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. Exercise-induced external iliac artery endofibrosis (EIAE) is an uncommon condition affecting high-end endurance athletes in the absence of classic risk factors for atherosclerosis. These athletes are asymptomatic at rest and become symptomatic, with complaints of thigh claudication and loss of power during maximal effort. This was first reported in 1984 in two competition cyclists.
Since then, EIAE has been described not only among cyclists but also in long-distance runners, triathletes, and speed skaters. EIAE has been described mostly in men, with women accounting for only 7% of the cases. The diagnosis is made by having the athlete exercise to the point of symptoms and obtaining ankle-brachial indices (ABIs) and duplex scanning after exercise. Multiple mechanisms have been proposed to explain EIAE, including increased cardiac output and adaptive systolic hypertension during strenuous effort, psoas muscle hypertrophy, presence of collaterals from the EIA to the psoas muscle, and repeated direct mechanical trauma on the fixed iliac arterial segment by the psoas muscle during hip flexion, and kinking as a result of excessive iliac arterial length. The final pathway is wall thickening, reduction in arterial lumen caliber, and restriction of blood flow during maximal exertion. We describe our experience with EIAE, our method of diagnosis, and propose a hypothesis for the mechanism involved in claudication associated with EIAE.
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