Primary Causes & Pathophysiology
Atherosclerosis is the primary mechanism, involving endothelial dysfunction, lipid accumulation, and inflammatory cell infiltration within the arterial intima. This leads to plaque formation, progressive luminal narrowing, and reduced distal perfusion pressure. During exertion, the metabolic demand of skeletal muscle exceeds the restricted blood supply, causing ischaemia and the accumulation of metabolites like lactate, which manifests as claudication. In advanced disease, resting blood flow becomes insufficient to maintain tissue viability, leading to rest pain, ulceration, and gangrene. Collateral vessel formation may partially compensate for occlusions but is often inadequate during increased metabolic demand or when microvascular disease coexists.
Endothelial injury and lipid deposition leading to intimal plaque formation, calcification, and progressive luminal narrowing of large and medium-sized arteries.
Non-atherosclerotic segmental inflammatory condition causing thrombosis of small and medium-sized arteries and veins, strongly linked to heavy tobacco use.
Inflammatory destruction of arterial walls (e.g., Takayasu arteritis, giant cell arteritis) leading to stenosis, occlusion, or aneurysm formation.
Anomalous anatomical relationship between the popliteal artery and surrounding myofascial structures, causing repetitive mechanical compression and secondary thrombosis or aneurysm.