Closure of Aortic Paravalvular Leak Under Intravascular Ultrasound and Intracardiac Echocardiography Guidance


Madan Sharma, MD*, Elaine Tseng, MD§,∞, Nelson Schiller, MD*, Phillip Moore, MD,
Kendrick A. Shunk, MD, PhD*,£

ABSTRACT: Aortic paravalvular leaks after aortic valve replacement surgery — though not uncommon as an incidental finding — may become clinically significant in up to 5% of patients. Open surgical correction by either direct suturing or patching of the defect or reoperative valve replacement is associated with significant morbidity and mortality. Relatively few case reports are available in the literature addressing percutaneous closure of aortic paravalvular leaks. We describe the novel use of intracardiac echocardiography and intravascular ultrasound to guide closure strategy selection and subsequent deployment of an Amplatzer duct occluder device. The patient experienced immediate subjective and hemodynamic improvement accompanied by rapid resolution of heart failure symptoms from New York Heart Association (NYHA) class IV to NYHA class II. This marked clinical improvement has been sustained at 40 months to date and 4-month follow-up echocardiography confirmed complete resolution of aortic regurgitation as the mechanism behind this improvement.

J INVASIVE CARDIOL 2011;23:E250–E254

Key words: aortic valve insufficiency, intravascular ultrasonography


Prosthetic paravalvular leaks (PVL) are common, occurring after 2–17% of prosthetic valve replacements.1,2 While small PVL may cause hemolysis, they are usually well tolerated. Larger PVL, however, may cause heart failure due to severe regurgitation. While the preferred option is surgical, reoperation is associated with significant morbidity and mortality.3,4,8–11 Percutaneous closure of the PVL is sometimes undertaken in patients with significant co-morbidities using any of a variety of devices originally intended for other purposes. Such “off-label” uses of these devices may result in under-reporting in the literature.13–27 Webb et al have reported one of the larger “series” of PVL managed percutaneously; however, only one of those cases was an aortic PVL.23 Here we describe the successful closure of an aortic PVL with an Amplatzer Duct Occluder (AGA Medical Corporation, Plymouth, Minnesota), using both intravascular ultrasound (IVUS) and intracardiac echocardiogram (ICE) for imaging of the PVL tract in order to inform specific occluder device selection and, in the case of ICE, to monitor progress and acute success of the procedure.

Case Report. An 81-year-old male, retired cardiac surgeon with a history of coronary artery disease and aortic stenosis had undergone 5-vessel coronary artery bypass grafting with a left internal mammary artery to the left anterior descending artery, saphenous vein graft to the right coronary artery, diagonal branch and a Y-anastomosis sequential saphenous vein graft to the obtuse marginal and the first diagonal branches, combined with aortic valve replacement (AVR) surgery with a 23 mm Magna pericardial bioprosthesis (Edwards Lifesciences, Irvine, California) in May of 2006 at an outside institution. The procedure was complicated by difficulty in valve sizing necessitating aortic root enlargement (Manougian procedure) using a Dacron patch (Hemashield; Boston Scientific, Natick, Massachusetts).12 His early post-operative course was complicated by mediastinal bleeding requiring re-exploration and delayed sternal closure. His subsequent hospital course was complicated by acute renal failure, nosocomial infections, respiratory insufficiency requiring tracheostomy and prolonged coma resulting in a 6-week prolonged stay in the intensive care unit. He subsequently recovered and was transferred to cardiac rehabilitation 7 weeks post-op with gradual recovery to New York Heart Association (NYHA) II functional status.

The patient then experienced worsening heart failure symptoms and was re-hospitalized in June of 2007 with acute decompensated heart failure, a new diastolic murmur, and a diastolic pressure consistently in the low 30s. Initial transthoracic echocardiogram demonstrated severe aortic regurgitation with reversal of flow in the descending aorta, a pressure half-time of 180 ms and calculated regurgitant fraction of 78%. A transesophageal echocardiogram (TEE) subsequently confirmed that the aortic regurgitation was due to a paravalvular communication between the left ventricular outflow tract and the left sinus of Valsalva (Figure 1). The patient underwent diagnostic cardiac catheterization with proximal aortography which confirmed severe aortic regurgitation (Figure 1).

