Background: External iliac artery endofibrosis (EIAE) classically presents in cyclists with intimal thickening of the affected arteries. We investigated possible anatomical predisposing factors including psoas muscle hypertrophy, arterial tortuosity, inguinal ligament compression, and arterial kinking via a case-control comparison of symptomatic and contralateral limbs.

Methods: All patients with unilateral EIAE treated surgically at our institution were reviewed. Each patient's symptomatic side was compared with their contralateral side using paired t-tests. Psoas hypertrophy was quantified by the transverse cross-sectional area (CSA) at L4, L5, and S1 vertebral levels, and inguinal ligament compression was measured as the anterior-posterior distance between the inguinal ligament and underlying bone. Tortuosity index for diseased segments and arterial kinking were measured on TeraRecon.

Results: Of 33 patients operated on for EIAE from 2004 to 2021, 27 with available imaging presented with unilateral disease, more commonly left-sided (63%). Most (96%) had external iliac involvement and 26% had ≥2 segments affected: 19% common iliac artery, 15% common femoral artery. The symptomatic limb had greater mean L5 psoas CSA (1,450 mm² vs. 1,396 mm², mean difference 54 mm², P = 0.039). There were no significant differences in L4 or S1 psoas hypertrophy, tortuosity, inguinal ligament compression, or arterial kinking. 63% underwent patch angioplasty, and 85% underwent additional inguinal ligament release. 84% reported postoperative satisfaction, which was associated with a greater difference in psoas hypertrophy at L4 (P = 0.022).

Conclusions: Psoas muscle hypertrophy is most pronounced at L5 and is associated with symptomatic EIAE. Preferential hypertrophy of the affected side correlates with improved outcomes, suggesting psoas muscle hypertrophy as a marker of disease severity.

Objective: High-performance athletes can develop symptomatic arterial flow restriction during exercise caused by endofibrosis. The pathogenesis is poorly understood; however, coagulation enzymes, such as tissue factor (TF) and coagulation factor Xa, might contribute to the fibrotic process, which is mainly regulated through activation of protease-activated receptors (PARs). Therefore, the aim of this explorative study was to evaluate the presence of coagulation factors and PARs in endofibrotic tissue, which might be indicative of their potential role in the natural development of endofibrosis.

Methods: External iliac arterial specimens with endofibrosis (n = 19) were collected during surgical interventions. As control, arterial segments of the external iliac artery (n = 20) were collected post mortem from individuals with no medical history of cardiovascular disease who donated their body to medical science. Arteries were paraffinized and cut in tissue sections for immunohistochemical analysis. Positive staining within lesions was determined with ImageJ software (National Institutes of Health, Bethesda, Md).

Results: Endofibrotic segments contained a neointima, causing intraluminal stenosis, which was highly positive for collagen (+150%; P < .01) and elastin (+148%; P < .01) in comparison with controls. Intriguingly, endofibrosis was not limited to the intima because collagen (+213%) and elastin (+215%) were also significantly elevated in the media layer of endofibrotic segments. These findings were accompanied by significantly increased α-smooth muscle actin-positive cells, morphologically compatible with the presence of myofibroblasts. In addition, PAR1 and PAR4 and the membrane receptor TF were increased as well as coagulation factor X.

Conclusions: We showed that myofibroblasts and the accompanying collagen and elastin synthesis might be key factors in the development of endofibrosis. The special association with increased presence of PARs, factor X, and TF suggests that protease-mediated cell signaling could be a contributing component in the mechanisms leading to endofibrosis.

High level endurance sports, like biking, may lead to a vascular pathology called endofibrosis. Its symptoms are an arterial wall thickening and a reduction of the artery lumen calibre. Cyclists are impacted in the iliac arteries due to a pinching and kinking mechanism, but other athletes may be vulnerable like rowers, triathletes or soccer players (Feugier and Chevalier Citation2004). This pathology was addressed increasingly over the years in the vascular surgery literature (INSITE Collaborators Citation2016). Arterial endofibrosis is a hypertrophic arterial remodelling pathology that affects a young and healthy population. According to Pr Feugier, specialist of this pathology in Lyon’s South Hospital (Feugier and Chevalier Citation2004), endofibrosis is close to another vascular pathology, called myointimal hyperplasia.

The development mechanisms of endofibrosis involves several factors and phenomena, such as hemodynamics, biochemistry, cells evolution, etc. We focus here on the biomechanical modelling of the endofibrosis in the iliac artery. Our goal is to bring a better understanding of this disease by a model that couples cell population evolution, hemodynamics, biochemical evolution of growth factors. The model is expected to permit a parametric analysis, and to provide prediction data about the most important mechanisms at play, which we illustrate here on a case of initially wounded artery.

Background: Exercise-induced external iliac artery endofibrosis (EIAE) is rare and has been described primarily in endurance male cyclists. Clinically, it presents as claudication during maximal exercise with quick resolution after exercise. Most patients have fibrotic changes within the external iliac artery (EIA). We describe our experience with EIAE and propose a hypothesis for the mechanism involved in the associated claudication.

Methods: This was a retrospective review of athletes who presented with symptomatic EIAE requiring operative repair between 2001 and 2010. Data collected included demographic information, initial presentation, type of exercise, repair, and long-term outcome. Diagnostic studies consisted of duplex evaluation, modified exercise treadmill test, and angiography.

Results: Eight women, presented with symptomatic EIAE. Two had bilateral EIAE. All were endurance athletes (three cyclists, one runner, and four were cyclists and runners). Median age at presentation was 42.5 years (range, 39-60 years). Median duration of symptoms was 5.5 years (range, 2-15 years). Diagnosis was confirmed with an exercise treadmill test modified to accommodate these patients' high level of conditioning and unmask the claudication. In the most recent two patients, marked EIA vasospasm was noted after exercise by duplex scanning. All patients were treated with EIA vein patch angioplasty. Follow-up ranged from 1 to 10 years. All had a normal result on the modified exercise treadmill test and resumed their athletic activities postoperatively.

Conclusions: This series highlights a possible mechanism to explain the claudication associated with EIAE. Vasospasm may be more important than wall thickening for the reduction of blood flow during extreme exercise in affected athletes. Routine duplex ultrasound imaging to measure EIA diameter and flow velocities before and after maximal exercise is needed to confirm this phenomenon.