Wire Entrapment Through an Aortic Paravalvular Leak

J INVASIVE CARDIOL 2010;22:E119–E121

Key words: A-PVL, complications    The occurrence of paravalvular leaks (PVL) after valve replacement surgery is not infrequent, however a small percentage of them are clinically significant.^1–3 The surgical repair of those leaks requiring closure is complex, with higher morbidity, mortality and significant recurrence.^4–8 Percutaneous closure of PVLs is becoming an acceptable treatment modality with low complication rates, although not always successful.^9–11    The use of guidewires is essential to initially cross the paravalvular track of the leak. Most wires are constructed with an inner core, which is wrapped with a much thinner wire to provide specific characteristics to their performance. More recently, the use of monolytic wires with hydrophilic coating has facilitated the passage through tortuous structures.    There are well-known complications from the use of wires, the most common ones described being dissection and perforation of structures.^12–15 A very unusual complication related to the use of a wire is the entrapment within anatomical structures. We describe a case of a coronary wire entrapped through a serpiginous aortic paravalvular leak (A-PVL).    Case Description. An 81-year-old male who had a bioprosthetic aortic valve replacement for aortic stenosis 5 months prior was referred with refractory congestive heart failure and hemolysis from a large A-PVL diagnosed by transesophageal echocardiography (TEE). The patient underwent 256-slice computed tomography angiography (CTA) with 4-D image volume-rendered reconstruction which confirmed and characterized the presence of the A-PVL with a serpiginous track originating underneath the right coronary cusp (Figures 1A and B). Due to the recent complicated post-operative course, the patient was referred for a percutaneous attempt to close the A-PVL.    Procedure. Bilateral femoral artery (FA) accesses were obtained with 6 Fr sheaths. An AR2 diagnostic catheter was advanced retrogradely over a 0.035-inch Glidewire (Terumo Medical Corp., Somerset, New Jersey) to engage into the A-PVL. After several unsuccessful attempts to cross the A-PVL leak, the Glidewire was exchanged for a 0.014-inch hydrophilic PT2 MS guidewire (Boston Scientific Corp., Natick, Massachusetts) which successfully crossed into the left ventricle (LV). Once this wire was positioned in the LV, it was redirected antegradely through the functional bioprosthetic valve orifice into the ascending aorta to obtain greater support and wire stability. The proximal tip of the wire was snared from the ascending aorta using a 25 mm Amplatz Goose Neck® snare kit (ev3, Inc., Plymouth, Minnesota) and the wire was exteriorized through the contralateral femoral artery access, forming an arterial-arterial loop (Figure 1C).    A 2.8 Fr Renegade™ microcatheter (Boston Scientific) was used to exchange the 0.014 inch hydrophilic wire for a 0.025 inch non-hydrophilic stainless steel wire in an attempt to increase support. Once the 0.025 inch wire and Renegade microcatheter were across the A-PVL leak, we were unable to further retrieve the guidewire. After several attempts to forcefully snare the wire, the proximal portion of the wire began to disintegrate in fragments. At this point, the wire, together with the Renegade microcatheter, was entrapped through the serpiginous PVL track.    Emergency surgery was required to remove the entrapped wire and catheter as well as to repair the A-PVL (Figure 1D). Surgical exploration revealed the entrapped wire across the polyester-covered suture ring of the prosthesis. The surgeons forcefully removed the wire, and with a pericardial patch stitched, closed the PVL. The patient recovered uneventfully and a follow-up echocardiogram revealed the presence of a small but persistent A-PVL.    Discussion. Wire entrapment is a rare complication described in a variety of anatomical structures based on the procedure performed.^16–20 Paravalvular leaks, a well-recognized surgical complication after valve replacement, poses a technical challenge for the surgeon and interventionist due to its variable nature with unique morphologies and locations.2,21 During percutaneous repair, a variety of wires and catheters are used to cross the PVL depending on the location and anatomical characteristics of the leak. In this case, we describe the use of a 0.014 inch hydrophilic coronary wire used to cross through an A-PVL with a serpiginous tract and the subsequent exchange for a 0.025 inch nonhydrophilic wire in an attempt to upgrade the support to deliver a closure device. In this attempt, the nonhydrophilic wire was entrapped at the PVL track and after forceful pulling of the wire fractured and disintegrated it.    Currently, hydrophilic wires are preferred to tract a difficult path; the risk of dissection and limited support obtained mandate the exchange for a different wire. In this case the entrapment of the nonhydrophilic wire by the polyester suture ring could have been potentially avoided by using only hydrophilic wires due to their characteristic lubricity.    The approach to remove entrapped wires percutaneously has been described by using different catheters and maneuvers depending on the location.^22,23 When the intrinsic stress that a wire has been designed to withstand is overcome by external forces, the outer coil can disintegrate and result in fragmentation.^12,24 As described during this case, the surgical removal of fragments or entrapped wires is the final resolution to this complication.²⁵    Conclusions. The entrapment of a wire through a PVL is a rare complication of percutaneous repair. Awareness of this risk is relevant for the selection of appropriate tools based on the characteristics of each PVL to avoid entrapment when performing transcatheter repair. Nonhydrophilic wires should not be used in percutaneous closure of paravalvular leaks in an effort to avoid the complication reported in this paper. From Department of Interventional and Structural Heart Disease, Lenox Hill Heart and Vascular Institute, New York, New York. The authors report no financial relationships or conflicts of interest regarding the content herein. Manuscript submitted October 27, 2009 and accepted December 4, 2009. Address for correspondence: Carlos E. Ruiz, MD, PhD, Lenox Hill Heart and Vascular Institute, 130 East 77th Street. 9th Floor Black Hall, New York, NY 10075. E-mail: cruiz@lenoxhill.net References

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