Case Report

Simultaneous Aortic and Mitral Metallic Paravalvular Leaks Repaired Through One Delivery Sheath

Claudia A. Martinez, MD, Howard Cohen, MD, Carlos E. Ruiz MD, PhD
Claudia A. Martinez, MD, Howard Cohen, MD, Carlos E. Ruiz MD, PhD

ABSTRACT: Paravalvular leaks (PVL) are a well-known complication after prosthetic valve surgery. Effective non-surgical repair techniques are being developed using several off-label transcatheter occlusive devices given that there is no unique technique applicable to repair each paravalvular leak. We describe a technique used to simultaneously repair several PVL percutaneously, in a patient with double mechanical prosthesis using a single delivery system, by taking advantage of specific anatomical factors and selecting the best applicable devices.

J INVASIVE CARDIOL 2011;23:E19–E21
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Paravalvular leaks (PVL) are a well-known complication after valve surgery, especially in heavily calcified annulus as well as post-infective prosthetic endocarditis.1,2 Treatment of PVL is required when patients become symptomatic with worsening heart failure or severe hemolysis. The conventional repair of these types of defects has been surgical, but the high morbidity and recurrence rates have motivated the search for alternative treatments.3–9 Transcatheter repairs of PVL have been reported since the early 1990s using a variety of closure devices designed for other structural and vascular indications (i.e., coils, occlusion devices, etc.) with variable success.10,11 Due to the wide anatomical variations of PVL, a standard routine closure technique is not applicable and innovative strategies are required.

We describe a case in which a technique was used to simultaneously close an aortic (A-PVL) and mitral paravalvular leak (M-PVL) in a patient with double mechanical valves through the same access site.

Case Report. A 54-year-old man with re-do metallic valves in the aortic and mitral position (4 years prior) due to history of endocarditis, was referred for transcatheter PVL repair because of severe hemolysis. He underwent 3-D transesophageal echocardiogram (TEE) as well as 4-D computed tomographic angiography (CTA) reconstruction that confirmed the presence of 2 M-PVL (at 9 and 11 o'clock visualized clockwise from the left atrium, when the aortic valve is considered in the 12 o'clock position) and 1 A-PVL close to the left coronary cusp. These images were further used to guide the procedure (Figure 1).

Procedure. Arterial and venous femoral accesses were obtained. An 8 French (Fr) Mullins sheath was introduced from the right femoral vein into the right atrium and with a Brokenbrough needle, trans-septal puncture was performed to obtain antegrade access into the left atrium (LA). A 6 Fr JL5 catheter was introduced through the right femoral artery into the ascending aorta to engage retrograde the A-PVL with a 0.035" glidewire. Once the glidewire was in the left ventricle (LV), a 6 Fr AR2 catheter was exchanged inside of the LV over the same glidewire to redirect it retrograde into the left atrium (LA) through the M-PVL. Once the wire was successfully placed in the left atrium retrograde through the A-PVL and M-PVL, a 4 Fr glidecatheter was advanced over the glidewire into the LA to obtain more support. A 25 mm Amplatz Goose Neck Snare kit (EV3 Inc., Plymouth, Minnesota) was then introduced antegrade through the trans-septal venous sheath into the LA to snare the glidewire and exteriorize it through the right femoral vein, creating an arterial-venous loop (A-V loop).

The trans-septal sheath was then exchanged for a 7 Fr delivery system and advanced antegrade through the M-PVL into the LV and through the A-PVL into the ascending aorta. An 8/6 mm Amplatzer Duct Occluder (ADO) device (AGA, Plymouth, Minnesota) was deployed at the A-PVL. The delivery sheath was then withdrawn into the LV and a 10/8 mm ADO device was deployed successfully through the same delivery system into the M-PVL (Figures 1 and 2). The normal function of the prosthetic valves during deployment and after release was confirmed by fluoroscopy and TEE performed during the procedure. Color Doppler revealed no residual PVL. A follow-up CTA confirmed the stability of the devices, including the occlusion of both of the M-PVLs with the same skirt of the ADO device that was positioned at one of the M-PVL (Figure 3). The patient was discharged home 2 days later and subsequent outpatient follow-up has been uneventful without further hemolysis.

Discussion. We present a patient with clinically significant A-PVL and M-PVL of 2 metallic prosthetic valves that were percutaneously closed through a single access. The advantage of accessing the LV retrograde through the A-PVL without interfering with the function of the metallic aortic valve prosthesis was a unique scenario that allowed for simultaneous retrograde access into the M-PVL from the transfemoral approach. The ADO is a self-expandable device made from a Nitinol wire mesh filled with polyester fabric that has a retention skirt in one side, designed for non-surgical closure of a patent ductus arteriosus. Based on the characteristics and anatomical locations of the PVL presented in this case, the ADO device was selected to percutaneously close the A-PVL and one of the M-PVL present, taking into consideration the size (measured by 3-D TEE and 4-D CTA) as well as the pressure difference in each chamber. For the A-PVL, due to the greater diastolic gradient at the aortic side, the retention skirt of the ADO was deployed at the ascending aortic side of the PVL. For the M-PVL ,the higher gradient is the one generated by the LV during systole, which is why the device was deployed antegrade with the retention skirt at the ventricular side (successfully occluding both M-PVLs initially present).

Conclusion. The percutaneous closure of PVL continues to be a technically challenging procedure. Although there are several approaches, attention to specific anatomical factors in each case will allow the interventionalist to select the best applicable technique.

References

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From the Department of Interventional and Structural Heart Disease, Lenox Hill Heart and Vascular Institute, New York, New York. Disclosure: Dr. Carlos Ruiz is a proctor for AGA. Manuscript submitted May 25, 2010 and accepted June 15, 2010. Address for correspondence: Carlos E. Ruiz, MD, PhD, FACC, FSCAI, Director of Structural Heart Interventions, Lenox Hill Heart and Vascular Institute, 130 East 77th Street, 9th Floor Black Hall, New York, NY 10021-10075. E-mail: cruiz@lenoxhill.net