Bilateral external iliac artery thrombosis due to endofibrosis in a 33-year-old female triathlete

Abstract

External iliac artery endofibrosis is a rare disease predominantly affecting young, elite male athletes. This case involves a 33-year-old female triathlete who presented initially with lower extremity claudication during training. After completing a triathlon 1 year later, the patient experienced acute-onset pain in both legs. Computed tomography angiography showed abrupt occlusion of the bilateral proximal external iliac arteries. The patient underwent a right and left external iliac artery reconstruction using the ipsilateral great saphenous vein and reported significant improvement of claudication symptoms. The case highlights a rare complication of acute bilateral arterial thrombosis.

An extremely rare disconnection of the external iliac artery and novel collateral remodeling in an endometrial stromal sarcoma woman

“…Whether it was caused by her own abnormal physical condition. External iliac artery endofibrosis (EIAE) can cause arterial thrombosis and rupture [ 13 – 17 ]. EIAE is defined as a specific intimal thickening of the wall of the artery.…”

External iliac artery endofibrosis in an elite female endurance cyclist

“…7 Because this condition is mostly seen in cyclists, some authors suggest that hyperflexion at the hip joint causes repetitive deformation of the EIA such as elongation, torsion, and stretching. 6,9 Also, these athletes are known for hypertrophy of the psoas muscle and this may exacerbate the trauma to the vessel by compression and displacement. 6,9 Some collateral vessels that anchor the EIAs to the psoas muscle may shorten the mobile portion of the artery and, together with the excessive length of the vessel, constitutes a risk factor for kinking and increased mechanical stress.…”

“…6,9 Also, these athletes are known for hypertrophy of the psoas muscle and this may exacerbate the trauma to the vessel by compression and displacement. 6,9 Some collateral vessels that anchor the EIAs to the psoas muscle may shorten the mobile portion of the artery and, together with the excessive length of the vessel, constitutes a risk factor for kinking and increased mechanical stress. 10 Besides all these extrinsic mechanical and anatomical mechanisms, the pathophysiologic mechanism could also be related to intrinsic factors, such as high cardiac output causing shear stress and stimulating endothelial dysfunction.…”

“…10 Besides all these extrinsic mechanical and anatomical mechanisms, the pathophysiologic mechanism could also be related to intrinsic factors, such as high cardiac output causing shear stress and stimulating endothelial dysfunction. 6,9 The histological findings of endofibrosis are quite distinct from those of atherosclerosis, which reveals loose connective tissue with moderate to high cellularity. 6,11 Calcification and inflammation are much more present in atherosclerotic lesions, with a major presence of lymphocytes and macrophages.…”

“…7,14 Stent fracture, migration, and plicature have also been described. 9 Although good short-term outcomes have been described with endovascular repair, symptom recurrence occurred in a significant number of patients. 7 Unsatisfactory long-term endovascular outcomes could be explained by the fact that the mechanical forces inherent to the condition are still acting, resulting in continuous arterial damage.…”