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September 2011 Supplement
Advances in Embolic Protection Devices
Will improvements in EPD design lead to safer carotid artery stenting procedures?
By Samir K. Shah, MD; Naveen Balansundaram, MD; and Daniel G. Clair, MD
Internal carotid artery stenting (CAS) has become an increasingly tenable alternative to carotid endarterectomy for occlusive disease in high-risk patients. Although CAS is advantageous in several respects relative to endarterectomy, both show risk for embolic stroke.1,2 Despite the absence of any form of embolic protection during initial CAS experiences, the potential for embolism during wire manipulation of the plaque with continuous antegrade blood flow is intuitively evident. 3 In fact, one would expect that the number of emboli produced during CAS would be substantially higher than that produced by carotid endarterectomy, and indeed, this has been shown in several studies.4,5 Although the clinical significance of emboli remains to be clarified (patients appear to tolerate some emboli as documented by transcranial Doppler or diffusion-weighted imaging [DWI] without sequelae6,7), it is likely that a reduction in distal embolization would improve the safety of CAS.
EMBOLIC PROTECTION DEVICES
Since the initial description of an embolic protection device (EPD) in 1990 by Theron et al, there have been numerous technological advances.8 Currently, three broad categories of EPDs exist: proximal occlusion devices, distal occlusion devices, and filters (Table 1).
Proximal Occlusion Devices
Proximal occlusion devices represent the most recent evolution
in EPDs and include the Mo.Ma Ultra (Medtronic
Invatec, Frauenfeld, Switzerland) and the GORE® Flow
Reversal System (Figure 1), which produce flow stasis and
flow reversal, respectively. The Mo.Ma device uses balloon
occlusion of the common carotid and external carotid arteries
to achieve cessation of blood flow before angioplasty and
stenting. The GORE® Flow Reversal System additionally
establishes a filtered arteriovenous shunt between the common
carotid and femoral vein to produce flow reversal.
The principal advantage of proximal occlusion devices is the avoidance of plaque disruption (provided the lesion begins distal to the origin of the external carotid artery) during EPD placement. The GORE® Flow Reversal System has the added benefit of actively removing particulate matter. Given that these devices sit proximally to the target lesion, there are no relevant landing zone requirements. Disadvantages include the need to separately place two balloons, a slightly larger 9- to 9.5-F compatibility, and potential intolerance to flow cessation.
Distal Occlusion Devices
Distal occlusion devices attempt to prevent embolization
via balloon occlusion of the internal carotid artery distal to
the lesion. The only currently available device is the
GuardWire system (Medtronic, Inc., Minneapolis, MN). The
device is 6-F compatible and is available with two balloon sizes to occlude vessels with 2.5- to 5-mm and 3- to 6-mm
diameters; crossing profiles are 0.028 inches and 0.036 inches,
respectively.
The balloon is equipped with a 2.5-cm nitinol distal tip and is advanced past the lesion and inflated using a 0.014-inch wire inflation system. The inflation device is then detached from the balloon and wire, which are used to complete the intervention. After stent placement, an aspiration catheter is advanced over the wire to evacuate debris before balloon retrieval. The aspiration catheter can also be used to flush debris from the “dead end” of the internal carotid artery below the inflated balloon into the external carotid artery, but this risks embolism via external to internal carotid collaterals.
Clear advantages of distal occlusion devices include a low crossing profile and a minimal 4.5-mm landing zone for the occlusion balloon. The need to traverse the lesion before intervention, mandatory use of aspiration, risk of embolism past the balloon, interference with visualization of the lesion, injury to the distal carotid artery, and intolerance to flow occlusion constitute its principal disadvantages.
Filter Devices
Filter devices are the most common EPD type and are
available in a broad variety of specifications (Figure 2). Many
filter EPDs come attached to a moldable wire tip and wire
body, whereas some may be advanced over a 0.014-inch wire
that has traversed the lesion. Filter details range widely with
regard to several specifications: crossing profile, landing zone
length, and pore size. Crossing profile ranges from 1.7 F
(FiberNet, Lumen Biomedical, Inc., Plymouth, MN) to 3.9 F
(Angioguard Rx, Cordis Corporation, Bridgewater, NJ). The
majority of filters can be primarily advanced past the lesion
without angioplasty; if needed, the lesion can be predilated
with a low-profile angioplasty balloon, although this risks
embolism. In addition to the smallest crossing profile, the
FiberNet filter also has a short landing zone (15 mm).
Although pore size typically ranges from 100 to 140 μm,
devices with substantially smaller (FiberNet, 40 μm) and larger
pores (SpideRX [Covidien, Mansfield, MA],167–209 μm)
are available.
Assessment of flow before filter retrieval is mandatory, as diminished flow may indicate clogging of the device with embolized debris. This requires aspiration of the debris and reassessment of flow to avoid embolism during retrieval. Persistent flow limitations may be due to arterial spasm, which can be treated with injection of a vasodilator (eg, nitroglycerin). Filter devices are easy to deploy, do not interfere with lesion visualization, and maintain antegrade blood flow. However, they also suffer from some disadvantages: the need to cross the lesion before implementation of protection, embolism through the filter both during the intervention and during recapture, and the need for a nontortuous landing zone. Absence of the latter may make performance of the procedure impossible and can allow embolism between the vessel wall and the filter when coaptation of the filter to the vessel wall is inadequate.
