These authors very admirably present their recommendations, strategies, and tips in utilizing filter embolic protection devices (EPD) during lower extremity percutaneous peripheral interventions (PPI).1 As a cardiovascular surgeon by training, and having witnessed the large amount of both atherosclerotic and thrombotic plaque burden inside infrainguinal vessels many times, I’ve often wondered where this debris goes during our PPIs and how we get by without at least some degree of embolization on every case. With the recent advent of atherectomy devices and EPDs that allow us to actually visualize this debris in the cath lab or endovascular suite, I believe I now know the answer. Very likely, some degree of embolization does occur with every PPI case, or a large percentage of our PPI cases. EPDs are considered the “standard of care” during carotid PPI, coronary artery bypass graft PCI, and mounting evidence supports consideration during renal PPI. I suggest it is now time for us to “get our heads out of the sand” and realize the clinical need for EPD in many, if not most, lower extremity PPIs, especially in those higher-risk patient populations, as defined by the authors and in patients with critical limb ischemia (CLI), who oftentimes have single-vessel runoff, at best, with compromised microcirculation who may not tolerate even the smallest distal embolic insult.
The published data supporting EPD use in lower extremity PPI are sparse and have been cited by the authors.
The patient with lower extremity disease, and especially CLI, is already predisposed to embolic risks during PPI, as they have multilevel disease with large pre-existing atherosclerotic plaque burdens, a likely high incidence of thrombus, high incidences of diabetes and hypercoagulability, and the PPI that occurs in a “low flow” environment as compared to PCI. These higher-risk patients need optimal “proximal protection” strategies with optimal anticoagulation and antiplatelet pharmacotherapy, coupled with optimal periprocedural techniques and potentially downstream “distal protection” with EPDs. Similar to these authors, we also advocate direct thrombin and GP IIb/IIIa inhibition in the highest-risk group, including CLI. We have reported safety and feasibility with this “endopharmacotherapeutic” approach with a slight trend towards improved outcomes, but multicenter, randomized data remain lacking.2–4
I believe the risk of distal embolization starts with the “needle stick” and can potentially increase exponentially with the manipulation of each wire, catheter, balloon, device, etc. We know this from the pattern and number of “hits” that occur during carotid PPI, as measured by transcranial Doppler. Why should this be any different during lower extremity PPI? I strongly suspect it is much worse, especially when considering the characteristics of infrainguinal arterial disease. The SilverHawk (FoxHollow Technologies, Inc., Redwood City, California) atherectomy device has frequently been implicated in generating distal embolic debris, but I strongly suspect PTA alone, balloon predilation, stent deployment, balloon postdilation, and even excimer laser therapy (Spectranetics, Colorado Springs, Colorado) can also generate embolic debris, especially if details to technique are not followed. The “cheese grater” effect with stent deployment with aggressive post dilatation very likely has the potential to generate significant micro and macrodebris. Rapid advancement of the laser probe, especially through highly calcified plaque, could also potentially generate downstream distal emboli.
The authors appropriately list 7 clinical scenarios in which they recommend EPDs. As with any device technology, as these devices are perfected, the indications for use can be expanded, and I can even envision EPDs becoming the “standard of care” in infrainguinal PPI as they have become in carotid PPI. Traditional dictum would require multicenter, randomized data for EPD to become a “standard of care” in lower extremity PPI. I would tend to agree, but I would raise the question as to why EPD during carotid PPI became a “standard of care” without a plethora of similar data. I suspect that the frequently made comment “the brain is not as forgiving as the leg” is also likely true with embolic debris and has a lot to do with the clinically rapid adoption of EPDs during carotid PPI. I would like to raise the issue against the statement that the lower extremity is not as clinically tolerant of embolic debris as generally perceived, especially the already compromised CLI limb. Just as a detailed neurologic exam by a neurologist and cerebral imaging post carotid PPI has surprisingly identified a high incidence of post PPI embolic debris sequelae, I suspect this same high likelihood of clinical sequelae could be identified in the small vessels and microcirculation of the foot, if only we had the objective clinical ability to do so. I wonder how many interventionalists (radiologists, cardiologists, and yes, surgeons) actually do a detailed physical exam and assessment of the foot before and after their PPI and are trained and committed to accessing even the “minor” clinical signs and symptoms of distal microcirculatory embolic debris.
As a trained and committed cardiovascular surgeon, I must admit that this post-PPI assessment is no easy task. Pain is a poor assessment for emboli, as most of the CLI patients have a severe diabetic neuropathy with an insensate foot and, therefore, cannot perceive pain. Massive distal emboli can be easily diagnosed, but not so for smaller debris that can be clinically asymptomatic, which I strongly suggest are clinically significant (Figure 1). Distal tissue and skin changes oftentimes occur 24–72 hours after the PPI and after discharge from the hospital and still can remain asymptomatic (Figure 2). Analogous to the lessons learned from the downstream microcirculatory distal emboli experience during PCI for acute coronary syndromes, I suspect similar microcirculatory injury frequently occurs during infrainguinal PPI, but we have no analogous biomarkers or tools to accurately assess the pedal microcirculation. When these tools become available, I believe we will identify a very high incidence of distal embolic debris during infrainguinal PPI and be able to fully assess their clinical significance. How do we know today that a poorly healing CLI ulcer or a new wound breakdown after a “successful” PPI with revascularization of the “culprit lesions” wasn’t caused by distal embolic debris? Postprocedural angiograms are necessary and can identify macrodebris, but infrapopliteal vessels are very prone to spasm and angiography is likely poor in assessing the small vessels and microcirculation of the foot.
