Embolic protection devices.

Percutaneous intervention for the treatment of coronary and peripheral atherosclerotic disease has become a well established technique, and has been recently extended also to the carotid arena. However, distal embolisation of particulate matter, including plaque debris such as fibrin, necrotic atheromatous core, foam cells, cholesterol clefts, and thrombus, at the time of balloon inflation or stent deployment, complicate percutaneous mechanical interventions more often than had been recognised before. The risk of distal embolisation is now considered significant in carotid arteries, degenerated saphenous vein graft, and in thrombotic lesions characterising the patient affected by acute coronary syndromes. The process of plaque embolisation catalyses a complex interaction also involving microvascular spasm and thrombosis. This often results in diminished blood flow to the distal vascular bed, potentially complicated by periprocedural ischaemia and/or infarction or stroke. 7 In particular, the risk of distal embolisation is especially high in degenerated saphenous vein grafts, with the “no reflow” phenomenon being reported in up to 31.8% of cases during treatment of thrombotic lesions and in up 7.9% of cases with no thrombus present. Although large particles (> 100 μm) may obstruct large, epicardial vessels, very small particles, as little as 15–50 μm, can also obstruct the microvascular bed causing microinfarcts and left ventricular dysfunction. In the setting of acute myocardial infarction, Ito and associates detected by myocardial contrast echocardiography a substantial “no reflow” area, potentially related to distal embolisation of atherosclerotic debris in 37% of patients with TIMI-3 flow shortly after reperfusion treatment. Those “infarctlets”, indicated by an increase in periprocedural creatine kinaseMB, have been recently associated with worse outcome at one year follow up, even in patients without any apparent procedure or in-hospital complications. Different approaches have been attempted in the past to reduce distal embolisation, including intracoronary administration of urokinase, extraction coronary atherectomy, directional coronary atherectomy, laser angioplasty, ultrasound thrombolysis, and AngioJet rapid thrombectomy. 17 The results, however, were not considered to be satisfactory in terms of achieving a significant reduction in distal embolisation. Over the last few years, several distal protection devices have been introduced to allow the capture and retrieval of friable, lipid-rich plaque constituents released after percutaneous interventional procedures, before they lodge in the distal microcirculation. Currently available technologies for embolic protections have focused either on conduit occlusion (proximal or distal) with subsequent aspiration or on distal filter capture debris (table 1).