Stent fracture in the coronary and peripheral arteries.

Inherent risks of stenting include restenosis and thrombosis. Recently, stent fractures have been recognized as a complication that may result in thrombosis, perforation, restenosis, and migration of the stent resulting in morbidity and mortality. Stent fractures were originally seen in the superficial femoral arteries but have since then been reported in almost all vascular sites including the coronary, renal, carotid, iliac, and femoropopliteal arteries. Fractures are the result of the complex interplay between stent manufacturing, the stented segment, pulsatile and nonpulsatile biomechanical forces, and plaque morphology at a particular vascular site. The presentation of a patient with a fracture is highly variable, ranging from asymptomatic in nature, detected on routine screening without any sequelae, to sudden cardiac death related to a thrombosed coronary artery. Despite being recognized as an important complication, consensus on routine surveillance and diagnostic methods to detect fractures continues to be lacking. Fortunately, most cases are relatively benign and can be managed conservatively if detected. In the setting of recurrent symptoms, further intervention is usually sought. In review of the literature most cases are managed with placement of a stent over the fractured area, the stent-in-stent technique, but several other alternatives may be available. As the knowledge of the variables that make stents prone to fracture are identified, better technologies and techniques can be employed to minimize the risk of this complication. This article reviews the available literature on stent fractures and complications using data found on PubMed, MEDLINE, the Manufacturer and User Facility Device Experience (MAUDE) database, and the Cochrane databases.

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