Several promising technologies are being developed to assess wound healing that also may hold promise in assessing microcirculatory anatomy and function before and after infrainguinal PPI. The OxyVu (Hypermed, Inc., Waltham, Massachusetts) utilizes medical hyperspectral imaging, a novel camera-based diagnostic tool that quantifies hyperspectral tissue oxygenation in diabetic foot ulcer wound healing, and therefore, has the potential to be an objective metric of microcirculatory function and disease. The Sensilase System (Vasamed, Inc., Eden Prairie, Minnesota) is a noninvasive laser Doppler test combining skin perfusion pressure (SPP) and pulse volume recording (PVR) to assess the capillary circulation and assess wound healing potentials. Both technologies are under investigation and may show promise as objective physiologic assessments of distal embolic debris during infrainguinal PPI.
Our single site experience with filter EPD in 70 infrainguinal PPI in primarily CLI patients began in July 2006. To date, 58 cases have been analyzed. PPI treatments included: sole laser = 4, sole plaque excision (PE) = 2, laser PTA = 16, PE PTA = 4, laser PTA/stent = 23, PE PTA/stent = 4, and PTA/stent = 5. The EPD delivery success rate was 58/59 (98%). There were no major EPD complications but 3/16 (18.7%) infrapopliteal deployments experienced vasospasm. Overall, particulate EPD debris was identified in 44/58 (76%) of cases. No EPD debris was found in 14/58 (24%) cases. Minor debris was identified in 37/58 (64%) and major debris in 7/58 (12%). Predictors of major debris included CTO, PE, PTA, and PTA/stenting, but minor debris occurred with all types of PPI including laser.
The technical tips provided by the authors are important and noteworthy. Additional lessons we have learned include:
1) We almost exclusively cross all lesions facilitated by the hydrophilic 0.035 mm Quick-Cross (Spectranetics Corporation, Colorado Springs, Colorado) catheter and deliver the Spider (eV3, Inc., Plymouth, Minnesota) filter EPD through the Quick-Cross catheter. As described by Dr. Shammas, we have also found the Spider EPD to be the most user friendly system currently available;
2) Avoiding movement of the EPD wire after deployment is very important to avoid complications. This can be very difficult to achieve, especially in more complex cases. Keeping the EPD in full view during all PPI maneuvers is paramount to avoiding EPD wire movement, especially in during device exchanges;
3) EPD movement induces vasospasm, especially in infrapopliteal vessels. Liberal use of antispasmodic agents is advocated and it is important not to oversize the EPD to the vessel size, especially in EPD deployment in infrapopliteal vessels;
4) Detailed final angiogram EPD scrutinization under cine magnification is recommended on all cases to identify debris before removal to strategize a removal plan. Partial filter capture is now recommended with the Quick-Cross catheter on all cases with debris identified on cine magnification. The inner Quick-Cross catheter edge is hydrophilic and the diameter of the catheter is larger than the existing Spider capture system, which facilitates partial filter capture and, therefore, less likelihood to extrude or “squeeze” debris through the filter pores during capture with a “full basket” (Figure 3);
5) The EPD has become just as important a tool in our “CLI toolbox” as any other revascularization device. It has become a “safety net” in many of our complex CTO or cases with large atherosclerotic or thrombus burdens. As a surgeon, EPDs have allowed me to be even more aggressive with endovascular treatments in higher risk cases, that, in the past, I would have selected an open surgical procedure as the index therapy due to high-risk of emboli during PPI. I now use creative EPD strategies in a great majority of my infrainguinal PPIs. As mentioned by the authors, even capture and removal of minor debris during PPI oftentimes prevents a more lengthy endovascular case, which at minimum will require extra fluro time, contrast volume, pharmaceutical-lytic agents, thrombectomy catheters, and devices, etc., which all have their own complications and clinical and economic costs.
This review does a nice job in identifying recommendations and strategies for EPD use during infrainguinal PPI. Naturally, multicenter, randomized data will likely be necessary before EPD use during lower extremity PPI will be considered a “standard of care”, or even more importantly in today’s environment, achieve FDA-approval in the periphery. I predict, though, that, unfortunately, this data will be difficult to accumulate analogous to the difficulty and lack of data in all other areas of peripheral endovascular therapy. I can now hear critics saying that thousands of lower limb PPIs are done yearly with few “clinically relevant” distal emboli, and that minor debris in a limb with 3-vessel runoff is not clinically important. That argument does hold some truth by our current objective assessments of infrapopliteal vessels and the microcirculation of the foot. I believe that concept will change in the near future. I would ask any of our readers (with 3-vessel infrapopliteal runoff) if they would be comfortable in losing their own 2.5 mm dorsalis pedis or posterior tibial artery or the corresponding pedal microcirculation today, even if they remained asymptomatic. I would think not. Hopefully, this ca also be avoided in our patients, especially when we have EPD systems that are proven simple, safe, cost-effective, and yes, effective in protecting the lower limb microcirculation from embolic debris during PPI.
In conclusion, I believe it is now time for us to “get our heads out of the sand” or embolic debris and dedicate the resources necessary to fully investigate the potential role of distal embolic debris and EPDs during infrainguinal PPIs. I hope clinicians, industry, and the FDA can work closely on this project, as I believe EPD use in infrainguinal PPI, especially in CLI, has the opportunity to further improve acute and longer-term outcomes.
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