## 1 Introduction  
Peripheral artery disease (PAD) represents a particular manifestation of systemic atherosclerosis, in which atheromatous plaques are located at the level of the peripheral arteries. In most cases, the peripheral location of atherosclerosis is associated with concomitant involvement of the coronary or carotid arteries or with multiple co-morbidities, such as hypertension, diabetes mellitus, dyslipidemia or obesity. The prevalence of peripheral artery disease is increasing with age, with an incidence of around 20% of patients after the age of 80; it is estimated that it affects more than 200 million people worldwide [1]. It has been recently suggested that the adipose tissue may play a significant role in the complex process of atheromatous plaque progression and destabilization [2]. Adipose tissue is a tissue present throughout the body and has multiple roles in the complex thermoregulation process. The main depots of adipose tissue are located subcutaneously. However, several particular distributions of the adipose tissue, such as epicardial, visceral or perivascular can have important consequences on the complex cardiometabolic balance. The role of white adipose tissue in the regulation of vascular health and in the local production of inflammatory cytokines has been recently described. Several authors have demonstrated the potential involvement of this tissue in the etiology of endothelial dysfunction [3; 4; 5]. Adipose tissue has been associated with insulin resistance and cardiovascular events, this interrelation being mediated by an exacerbated inflammatory response triggered by local or systemic mediators released by adipokines [6]. The white adipose tissue contains adipocytes, macrophages, T cells and collagen fibers, at the same time secreting chemokines, leptin, adiponectin, resistin, vasoactive substances and free fatty acids. It is well-known that one of the most important adipokines released by the adipose tissue, tumor necrosis factor \(\alpha\), stimulates production of proinflammatory mediators such as interleukin 6 or monocyte chemotactic protein 1 [7; 8]. In the presence of glucocorticoids, tumor necrosis factor \(\alpha\) also increases leptin expression in the adipose tissue [8]. An increased leptin level is strongly associated with inflammation. Nevertheless, increased leptin levels are not only present in acute infections, inflammation and sepsis, but it is also involved in the pathophysiology of several chronic inflammatory or autoimmune diseases [9]. Multiple studies have investigated the association between perivascular adipose tissue and major vascular diseases. To date, most of these studies focused on the relationship between the epicardial adipose tissue and the presence of coronary artery disease. Epicardial adipose tissue, which is the fat surrounding the coronary arteries, has been demonstrated to represent a powerful marker of atherosclerosis. An increased epicardial fat volume has been associated with a higher vulnerability of the atheromatous coronary plaque and has been recorded in larger amounts in patients with acute myocardial infarction [10]. However, there is no study so far that has investigated the potential role of the perivascular adipose tissue, located at the level of iliac arteries, in the complex pathophysiology of peripheral arterial diseases. This is probably due to the difficulty to quantify the periiliac adipose tissue using standard imaging techniques, such as vascular ultrasound. The aim of our study was to develop a semi-automated, computer-aided imaging technique to quantify the amount and assess the distribution of perivascular fat at the level of the iliac arteries, and to demonstrate the reliability of this technique in assessing the complexity of vascular disease in patients with atherosclerotic lesions at this level as expressed by presence of lower limb ischemia.