EFFECTIVENESS
There have been numerous studies establishing the safety of individual devices (Table 2). Nonetheless, it is difficult to arrive at any robust conclusions regarding the relative effectiveness of particular EPDs because of differences among studies with respect to patient comorbidities, degree of carotid stenosis and symptomatology, carotid stents, operator experience, and other factors that could feasibly affect outcomes. The ideal test to determine EPD effectiveness would be a comprehensive comparative randomized trial involving multiple EPDs; regrettably, there is no such study. To make matters worse, as stated previously, knowledge regarding the number and size of emboli required to produce clinical sequelae is lacking.
More problematic is the absence of clear evidence of the general effectiveness of EPDs. No clinical trial has shown improved outcomes from EPD use despite the instinctive sense that they must improve safety. Macdonald et al compared 15 CAS patients who underwent treatment with the Emboshield filter (Abbott Vascular, Santa Clara, CA) with 15 patients who underwent unprotected CAS, using DWI magnetic resonance imaging and transcranial Doppler signals as surrogates for stroke.7 There was a statistically greater number of signals consistent with embolism on transcranial Doppler in patients with filter placement than in those without. Similarly, there was an increased, but statistically nonsignificant, number of new white lesions indicating emboli on DWI in patients with EPD. The increased number of emboli in EPD patients was generated during filter installation and retrieval.
A similar randomized study by Barbato et al using the RX Accunet embolic protection system (Abbott Vascular) in 35 patients found that there was no statistical difference in the number of lesions detected by DWI between the EPD and non-EPD cohorts.6 Both of these studies have a number of weaknesses—most importantly, the small sample size and the use of proxy imaging measurements instead of actual clinical stroke. The latter point cannot be overemphasized, and one must be cautious when interpreting the clinical significance of these findings. Whether or not these potential drawbacks are limited to filter devices or extend to all current EPDs is unknown. Some studies have suggested reduced embolism with distal occlusion9 or proximal occlusion devices relative to filters.10
It is important to be mindful that filter use may not be as protective as once thought and has the potential to paradoxically increase embolic phenomena. Despite these issues, most agree that the use of embolic protection is mandatory, and evidence for this comes from several sources. First, the capture rate for visible debris in filters is very high and has been noted at 60% when evaluated by Sprouse et al.16 Second, experimental ex vivo assessments of EPDs reveal that they all trap debris typically released during CAS.17,18 Finally, large registries that have compared outcomes with and without protection have found significant reductions in neurologic events among patients who were treated with EPDs.19-21 It is unclear whether data that do not support the use of these devices reflect a failure of the device, some problem with the devices inducing embolization, or the inability of the devices to trap microparticles. In this regard, the use of proximal protection has the distinct advantages of protected lesion crossing, trapping of debris of all sizes, and no injury beyond the area being protected.
A thoughtful paradigm for choosing EPD type has been outlined by Schneider and Ansel.22 Briefly, these authors recommend the use of proximal protection in the setting of complex lesions and in those with limited cerebral reserve, filters in the setting of poor collaterals, and a device of the interventionist's choice in situations that do not fall into any of these categories. What is perhaps most important in the performance of CAS is the understanding that adequate experience with every available device is unattainable, and each interventionist should choose one proximal protection system and one distal protection system (filters most commonly) to achieve familiarity and develop a procedural routine. This will limit intraprocedural complications related to deployment and use problems.
CONCLUSION
Embolic stroke remains one of the principal risks of CAS. EPDs attempt to reduce this risk via proximal or distal occlusion or filtration. Although seemingly obvious, evidence regarding the effectiveness of EPD use and of the superiority of one EPD over another is lacking, and we are unlikely to ever see randomized data regarding the use of these devices. Further study is needed to clarify the role of EPDs during CAS. For example, what are the implications of embolic debris below the threshold of filter trapping? Are symptomatic and elderly patients more susceptible to microembolic debris (as an explanation for increased neurologic events in these patient groups)?
Advances in CAS are likely to continue and will be related to the systems used to introduce equipment into the carotid artery, embolic protection, and stent design. Of all of these areas, the majority of advancements to date have been in the design of EPDs, which are now specifically engineered for CAS. I believe that CAS has been made safer because of these advances, and further iterations of these devices will likely lead to continued improvements in the safe performance of this procedure. One can easily envision the day when performance of CAS will be the primary method of treating carotid disease because of successful efforts to limit neurologic sequelae as is already being seen in the development of EPDs.
Samir K. Shah, MD, is with the Department of Vascular Surgery, The Cleveland Clinic Foundation in Cleveland, Ohio. He has disclosed that he has no financial interest related to this article.
Naveen Balasundaram, MD, is with the Department of Vascular Surgery, The Cleveland Clinic Foundation in Cleveland, Ohio. He has disclosed that he has no financial interest related to this article.
Daniel G. Clair, MD, is Chair of the Department of Vascular Surgery, The Cleveland Clinic Foundation in Cleveland, Ohio. He has disclosed that he is a paid consultant to Endologix, Inc., Minnow Medical, Boston Scientific Corporation, and Medtronic, Inc. Dr. Clair may be reached at (216) 444-3857; claird@ccf.org.
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