Second Valve Implantation for the Treatment of a Malpositioned Transcatheter Aortic Valve

Abstract: Background. Unfavorable immediate or delayed results after transcatheter aortic valve implantation (TAVI) may be a consequence of bioprosthesis malfunctioning, malpositioning, embolization, or degeneration. Deployment of a second valve within the first one implanted (TAVI-in-TAV) may be a potentially helpful therapeutic strategy. Methods. Six out of 412 patients undergoing TAVI had TAVI-in-TAV implantation for the treatment of a too high (n = 4) or too low position (n = 2) of the first implanted valve. Results. All TAVI-in-TAV procedures were successfully performed. The calculated valve area after second valve implantation was 1.6 ± 0.3 cm² with a mean gradient of 7.3 ± 2.2 mm Hg. Residual aortic regurgitation (AR) was mild in 5 patients and moderate in 1. At mid-term follow-up (30-724 days) neither the mean valve area (1.47 ± 0.31 cm²), the mean gradient (7.5 ± 3.6 mm Hg; 3.0–13.0 mm Hg) nor the degree of AR had changed significantly. Conclusion. TAVI-in-TAV for correction of malpositioned or embolized valves is technically feasible and leads to favorable functional results during mid-term follow-up.   

J INVASIVE CARDIOL 2012;24(9):457-462

Key words: aortic valve, heart valve prosthesis implantation, percutaneous, malpositioning, valve-in-valve

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The prevalence of valvular heart disease increases in parallel to the aging of the population. As a consequence, degenerative aortic valve stenosis has become the most common valvular heart disease in developed countries, affecting  2%-7% of individuals over the age of 65.^1,2 Once symptomatic, aortic valve stenosis is associated with poor prognosis and reduced survival.³ Transcatheter aortic valve implantation (TAVI) has emerged as an alternative to surgical aortic valve replacement among surgically high-risk patients.⁴

Despite the rapidly growing experience with this intervention, with more than 50,000 procedures performed so far, data on the incidence, cause, results, and long-term follow-up of transcatheter bioprosthesis-in-bioprosthesis implantation are scarce. This report focuses on the procedural and follow-up aspects of implantation of a second bioprosthesis within the first valve (TAVI-in-TAV), either during the initial or as a second intervention, to correct  hemodynamically unfavorable results after the first TAVI.

Methods

Data from 412 high-risk surgical patients who underwent TAVI for treatment of severe aortic stenosis between July 2007 and November 2011 were prospectively collected. Before the intervention, all cases were reviewed by the local heart team, an interdisciplinary group formed by interventional cardiologists and cardiac surgeons, to define the best treatment approach and device selection for each patient. This decision was made based on a thorough evaluation that considered the clinical characteristics of the patient, the risk assessment based on the Euroscore and  STS score, and the results of the preintervention screening investigation that comprised cardiac catheterization, transthoracic (TTE) or transesophageal echocardiography (TEE), computer tomography (CT), angiography of the aorta and iliofemoral vessels, carotid Duplex sonography, and pulmonary function tests.⁵ After the screening, 227 patients (55.1%) underwent transfemoral TAVI using a CoreValve device and 97 (23.6%) received an Edwards SAPIEN valve. The latter was implanted via transapical access in 83 patients (20.1%) and a CoreValve was deployed via trans-subclavian access in 5 patients (1.2%). Six patients (1.7% of the total) who had undergone transfemoral TAVI underwent implantation of  a second prosthesis without retrieval of the first one (TAVI-in-TAV), either as bail-out (n = 5) or during an elective re-intervention procedure (n = 1). These 6 patients form the cohort of this report.

All procedures were performed under local anesthesia with conscious sedation and monitored anesthetic care. Transfemoral access was gained as previously described.⁶ The radiographic projection that delineated the cusps of the 3 native aortic valve leaflets in a single line defined the optimal C-arm angulation used for valve implantation. Initial balloon dilatation was performed in all cases under rapid pacing (160-200 beats/min) by means of a temporary pacemaker previously inserted via jugular vein into the right ventricle. All valves were deployed under fluoroscopic guidance. As the need for TAVI-in-TAV was defined, and in case the guidewire had been removed after implantation of the first valve, correct re-insertion of the guidewire through the implanted TAVI prosthesis was carefully monitored. The same implantation technique and the same prosthesis type and size were used in all cases but one, in which case a second larger device was chosen.

