Atheroemboli during Peripheral Arterial Interventions
Atheroemboli during percutaneous peripheral arterial interventions (PAI) complicate about 1–2% of procedures, with serious adverse outcomes, although their true incidence is estimated to be much greater.1 In the era of increasing number and complexity of percutaneous peripheral arterial revascularization procedures, it is important to provide operators with guidance regarding the predictors of this rare though serious complication. The rarity and often unpredictability of atheroembolic complications during PAI makes this article by Shammas et al extremely relevant to today’s endovascular specialist.2
This feared sequela of PAI might either result in abrupt occlusion of large conduit runoff vessels and/or impede microcirculatory flow. Doppler-signal recording of distal embolization (DE) is registered during 100% of PAI,3 however angiographic slow or cessation of antegrade flow occurs in 3.8–24% of cases.1 The frequent incidence of DE is largely due to anatomic and procedural variability amongst published reports, with local intra-arterial thrombolysis linked with the highest risk of DE.1 Acute or subacute lower-limb ischemia, endovascular treatment of chronic total occlusions and use of atherectomy techniques have also been reported to be independent predictors of DE.4 The SilverHawk Plaque Excision Atherectomy device (FoxHollow Technologies, Redwood City, California) and laser atherectomy have both been linked to distal athero-embolization during PAI, with debris collected in distal filter-based embolic protection devices (EPD) in 20–50% of cases.5 Similarly, angioplasty with provisional stent implantations during infra-inguinal PAI may also be a source of significant DE. Clinically significant DE was reported in nearly 30% of angioplasty and/or stent procedures and in 90% of atherectomies reported in the Preventing Lower Extremity Distal Embolization Using Embolic Filter Protection (PRO-TECT) registry.6
In this issue of the Journal of Invasive Cardiology, the Shammas et al report results form a large cohort of PAI from a single center. Although the analysis is retrospective, the prospective data collection and outcomes adjudication make this report significant and relevant to endovascular specialists. Especially noteworthy is the wide discrepancy in the literature-reported incidence of DE and the need for a clinically necessary mechanical and/or pharmacologic intervention. Though it is important to highlight that this determination, as reported by Shammas et al, is not without bias; the 2.4% incidence of operator-adjudicated DE requiring treatment allows us to predict the true incidence of clinically meaningful athero-embolic complications anticipated by operators performing PAI in a real-world practice setting.2 The authors also present independent clinical and procedural factors that heighten the risk of DE during PAI, like the presence of prior amputations, visible intravascular thrombus and complex lesion features characterized per the TransAtlantic InterSociety Consensus classification (original TASC-2000) as TASC D.2
Though Shammas et al recognize the important limitations of their report, it is worth adding that the report does not address the specific clinical and procedural details that led to the operators adjudicating some, but not all, cases of DE as clinically relevant and requiring treatment. The timing of DE and association with specific devices are crucial factors to planning a PAI, and the inclusion of such details may have provided some meaningful pointers to the readers. Instrumentation in the distal infrarenal aorta, arterial access and/or sheath insertions have all been linked to athero-embolization, as are non-procedure-related factors like the presence of large, mobile aortic atheroma, warfarin therapy associated “blue-toe syndrome,” cardio-embolic events, and others.7 In Figure 1, we present a case of massive DE after contralateral arterial sheath placement. Most importantly, as in the native percutaneous coronary and saphenous aorto-coronary vein graft interventions, the reported incidence of DE may not justify the recommendation for the use of EPD without a controlled strategy trial.8 Most DE during PAI occur during stent deployment, similar to what has been reported during carotid interventions by Casserly et al, and its negative association with preprocedural antiplatelet therapy with aspirin during renal artery stenting.9 Moreover, the presence of intravascular thrombus is underappreciated using conventional angiographic techniques in patients with acute or subacute lower-limb ischemia. Intravascular ultrasound (IVUS) imaging has demonstrated the presence of thrombus in about 94% of patients with acute or subacute presentations.10 It is also important to highlight that IVUS may not be ideally suited for imaging fresh clot, and a strategy of compulsive aspiration thrombectomy, with or without visible thrombus, may be reasonable and should be tested in a clinical strategy trial, as validated during coronary interventions for acute ST-segment-elevation myocardial infarctions. The conversation about athero-emboli during PAI would be incomplete without mentioning adjunctive pharmacotherapy with antiplatelet and antithrombotic agents, a topic that has largely been neglected. Intensification of adjunctive therapy with warfarin, along with aspirin, clopidogrel or ticlopidine in patients with peripheral arterial disease, did not show improved outcomes, and reported a significant increase in hemorrhagic complications.11 Similarly, periprocedural use of abciximab (a glycoprotein IIb/IIIa inhibitor), in addition to aspirin and clopidogrel during PAI of long and complex lesions, was not associated with improved mortality or ischemic outcomes, and resulted in excess bleeding (5.1% vs. 1%; p = 0.02).12 However, DE as defined by angiography, occurred in 6.1% of patients in the abciximab group, and 12.3% of controls (p = 0.02); representing a 55% decrease in the adjusted risk associated with triple antiplatelet therapy.13 This may suggest the possible role of glycoprotein IIb/IIIa inhibitors as adjunctive therapy in patients at high risk for DE or slow-flow states.
