Unintended Consequences of Femoral Artery Closure Devices

J INVASIVE CARDIOL 2010;22:358–359

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Vascular closure devices (VCDs) were developed in the mid-1990s to provide more effective hemostasis for femoral artery access sites, largely in response to the large-bore sheaths used for atherectomy devices and the emerging stent therapy requiring extensive anticoagulation.¹ These devices have undergone extensive modification improving their effectiveness and safety, with recent large single-center^2,3 and post hoc data from the ACUITY trial⁴ suggesting that VCDs reduce the incidence of major bleeding at the access site. Vascular complications associated with femoral arterial access use have been well recognized since the introduction of the percutaneous access technique in the 1950s. Despite a better understanding of potential factors that influence the risk of a vascular complication, an improvement in access technique and use of smaller sheath sizes, there remains a low but persistent rate of vascular complications after femoral artery access. Similarly, rates of vascular complication after the use of VCDs appear to have diminished over the past decade, likely in response to better devices as well as a better understanding of the optimal circumstances in which they should be used.³ However, there remains a low incidence of significant vascular complications, some of which appear to be unique to closure devices. There are two vascular complications in particular with substantial morbidity and potential mortality complicating femoral artery access: bleeding resulting in retroperitoneal hemorrhage, and partial or total occlusion of the femoral artery resulting in acute leg ischemia. Prior to the introduction of VCDs, surgical repair for laceration or threatened ischemia was reported in 0.5–1.9% of balloon angioplasty registries.⁵ In a more recent study, the rate of intervention for major bleeding at the access site was 0.4%.⁴ In this issue of the Journal, Brueck et al⁶ describe six cases of partial or complete occlusion of the femoral artery by the Angio-Seal closure device in 8,587 consecutive Angio-Seal deployments, which represents an incidence of 0.07%. All but one of the cases occurred within a few hours of the procedure and required urgent intervention to relieve threatened limb ischemia. In one case, symptoms developed shortly after the procedure, requiring intervention within a week of the procedure. In the absence of a closure device, one presumes that local arterial injury, most likely in the setting of preexisting atherosclerotic disease, stimulates the thrombotic process, culminating in acute thrombosis of the common femoral artery. Given that the common femoral artery is the sole conduit of blood supply to the leg, any interruption of flow will result in limb ischemia. In fact, preexisting atherosclerotic disease appears to be the important substrate in vessel occlusion after manual compression as well as after the use of a closure device as reported by Brueck et al.⁶ Using Doppler ultrasound, they were able to demonstrate that the collagen sponge was deployed intra-arterially (rather than external to the artery) in three of the six cases. In two cases, the anchor of the device was trapped under a plaque of the posterior wall with vessel occlusion due to physical collapse of the artery resulting from retraction against the collagen sponge outside of the vessel wall. It should be noted that vessel occlusion following closure device use is not unique to the Angio-Seal device, as case reports have documented this uncommon complication after use of suture-based, clip or external sealant devices as well.⁷ Fortunately, in the cases described here, the authors were able to use a percutaneous rescue technique that allowed reperfusion of the affected limb without the need for an open surgical repair. What lessons can we learn from these cases? First, the authors acknowledge that the Angio-Seal device was deployed in the majority of their patients without performing femoral arteriography before device placement. To their credit, they have now adopted universal femoral artery angiography before device use to ensure optimal local anatomy (i.e., a common femoral artery access site), as well as the absence of significant local atherosclerotic disease. Second, this Angio-Seal experience extends from 1995 to 2009, during which at least eight substantial device modifications were made to improve the effectiveness and the safety of the device. In particular, the newest modification of the device, the Evolution, incorporates automated compaction of the external collagen sponge against the anchor, which potentially should minimize the risk of pushing the external collagen sponge into the vessel itself due to vigorous manual compaction. To this point, in 1,010 Angio-Seal deployments in the Evolution Registry,⁸ there were no partial or complete vessel occlusions. Third, the incidence of this potentially grave, but infrequent complication should be placed in perspective. The incidence of 0.07% in this series is lower than that observed in the manual compression arm of several recent large single-center experiences,^2,3 and is substantially lower than that observed with most publicized experiences using the brachial artery as an access site (which is also an end-artery, and occlusion results in limb ischemia). Fourth, the percutaneous management of the partial and complete vessel occlusion provided satisfactory results with resolution of limb ischemia in the hands of these expert operators. Whether similar excellent outcomes would occur in the hands of less experienced operators remains to be determined. Open surgical repair can be done through a limited incision and would provide a definitive alternative solution to this uncommon problem. Going forward, the unintended consequence of the use of a closure device resulting in partial or complete vessel occlusion, rather than hemostasis and patency, remains a challenge for those participating in percutaneous therapies of the vascular system. While “extravascular” closure such as can be achieved with a sealant or a clip offers a theoretic solution to this particular device-related complication, the optimal solution to hemostasis at the access site free of any other complication awaits development.

References

1. Dauerman HL, Applegate RJ, Cohen DJ. Vascular closure devices: The second decade. J Am Coll Cardiol 2007;50:1617–1626. 2. Arora N, Matheny ME, Sepke C, Resnic FS. A propensity analysis of the risk of vascular complications after cardiac catheterization procedures with the use of vascular closure devices. Am Heart J 2007;153:606–611. 3. Applegate RJ, Sacrinty MT, Kutcher MA, et al. Trends in vascular complications after diagnostic cardiac catheterization and percutaneous coronary intervention via the femoral artery, 1998–2007. JACC Intervent 2008;1:317–326. 4. Sanborn TA, Ebrahimi R, Manoukian SV, et al. Impact of femoral vascular closure devices and antithrombotic therapy on access site bleeding in acute coronary syndromes: The Acute Catheterization and Urgent Intervention Triage strategy (ACUITY) trial. Circ Cardiovasc Interv 2010;3:57–62. 5. Popma JJ, Satler LF, Pichard AD, et al. Vascular complications after balloon and new device angioplasty. Circ 1993;88(Part 1):1569–1578. 6. Brueck M, Bandorski D, Rauber K, Boening A. Percutaneous transluminal dilatation of inadvertent partial or complete occlusion of the femoral artery caused by Angio-Seal™ deployment for puncture site closure after cardiac catheterization. J Invasive Cardiol 2010;22:353–357. 7. Turi ZG. Vascular occlusion after vascular closure: Rare but not rare enough. Catheter Cardiovasc Interv 2008;72:525–526. 8. Applegate RJ, Turi ZG, Sachdev N, et al. The Angio-Seal Evolution registry: Outcomes of a novel automated Angio-Seal vascular closure device. J Invasive Cardiol 2010, accepted for publication.

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From the Wake Forest University School of Medicine, Winston-Salem, North Carolina. The author reports no conflicts of interest regarding the content herein. Address for correspondence: Robert J. Applegate, MD, FACC, Section of Cardiology, Wake Forest University School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157-1045. E-mail: bapplega@wfubmc.edu