Coronary and graft angiography showed that the left anterior descending and left circumflex arteries had proximal segment high-grade stenosis; the right coronary artery had luminal irregularities only.The left internal mammary graft to the left anterior descending artery was patent; the saphenous vein graft to the diagonal and obtuse marginal branches had severe stenosis in its proximal shared segment.

Revascularization and redo-aortic valve replacement surgery (AVR) were discussed in detail in a series of interdisciplinary conferences, including several members of the cardiothoracic surgery, non-invasive cardiac imaging, and interventional cardiology teams. Given his prior post-operative course and multiple co-morbidities, the patient was deemed an unacceptable risk for open repair by two independent and highly-experienced academic cardiothoracic surgery teams. The patient refused an offer for hospice care. A trial of intensive medical therapy ensued, but after 4 weeks in the hospital, he remained in NYHA class IV heart failure, unable to speak in complete sentences due to dyspnea at rest. Following a series of detailed strategic and technical discussions of potential options with the patient (a highly informed and competent retired cardiac surgeon) and his son (a practicing cardiac anesthesiologist), an attempt at percutaneous closure was offered and enthusiastically accepted.

Procedure. After obtaining appropriate femoral arterial and venous access, the patient was given repeated small boluses of heparin to achieve an activated clotting time that ranged from 228–242 seconds during the procedure. An 8 French (Fr) ICE catheter (ACUSON AcuNav; Siemens, New York, New York) was advanced via an 8 Fr right femoral venous sheath to the right atrium for imaging of the aortic bioprosthetic valve and the paravalvular leak (Figure 2). A 6 Fr Amplatz ALR guide catheter was advanced via a 6 Fr right femoral arterial sheath to the aortic root. A 300 cm, 0.014" diameter, balanced middle-weight coronary guidewire (BMW; Abbott Vascular, Santa Clara, California) was then advanced through the ALR across the paravalvular tract into the left ventricle. A 40 MHz, mechanically-rotating IVUS catheter (Atlantis Pro; Boston Scientific) was advanced over the guidewire to image the paravalvular tract using an automated pullback at 0.5 mm/s. The tract was irregular, with a somewhat crescent-shaped cross-section profile and a minimum unstretched dimension of 2 mm at the expected point immediately adjacent to the sewing ring (Figure 2). After assessment of the morphology and dimensions of the paravalvular tract with both IVUS and ICE was completed, left coronary angiography was performed via a separate 4 Fr sheath in the left femoral artery to define the origin of the left main artery in relation to the PVL.

Using a 100 cm, 5 Fr glide catheter (Terumo, Elkton, Maryland), the BMW guidewire was exchanged for a 260 cm, 0.035" diameter, Amplatz super-stiff guidewire (Boston Scientific) in the left ventricle. A Powerflex P3 catheter (Cordis Corporation, Miami Lakes, Florida) was advanced over the Amplatz wire spanning the paravalvular leak. It was gently inflated at low atmospheric pressure to further define the contour of the tract and to assess the effect on the leak by ICE with color Doppler as well as simple arterial pressure waveform monitoring (Figure 2). The diastolic pressure increased from 30 mmHg to 50 mmHg with balloon occlusion of the PVL tract. The balloon was deflated and removed. After review of the images and measurements, available options for closure were reviewed. Given the size of the PVL, the proximity to the prosthetic leaflets and the left main coronary origin, and the forces likely to be present on the device due to the pressure gradient between the aorta and the left ventricle, a device with a wide mid-portion and a flange on either end would have been the ideal intuitive choice. Although the Amplatzer muscular VSD device fits the description, it was not an available option in the United States at that time. After consideration of all available alternatives, including coils, PFO, and ASD devices, an Amplatzer Duct Occluder was selected. To compensate for the lack of a flange on the proximal end, it was decided to deploy an oversized 10/8 Amplatzer Duct Occluder device with the goal of obtaining a waist at the sewing ring and a flare above it, as the flange of the device would be below the valve in the outflow tract.

