Peripheral arterial disease (PAD) is a form of cardiovascular disease caused by a build‑up of fatty deposits in the arterial walls of the leg. These fatty deposits, called atheroma, narrow the arteries in a process known as atherosclerosis. PAD is estimated to affect 1 in 5 people aged over 60 years in the UK and its incidence increases with age, according to NICE's quality standard on peripheral arterial disease. It is more common in people with diabetes, high blood pressure or high cholesterol, and in those who smoke. PAD is more common in men, with an overall incidence of 8.2% compared with 5.5% in women (Kroger et al. 2006).

Although some people with PAD may have no symptoms, it often causes muscle pain and aching (known as claudication) in the affected leg. PAD can cause severe claudication, making walking painful and reducing quality of life. In approximately 1 in 5 people with PAD, the narrowing of the arteries leads to increasingly severe symptoms with the development of critical limb ischaemia. Symptoms of critical limb ischaemia include gangrene and ulcers (NHS Choices) and it is the most common cause of leg amputation in the UK.

PAD is also a risk factor for other cardiovascular events, such as heart attack and ischaemic stroke; people with PAD have a 3–4‑fold increased risk of such an event.

Peripheral vascular grafts are used during vascular bypass procedures, which are done to restore blood flow to the lower limbs. This is achieved through bypass of the diseased (blocked) portion of the blood vessel with a portion of healthy vessel or, if no healthy vessels are available, with an artificial graft.

During bypass surgery, a healthy vein is taken from another part of the leg and joined, or grafted, above and below the blocked artery. This procedure, referred to as an autologous graft, allows the flow of blood to be rerouted to avoid the blockage and maintain an efficient blood supply. A vascular surgeon assesses whether a vein is available and suitable for the procedure. Autologous grafts have a lower failure rate than prosthetic grafts and are used wherever possible. However, when it is not feasible to use a healthy vein, an artificial graft may be used. PTFE is commonly used in the manufacture of artificial grafts.

Reduction in the patency of grafts can lead to graft failure. Early failure (within the first 30 days) is usually due to technical issues. A common cause of mid‑term (1–18 months) graft failure is thrombosis resulting from neointimal hyperplasia (NIH), an accumulation of vascular smooth muscle cells at the furthest attachment of the graft (the distal anastomosis). NIH causes thickening of the graft walls and narrowing of the vessel, which reduces blood flow and can lead to graft failure. Late failure (after more than 18 months) is usually due to progression of atheroma above or below the graft.

Factors that could affect patency rates include the location of the distal anastomosis and run‑off, severity of disease, use of adjuvant techniques and compliance with medications, previous intervention, sex and smoking status.

Further surgery may be needed to salvage or re‑open the graft using techniques such as endovascular thrombolysis, angioplasty, stent placement or mechanical thrombectomy to restore blood flow. If this is unsuccessful, and if all other revascularisation options have been exhausted, the affected limb may have to be amputated. Artificial grafts that are designed to reduce the risk of thrombosis may be less prone to failure than standard prosthetic grafts.

The anticoagulant drug heparin is widely used to prevent clot formation and to treat the symptoms associated with PAD and other thrombotic diseases. patients with PAD may have systemic (whole‑body) anticoagulants to protect against cardiovascular events such as stroke or heart attack, although they carry some risk of causing excessive bleeding. In recent years, heparin has also been bonded directly to artificial grafts. The aim is to prolong graft patency by making use of heparin's antithrombogenic properties to reduce the risk of graft occlusion. It is also thought that heparin may reduce or delay the development of NIH (Daenens et al. 2009, Dorigo 2012).

A potential concern about the use of heparin to coat vascular grafts is the possible development of an adverse drug reaction called heparin‑induced thrombocytopaenia (HIT). HIT type 1 is benign and not associated with an increased risk of thrombosis but HIT type 2 is caused by an immune response to heparin, leading to clumping and trapping of platelets. It is associated with significant morbidity and mortality if untreated. The incidence of HIT type 2 is rare.

Kasirajan (2012) evaluated 27 cases of suspected HIT following implantation of PROPATEN heparin‑bonded grafts. He concluded that the graft does not appear to induce an immune response associated with the development of HIT, and that this complication was more likely attributable to the systemic administration of heparin.