Haemodynamics and flow modification stents for peripheral arterial disease:a review

Endovascular stents are widely used for the treatment of peripheral arterial disease (PAD). However, the development of in-stent restenosis and downstream PAD progression remain a challenge. Stent revascularisation of PAD causes arterial trauma and introduces abnormal haemodynamics, which initiate complicated biological processes detrimental to the arterial wall. The interaction between stent struts and arterial cells in contact, and the blood flow field created in a stented region, are highly affected by stent design. Spiral flow is known as a normal physiologic characteristic of arterial circulation and is believed to prevent the development of flow disturbances. This secondary flow motion is lost in atheromatous disease and its re-introduction after endovascular treatment of PAD has been suggested as a method to induce stabilised and coherent haemodynamics. Stent designs able to generate spiral flow may support endothelial function and therefore increase patency rates. This review is focused on secondary flow phenomena in arteries and the development of flow modification stent technologies for the treatment of PAD

Interleukin-8 (IL-8) may contribute to the activation of neutrophils in patients with peripheral arterial occlusive disease (PAOD)

AbstractObjectives: to investigate the levels of interleukin-8 (IL-8) in patients with peripheral arterial occlusive disease (PAOD) and healthy control subjects both before and after an acute exercise test. Materials and methods: twenty-six patients with intermittent claudication and 22 matched healthy control subjects each had IL-8 levels measured before and after a standard acute treadmill-exercise test. Subjects walked for 10 min or until stopped by claudication pain. Serum IL-8 levels were measured before exercise was commenced and 1, 5 and 10 min after exercise was stopped.Results: patients with PAOD had statistically significantly higher levels of IL-8 than healthy control subjects, before and after an acute exercise test (p <0.00001, Mann–Whitney). Ratios of the change of IL-8 levels post-exercise showed a statistically significant difference at the post-5-min time point (/E2>p =0.005), showing a difference in the change of IL-8 levels at this time point between the patient group and control group. Conclusions: The increased levels and the failure of the cytokine levels to fall by the same extent after exercise in the patient group may be due to a combination of increased neutrophil activation, reduced blood flow and increased cytokine production during ischaemia–reperfusion, which is not observed in the healthy controls