The AGA duct occluder delivery sheath proved too short to reach the left ventricle over the super-stiff wire and was subsequently exchanged for a 90 cm, 8 Fr Cordis Brite tip guide sheath, which was advanced across the leak and positioned in the left ventricle. The Amplatzer Duct Occluder 10/8 device was then advanced with a standard deliver cable via the 90 cm sheath into the left ventricular cavity. The device was positioned under fluoroscopic and ICE guidance (Figure 3). ICE images showed minimal residual aortic regurgitation. Repeat left coronary angiography confirmed that the device would not infringe upon the left main coronary artery (Figure 3). After satisfactory confirmation of appropriate positioning, conformation, and hemodynamic effect, the device was fully released from its delivery cable (Figure 3). The patient reported immediate subjective improvement in dyspnea at the appropriate time during the procedure. The diastolic pressures rose from 36 mmHg at baseline to 53 mmHg and ICE confirmed acute reduction in the size of the aortic regurgitation jet (Figure 4).

By hospital day 4, the patient was able to ambulate 150 feet without dyspnea. A repeat transthoracic echocardiogram performed post-procedure day 1 showed only mild aortic regurgitation and the patient reported resolution of the symptom of exertional dyspnea. The remainder of the hospitalization was uneventful and the patient was successfully discharged home. The clinical improvement has been sustained at 9 months (to date). An echocardiogram performed at 4 months showed the device in its expected location with complete resolution of the aortic regurgitation by Doppler. His clinical improvement has been durable to 40 months (to date).

Discussion. PVL usually become clinically evident in the first year after valve replacement surgery. Aortic PVL can be seen in 47.6% of patients by Doppler echocardiography, though 90% of them are small, and their clinical course is benign.5 However, in 1–5% of patients, a larger clinical leak is seen.3,6 Redo-aortic valve replacement is associated with significant mortality and a substantial risk of recurrent paravalvular insufficiency.3,4,8–11

Percutaneous closure of PVL has been attempted since 1987. Hourihan et al reported 3 patients with successful closure of aortic PVL with the double-umbrella Rashkind device.13 Earlier devices had an unacceptable rate of embolization, and other devices have since been used including the Bard PDA Occluder, coils, and Amplatzer devices that are indicated for atrial septal defect or arterial duct closure.13–27 Most of the reported literature relates to closure of mitral as opposed to aortic PVL.13–27 Percutaneous closure of an aortic PVL has been reported very infrequently.20,21

The procedure is also limited by the anatomical complexity of the leak tract. PVL that come to intra-operative surgical inspection are typically described as irregular, tortuous, and crescent-shaped, resulting in difficulties in 3-dimensional assessment, device selection and device delivery.20,21 Larger defects sometimes require more than one device.19 The complex morphology benefits from dimensional assessment with multiple imaging modalities for rational device selection and delivery.

This case differs significantly from the few earlier reports,13–28 in that we used both ICE and IVUS to visualize the complexity of the PVL tract from within and without. While it may be argued that IVUS, while interesting, added little incremental information, we feel that it is the appropriate modality to study the morphology of the tract. Both the deployment of the device and immediate post-deployment results were also assessed by ICE. Since no “on-label” devices exist for percutaneous aortic PVL closure, a careful and rational strategy for selection of the “least unfavorable” option is critical. IVUS and ICE are particularly useful in this regard and are readily available adjunctive imaging support tools.

As this case also demonstrates, when all other potential management options, including surgery, medical management, and hospice care, are thoughtfully and rationally eliminated, percutaneous PVL may be the only remaining option. Provided it is approached with a thoughtful and deliberate manner, taking advantage of all available expertise and resources, it has the potential to provide an extremely gratifying outcome. Until “purpose-built” PVL closure devices are available, studied and approved, this sort of approach is an excellent alternative.


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From the *Department of Medicine, Division of Cardiology, and §Department of Surgery, Cardiothoracic Division, and Department of Pediatrics, University of California San Francisco, San Francisco, California and £Department of Medicine, Section of Cardiology, and Department of Surgery, Cardiothoracic Section, San Francisco Veteran Affairs Medical Center, San Francisco, California.
The authors report no conflicts of interest regarding the content herein.
Manuscript submitted April 13, 2010, provisional acceptance given April 19, 2010, final version accepted May 3, 2010.
Address for correspondence: Kendrick A. Shunk, MD, PhD, FACC, Department of Medicine, Section of Cardiology, Cardiology 111C, San Francisco VA Medical Center, 4150 Clement Street, San Francisco, CA 94121. E-mail:

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