Devices for distal protection during percutaneous coronary revascularization.

Despite early perceptions that distal embolization of atherosclerotic plaque contents was a rare event during balloon angioplasty, it has now become clear that manipulation of atherosclerotic lesions with wires, balloons, atherectomy catheters, or stents does liberate plaque debris. The tendency of this liberated debris to cause clinical manifestations depends on the amount of debris, the size of particles, and the sensitivity of the perfused organ. Additionally, clinical experience with various embolic protection devices (EPDs) has shown that the capture and retrieval of potentially embolic debris reduce adverse events in situations where the amount of debris is largest (eg, saphenous vein grafts [SVGs]) and where the end organ is most sensitive (myocardium, with no reflow and creatine kinase [CK]-MB release; brain with new lesions on magnetic resonance imaging or clinical stroke). In contrast, other adjunctive medical therapies such as glycoprotein IIb/IIIa receptor antagonists, which have been shown to reduce overall rates of CK-MB release during other coronary interventional procedures, have failed to mitigate the impact of distal embolization in SVG intervention.1–3 Embolic protection is thus now firmly established as a routine component of SVG and carotid stenting, although randomized trials have not been performed for the latter indication.4,5 Although it is almost certain that atherosclerotic or atherothrombotic debris is released during other interventions on peripheral, renal, and native coronary arteries, the link between such embolization and clinical events (and hence the rationale for embolic protection) has been more difficult to demonstrate. This may be due to smaller amounts of embolic debris, less sensitive metrics of end-organ damage, or less complete capture of debris by devices tested to date in those locales. For example, initial trials of distal embolic protection in native coronaries during primary angioplasty for acute myocardial infarction have shown retrieval of smaller amounts of debris than seen during SVG intervention,6 in a clinical setting where the background elevation of CK and size of infarction may make it more difficult to discern any incremental reduction provided by embolic protection. Moreover, early generations of EPDs were themselves burdened by large-sized delivery systems and incomplete retrieval of liberated debris (due to poor wall apposition, stagnant pools of debris liberated after device retrieval, shunting of debrisladen blood into proximal side branches, etc). The purpose of the present review is to examine the classes of EPDs, consider specific examples therein, and summarize clinical evidence with regard to their use.