Distal embolic protection devices (DEPD) were developed from the necessity of protecting against macroparticle embolization. These devices are routinely used in saphenous vein graft (SVG) interventions and carotid artery stenting, and have demonstrated clinical efficacy. The results led investigators to pursue their use in native coronary artery interventions during acute coronary syndromes. Currently available embolic protection devices utilize one of three mechanisms: distal filtration, proximal occluders and distal occluders.
       The release of embolic debris occurs in nearly 80% of successful primary percutaneous coronary interventions (PCI).¹ Emboli impair the distal microvascular circulation by direct occlusion and release of vasoactive substances by the endothelium.² This can result in cellular edema and impaired cellular function. Because restoration of TIMI 3 flow is correlated with improved outcomes and microvascular perfusion influences epicardial blood flow, protection against distal embolization should theoretically improve outcomes. Angiographic evidence of epicardial blood flow, however, correlates poorly with microvascular perfusion. Consequently, TIMI frame count, myocardial blush grade (MBG), and rapidity of ST-segment resolution are used as surrogate indicators of embolization. These indicators are highly predictive of clinical and functional outcome.^1,3–5
       Several trials have demonstrated efficacy in the use of DEPDs in saphenous vein grafts which frequently carry a high atherothrombotic burden. The SAFER trial demonstrated a significant reduction in the incidence of myocardial infarction (MI) and the no-reflow phenomenon with the use of the PercuSurge GuardWire® device (Medtronic Vascular, Minneapolis, Minnesota).⁶ The GuardWire is a temporary occlusion-aspiration system that relies on arresting antegrade flow. The FIRE trial compared the GuardWire with the FilterWire™ EX embolic protection system (Boston Scientific Corp., Natick, Massachusetts), and revealed a similar composite endpoint of death, MI and target vessel revascularization.⁷ The Filterwire is a nonocclusive filter mounted on its own guidewire. The PRIDE trial demonstrated that the TriActiv® embolic protection system (Kensey Nash Corp., Exton, Pennsylvania), a balloon protection and extraction device, is not inferior to the FilterWire or the GuardWire.⁸
       Initial feasibility studies of DEPDs in primary PCI suggested a higher occurrence of grade 3 MBG, more frequent resolution of ST-segment elevation, lower peak CK-MB and greater improvement in left ventricular ejection fraction at 30 days;1 however, randomized clinical trials have not been so encouraging. The EMERALD trial randomized 501 acute STEMI patients undergoing primary PCI within 6 hours of symptoms to either PCI with GuardWire distal protection or PCI alone.⁹ The primary endpoints of ST-segment resolution and infarct size, as well as the secondary endpoint of major adverse cardiovascular events (MACE) were equivalent in both groups. The PROMISE trial also had similar results utilizing the FilterWire system.¹⁰ DEPD may not have proven beneficial in primary PCI of native vessels because of the difficulty in protecting side branches, delayed reperfusion due to occlusive devices and embolization from crossing the lesion with the device.
       Filter devices have the advantage over occlusion balloons by preserving antegrade flow; however, they rely on a bulky guidewire that must cross the lesion. The Spider™ device (ev3, Inc., Plymouth, Minnesota) is a novel DEPD that incorporates a nitinol filter to capture embolic particles > 100 micrometers. The initial feasibility study demonstrated a 95% technical success rate, with no MACE related to the device in 20 patients undergoing primary PCI for acute MI. Patients who underwent rescue PCI after thrombolysis were excluded. The study utilized ST-elevation resolution as the surrogate marker of myocardial reperfusion, and achieved a > 50% reduction in 90% of patients. These results merit a randomized clinical trial with comparison to standard interventional treatment to determine if there is any advantage to the use of the Spider DEPD.
       The Spider device differs from other filter-type devices in that the choice of guidewire used to cross the lesion and deliver the device is left to the discretion of the operator. This choice allows access to the distal artery based on anatomic and morphologic characteristics of the vessel. It is this innovation that is credited to the high success rate of the initial study.
       The disparate results between DEPD in SVG and native coronary arteries suggest that atherosclerotic composition and endothelial characteristics differ between the substrate. Newer devices must incorporate a better understanding of these differences and take into consideration cost, risk, increased procedure time and the learning curve of the operator. Furthermore, previous studies have failed to demonstrate benefit with the use of DEPD or embolectomy with aspiration or rheolytic systems. Indeed, MACE rates in some trials are increased with the use of these devices. Strategies that target the common final pathway — at the cellular level — will ultimately be necessary to see a clinical benefit. Perhaps adjunctive pharmacotherapy is required in addition to these interventional devices to see a clinically significant result. After all, if it were only about thrombus, we would pre-treat all lesions with intracoronary thrombolytics.