Postprocedural medication consisted of acetylsalicylic acid 100 mg/day and clopidogrel 75 mg/day for 6 months. Adverse events including cardiovascular mortality, myocardial infarction, stroke, bleeding, acute kidney injury, and vascular access-site and access-related complications were defined and summarized according to the Valve Academic Research Criteria (VARC).⁷ Clinical and echocardiographic follow-up were scheduled to be performed within 30 days and at 6 and 12 months after the procedure.

Results

Baseline clinical characteristics and procedural results are presented in Table 1. Procedural success, defined as final stable placement of the second device, residual mean gradient less than 20 mm Hg, and absence of major cardiac and cerebral adverse events during the first 48 hours after implantation was achieved with all patients. Different mechanisms led to the need of a TAVI-in-TAV implantation for individual patients as described below.

Case 1. The first patient presented with severely calcified aortic leaflets requiring a stepwise dilatation of the valve. The passage of a 26 mm CoreValve prosthesis through the aortic valve was difficult, and during the deployment phase the valve dislodged cranially and was placed too high within the native annulus. As significant paravalvular aortic regurgitation (AR) was noted, postdilatation was performed in order to further expand the prosthesis and  improve the degree of regurgitation. This led to embolization of the device into the ascending aorta. The valve was then snared to a higher position in the ascending aorta in order to avoid occlusion of the coronary ostia, and a second 29 mm CoreValve was successfully  implanted into the aortic valve annulus with good result and only mild residual AR.

Case 2. A 26 mm CoreValve was implanted too low within the native aortic valve annulus, resulting in significant AR. Snaring of the bioprosthesis was attempted as a corrective measure, which led to dislodgment of the valve into the ascending aorta. A second 26 mm CoreValve prosthesis was then adequately implanted into the aortic annulus with a satisfactory final result.

Case 3. Severe angulations of the aortic arch caused distal dislodgment of a 29 mm CoreValve during deployment, resulting in severe AR. Attempts to snare and mobilize the prosthesis were unsuccessful. As a consequence, implantation of a second 29 mm valve was performed in appropriate position and improved the AR from severe to a moderate degree.

Case 4. The fourth case refers to an initially well-deployed 26 mm CoreValve prosthesis. However, one of the hooks connecting the valve to the delivery catheter remained attached to the catheter despite full deployment due to a high tension on the system. This led to a dislodgment of the valve into the ascending aorta while retrieving the delivery system. A second 26 mm CoreValve was successfully implanted in series, and the overall result was favorable.

Case 5 (Figure 1). This patient received primarily a 26 mm CoreValve. Despite slow and controlled stepwise deployment approximately 4 mm below the aortic annulus, cranial migration of  the prosthesis was observed during the final release with embolization into the ascending aorta. The valve was then pulled back by means of a snare to avoid occlusion of the coronary ostia, and a second 26 mm CoreValve was implanted in adequate position.

Case 6. Implantation of a 29 mm CoreValve too deep relative to the native aortic annulus resulted in moderate paraprosthetic residual AR despite postdilatation. The patient was asymptomatic, but an increase in left ventricle diameters (51 mm to 57 mm systolic and 62 mm to 71 mm diastolic) and a hemodynamically significant AR were measured at echocardiography follow-up after 1 year. A second 29 mm CoreValve was implanted within the first prosthesis at a higher position and AR was reduced to grade I. 

In-hospital outcome was complicated by major bleeding and acute renal injury in 1 patient, a major vascular complication in 1 patient, and a minor vascular complication in 1 patient. A definitive permanent pacemaker implantation was indicated in 2 out of 6 patients.

During mid-term follow-up (range, 30-724 days after intervention), 1 patient died of cancer 7 months after TAVI. Symptoms improved in 2 patients to New York Heart Association (NYHA) functional class I and in 4 patients to NYHA class II. Follow-up echocardiography revealed a calculated mean valve area of 1.47 ± 0.31 cm2 (range, 1.0-1.7 cm2) with a  mean aortic transvalvular gradient of 7.5 ± 3.6 mm Hg (range, 3.0-13.0 mm Hg). Residual regurgitation was none in 2 patients, mild in 3 patients and moderate in 1 patient (Table 2).

Discussion

TAVI-in-TAV was defined as the transcatheter insertion of a second bioprosthetic aortic valve within a previously implanted transcatheter bioprosthesis. This term is proposed to differentiate such procedures from those in which a percutaneous valve is implanted to treat a failed surgical bioprosthesis (valve-in-valve).

