 Introduction/Background Lower-extremity vascular diseases span a diverse range of etiologies and may be autoimmune, congenital, degenerative, inflammatory, infectious, metabolic, neoplastic, or traumatic in nature. Examples of such conditions include, but are not limited to, aneurysm formation, atherosclerosis, Buerger disease, cystic adventitial disease, dissection/transection, deep vein thrombosis, external iliac artery endofibrosis (EIAE), fibromuscular dysplasia (FMD), popliteal arterial entrapment syndrome (PAES), segmental arterial mediolysis (SAM), and genetic syndromes such as Marfan syndrome (MS), Loeys-Dietz syndrome (LDS), and vascular Ehlers-Danlos syndrome (EDS). Because of the plethora of potential underlying disease processes, imaging is often employed to secure a diagnosis and assist in guiding clinical management. Accurate vascular imaging relies upon visualization of the vessel lumen, vessel wall, and surrounding soft-tissue structures, with some modalities also offering the ability to characterize blood flow direction and velocity. Furthermore, nonvascular findings are often paramount in supporting a suspected clinical syndrome [1-4] or guiding surgical management [5-8]. Guidelines proposed in this document focus on nonatherosclerotic, arterial lower-extremity vascular disease. PAES is the most common cause of surgically correctable lower-extremity vascular insufficiency in young adults and consists of anatomic and functional subtypes. Patients with PAES present with calf claudication, paresthesia, and swelling during exercise. In anatomic PAES (Types I, II, III, and V), the extravascular structures within the popliteal fossa compress the popliteal artery and/or the popliteal vein, which results in compression and stenosis or occlusion during plantar flexion. Functional PAES (Type IV) results in compression of the popliteal artery despite the presence of an anatomically normal popliteal fossa; its etiology remains unclear.
Nonatherosclerotic Peripheral Arterial Disease.  Introduction/Background Lower-extremity vascular diseases span a diverse range of etiologies and may be autoimmune, congenital, degenerative, inflammatory, infectious, metabolic, neoplastic, or traumatic in nature. Examples of such conditions include, but are not limited to, aneurysm formation, atherosclerosis, Buerger disease, cystic adventitial disease, dissection/transection, deep vein thrombosis, external iliac artery endofibrosis (EIAE), fibromuscular dysplasia (FMD), popliteal arterial entrapment syndrome (PAES), segmental arterial mediolysis (SAM), and genetic syndromes such as Marfan syndrome (MS), Loeys-Dietz syndrome (LDS), and vascular Ehlers-Danlos syndrome (EDS). Because of the plethora of potential underlying disease processes, imaging is often employed to secure a diagnosis and assist in guiding clinical management. Accurate vascular imaging relies upon visualization of the vessel lumen, vessel wall, and surrounding soft-tissue structures, with some modalities also offering the ability to characterize blood flow direction and velocity. Furthermore, nonvascular findings are often paramount in supporting a suspected clinical syndrome [1-4] or guiding surgical management [5-8]. Guidelines proposed in this document focus on nonatherosclerotic, arterial lower-extremity vascular disease. PAES is the most common cause of surgically correctable lower-extremity vascular insufficiency in young adults and consists of anatomic and functional subtypes. Patients with PAES present with calf claudication, paresthesia, and swelling during exercise. In anatomic PAES (Types I, II, III, and V), the extravascular structures within the popliteal fossa compress the popliteal artery and/or the popliteal vein, which results in compression and stenosis or occlusion during plantar flexion. Functional PAES (Type IV) results in compression of the popliteal artery despite the presence of an anatomically normal popliteal fossa; its etiology remains unclear.