The risk that recurrent stenosis (restenosis) may develop is the most important weakness of endovascular interventions. Local deposition of thrombocytes and an inflammatory reaction occur as a consequence of mechanical injury to the vessel wall occurring during treatment. Together they induce intimal hyperplasia. Most recurrent stenoses occur within 6 months of the intervention. Gradual resolution of the intimal hyperplasia at the stent site has been observed in patients after more than 12 months since the intervention.

Muscular arteries (permitting active vessel diameter changes in response to end-organ need) such as the coronary, arm, and leg arteries are at greatest risk. This makes sense when one considers that an essential component of intimal hyperplasia is the migration and proliferation of smooth muscle cells. The recurrence rate for vascular occlusion is generally higher than for stenosis. Diabetes mellitus increases the risk of recurrent stenosis.

Recurrent stenoses have been observed in up to 53% of cases in the legs, whereas the rate for the carotid arteries is only 5 to 8%. The rates of restenosis in the subclavian artery are equally low at 5 to 7%. In the iliac arteries, a restenosis rate of only 6% was observed after placement of a nitinol stent. Renal arteries treated for arteriosclerotic stenosis with stent placement show a restenosis rate of 14 to 25%. The recurrence rates in renal arteries less than 4 mm in diameter and in smokers are higher (Kedhi et al 2008).

Platelet Aggregation Inhibitors

Aspirin and clopidogrel play an important role in prophylaxis against recurrence. This is because the initial reaction to the trauma of intervention is the deposition of thrombocytes. Via growth factors, these thrombocytes stimulate the proliferation of smooth muscle cells and their migration into the neointima.

Avoidance of Unnecessary Injuries to the Vessel Wall