TAVI-in-TAV may be required either as bail-out or elective procedure, to deal with structural dysfunction, malpositioning, or embolization of the first implanted transcatheter valve. This strategy, however, has also been employed to treat other unusual conditions, such as the occurrence of a ventricular septal defect immediately after TAVI.⁸ Table 3 summarizes some possible indications for TAVI-in-TAV.

Structural dysfunction of the prosthesis can occur either acute, subacute, or during long-term follow-up. Pasupati et al described a case in which all three leaflets of an Edwards-SAPIEN valve remained immobile after implantation, despite perfect positioning of the valve. Due to acute severe AR, the patient suffered a hemodynamic collapse that was successfully treated with a second Edwards SAPIEN valve implanted in series. The authors attributed the acute structural valve failure to two concurrent mechanisms: poor mobility of prosthesis (frozen) leaflets — which were previously preserved in glutraldehyde — as well as lack of sufficient diastolic pressure gradient to ensure leaflet closure, due to high left ventricular end-diastolic pressure as a result of significant AR after balloon dilatation.⁹ Pagnotta et al reported a subacute (few days) cusp rupture of a CoreValve bioprosthesis probably secondary to minor structural damage of the valve cusp after postdilatation that progressed under continuous shear stress. AR was corrected by means of implantation of a second CoreValve prosthesis.¹⁰ The diagnosis of structural dysfunction of the bioprosthesis may be considered when in  TEE a transvalvular rather than paravalvular aortic regurgitation is recognized.

Long-term durability of transcatheter valves remains to be determined. Transcatheter aortic valves implanted transfemorally need to have a low profile in order to prevent vascular access complications. As a consequence, the valvular tissue shall remain as thin as possible as long as durability of the tissue is not compromised. Especially for the CoreValve prosthesis, the valvular tissue is thinner than in surgically implanted valves. Pathological reports have been encouraging and no difference with respect to pattern of re-endothelization between the two CE-approved devices has been observed so far. It is, however, predictable that transcatheter valves will degenerate over time and the optimal treatment strategy for such cases has not been yet defined. Hammerstingl et al reported on a favorable outcome in a patient suffering from a severely stenosed CoreValve implanted 5.5 years earlier with the implantation of another CoreValve at the same level, stressing however the technical challenges that this procedure may impose.¹¹

Malposition of the implanted prosthesis is a main concern, considering that once implanted, neither of the currently available devices is re-positionable. The reported incidence of valve malpositioning (landing site too low or too high) ranges from 2.6% to 8.1% for the CoreValve and from 2.0% to 5.3% for the Edwards SAPIEN valve.^8,12-15 The learning curve of the operator plays a key role in this setting. Lange et al reported malpositioned valves in 7% of the first 300 cases, followed by only 1.8% in the subsequent 112 cases in a series of 412 TAVI patients, indicating that malpositioning remains  an issue even in experienced hands.¹⁴ In addition to the level of operator’s expertise, causes of malpositioning are related to patient characteristics or to procedural and anatomical characteristics, such as the size of aortic annulus and its ratio to the implanted prosthesis (which should be at least 1.1), the lack of native valve calcification, severe angulation of the aortic arch or unfolding of the ascending aorta, a small size of the left ventricular cavity with a prominent septal bulge, preexistent or sudden-onset of severe AR leading to dynamic movements of the delivery catheter, the use of inadequate angiographic projections during implantation, postdilatation of the implanted valve and errors related to pacemaker, balloon inflation or deflation (for the Edwards valve) or an incomplete release of the prosthesis from the delivery catheter (for the CoreValve). TAVI prostheses implanted too low carry the inherent risk of interference with the atrioventricular conduction system or the mitral valve apparatus. It has been reported that a CoreValve implanted too low in the left ventricle is associated with a greater need for pacemaker implantation and might impinge the anterior mitral valve leaflet. Mobile native aortic leaflets following a too deep implantation of the Edwards SAPIEN valve can  theoretically result in insufficient closure and coaptation of the leaflets of the bioprosthesis and lead to severe AR. Moderate or severe AR may also result from incomplete sealing of the device in a highly calcified annulus, especially in cases with low implantation. Conversely, a too high, supra-annular implantation can result in an impingement of the coronary ostia or embolization of the prosthesis into the ascending aorta. In summary, TAVI prosthesis malposition associated with severe aortic regurgitation is the main indication for implantation of a second valve. The reported incidence of TAVI-in-TAV treating this complication varies from 2.0% to 8.5% in different studies.^8,9,13-21