In conclusion, this article by Shammas et al provides valuable insight into predictors of athero-embolic complications during PAI from a high-volume center and brings to the forefront the often-forgotten need for a controlled, clinical-strategy trial dedicated to the use of EPD during PAI.
Acknowledgements. The authors acknowledge the grant support from the Clark Gregg Fund of the Harris Methodist Foundation of Fort Worth, Texas, and that of Avantika Banerjee, for her technical help in the preparation of this manuscript.
From the VA North Texas Healthcare System and University of Texas Southwestern Medical Center, Dallas, Texas.
The authors report no conflicts of interest regarding the content herein.
Address for correspondence: Subhash Banerjee MD, 4500 S. Lancaster Road (111a), Dallas, TX 75216. E-mail: Subhash.email@example.com
1. Karnabatidis D, Katsanos K, Kagadis GC, et al. Distal embolism during percutaneous revascularization of infra-aortic arterial occlusive disease: an underestimated phenomenon. J Endovasc Ther 2006;13:269–280.
2. Shammas N, Shammas GA, Dippel EJ et al. Predictors of distal embolization in peripheral percutaneous interventions: A report from a large peripheral vascular registry. J Invasive Cardiol 2009;21:628–631.
3. Lam RC, Shah S, Faries PL, et al. Incidence and clinical significance of distal embolization during percutaneous interventions involving the superficial artery. J Vasc Surg 2007;46:1155–1159.
4. Wholey MH, Maynar MA, Wholey MH, et al. Comparison of thrombolytic therapy of lower-extremity acute, subacute, and chronic arterial occlusions. Cathet Cardiovasc Diagn 1998;44:159–169.
5. Kaid KA, Gopinathapillai R, Qian F, et al. Analysis of particulate debris after superficial femoral artery atherectomy. J Invasive Cardiol 2009;21:7–10
6. Shammas NW, Dippel EJ, Coiner D, et al. Preventing lower extremity distal embolization using embolic filter protection: Results of the PROTECT registry. J Endovasc Ther 2008;15:270–276.
7. Banerjee S, Keber R, Barnett M, et al. Warfarin therapy and risk of embolic events in elderly stroke patients with aortic atheroma. Vascular Disease Management 2006;3:339–344.
8. Banerjee S, Brilakis ES. Embolic protection during saphenous vein graft interventions. J Invasive Cardiol 2009;21:415–417.
9. Casserly IP, Abou-Chebl A, Fathi RB, et al. Slow-flow phenomenon during carotid artery intervention with embolic protection devices: Predictors and clinical outcome. J Am Coll Cardiol 2005;46:1466–1472.
10. Shammas NW, Dippel EJ, Shammas G, et al. Dethrombosis of the lower extremity arteries using the power-pulse spray technique in patients with recent onset thrombotic occlusions: Results of the DETHROMBOSIS Registry. J Endovasc Ther 2008;15:570–579.
11. Warfarin Antiplatelet Vascular Evaluation Trial Investigators. Oral anticoagulant and antiplatelet therapy and peripheral arterial disease. N Engl J Med 2007;357:217–227.
12. Baumgartner I. Reopro and peripheral arterial intervention to improve clinical outcome in patients with peripheral arterial disease (RIO Trial). European Society of Cardiology Congress 2007; September 3, 2007; Vienna, Austria. Hot line II.