Embolic Protection Devices in Aortocoronary Saphenous Vein Graft Intervention

E mbolic protection devices (EPDs) were first developed to provide cerebral protection during carotid artery stenting and have led to marked reductions in the combined endpoints of stroke or death.1,2 Therefore, it was natural that these devices should be applied to native coronary and aortocoronary saphenous vein graft (SVG) interventions to reduce clinically significant atheroand thromboembolism. Despite multiple clinical trials, few data currently exist to support the routine use of any EPD in patients with acute coronary syndromes undergoing percutaneous native coronary intervention.3 Reasons for this are likely multiple, including a markedly prothrombotic milieu, liberation of small thrombi or vasoactive substances that may pass through an EPD, or in situ thrombus formation distal to the site of protection. Based on current clinical data, SVGs have emerged as the primary target for EPDs. SVG interventions are known to result in a high risk (~20%) of major adverse cardiac events (MACE) and a significant risk of slowor no-reflow, resulting in periprocedural myocardial infarction.4 The reason for the differential benefit of EPDs in SVGs over native coronaries reflects the disparate composition of plaque between these two vessel types. SVG athero-occlusive disease tends to be rich in cholesterol, with less calcium and intimal proliferation than in native coronary arteries.5 Slowor no-reflow in SVG intervention is more often related to distal embolization of friable, lipid-rich plaque than thrombus.6 This concept has been demonstrated in aspirate analyses after SVG intervention during distal balloon occlusion in which copious plaque constituents (cholesterol crystals, foam cells, fibrous plaque, and necrotic core) were recovered.7,8 The preponderance of nonthrombotic, plaque-rich emboli explains why glycoprotein (GP) IIb/IIIa inhibitors have not been as efficacious in SVG intervention as they are in native coronaries.9,10