cm to 3 cm postprocedural. The patient was discharged from the hospital after 3 days, therapeutic dosage of enoxaparin was continued for the next 2 weeks, and after that switched to rivaroxaban. In control interval (1 and 3 months), the patient was without complaints and DUS showed normal venous flow. Duration of anticoagulant therapy after venous stent is questionable, but since our patient has AF, anticoagulation is, in this case, permanent. **Conclusion:** For patient with chronic iliac vein compression and severe leg problems, endovascular intervention and venous stenting can provide complete resolution of symptoms. Further studies are necessary to identify optimal anticoagulant regimen after venous stenting in MTS.

Keywords

chronic venous compression, venous stent

DOI

Literature

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