The occurrence of AR ≥2 after TAVI has shown to be an independent predictor of mortality between 30 days and 2 years.^22,23 Accordingly, postprocedural moderate to severe AR should not be left untreated and TAVI-in-TAV has been described as a valuable therapeutic approach to correct this complication after TAVI. Other measures include postdilatation of the prosthesis in correct position or snaring a malpositioned device implanted too low in the left ventricle. The main mechanisms for relevant paravalvular AR after TAVI are incorrect sizing of the implanted valve (annulus-prosthesis mismatch) and heavy or unevenly distributed valvular calcification. The implantation of a second valve might result in more complete sealing and increase the radial force in a heavily calcified annulus, mitigating a potential recoil effect.^8,14,19,24

Of note, an imprecise or incomplete imaging of the aortic root may lead to improper device selection. In an attempt to overcome such limitations, new diagnostic tools are used to enable detailed anatomic analysis, optimal implantation projections, and deployment simulations. The case of the patient who developed a significant late AR (Case 6) was retrospectively analyzed with the 3mensio Valves imaging software (3mensio Medical Imaging BV), unavailable at the time of valve implantation. It showed an elliptic aortic annulus, not adequately appreciated by conventional CT measurements on which the device selection was based. Despite the adequate matching of the 29 mm implanted prosthesis to the 26 mm annulus measured by CT, the 82 mm perimeter of a fully-expanded 29 mm CoreValve was probably too small to match the 90 mm perimeter of this particularly elliptical annulus (Figure 2), representing an example of incomplete device apposition along the annulus circumference and being responsible for worsening of AR.

One of the concerns regarding TAVI-in-TAV refers to the smaller effective valve area which potentially leads to prosthesis-patient mismatch and perhaps less favorable hemodynamics and less improvement of clinical symptoms after TAVI.²⁵ According to the American Society of Echocardiography guidelines for evaluation of prosthetic heart valves,²⁶ this mismatch is considered to be hemodynamically insignificant if the indexed effective valve area is larger than 0.85 cm2/m2, moderate if 0.65 to 0.85 cm²/m², and severe if smaller than 0.65 cm²/m². Four patients of this series had TAVI-in-TAV after embolization and retrieval of the first implanted valve to the ascending aorta. As a consequence, there was just one prosthesis implanted at the native annular level at the end of the intervention. Accordingly, the mean indexed effective valve area in these patients was 0.97 ± 0.17 cm²/m², resulting in no prosthesis-patient mismatch, and the final mean transvalvular gradients were low, at 6.3 ± 1.6 mm Hg. The remaining two patients had two CoreValves implanted at the annulus level. The final calculated indexed effective valve areas were 0.85 cm²/m² and 0.61 cm²/m², respectively, with a mean residual transvalvular gradient of 10 mm Hg in both cases. Therefore, except for 1 case, significant prosthesis-patient mismatch was not observed after TAVI-in-TAV in this cohort of patients. This observation is in agreement with the findings of Kempfert et al, who demonstrated consistently low immediate residual transvalvular gradients after transapical TAVI-in-TAV in 15 patients.⁸

Last, but not least, the impact of a TAVI-in-TAV on long-term durability of the valve remains to be determined. Albeit not proven, TAVI-in-TAV should theoretically not affect valve durability, as in essence there is just one functional valve. Our results confirm favorable clinical outcome of patients receiving two devices as reported in a prior publication.²⁷ Accordingly, at the latest available follow-up of our patients, no significant increase in transvalvular gradient was observed. The longest period of follow-up after TAVI-in-TAV was reported by Ruiz et al, reporting on no change of transvalvular gradient up to 3 years after a second CoreValve deployment for the treatment of severe AR.²⁸

Conclusion

TAVI-in-TAV is a technically feasible strategy to treat relevant residual aortic regurgitation due to malpositioning or embolization of the first implanted valve and results in hemodynamically and clinically favorable outcome during mid-term follow-up.

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From the ¹Department of Cardiology and ²Cardiovascular Surgery, Swiss Cardiovascular Center Bern, University Hospital Bern, Bern, Switzerland, and ³Centro de Cardiopatias Congênitas e Estruturais do Paraná, Curitiba, Brazil.
Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. Dr Büllesfeld reports paid consultancy with an unspecified company. Dr Khattab reports paid consultancy, honoraria, and participation in a speaker’s bureau for unspecified companies. Dr Huber is a consultant for Medtronic/Edwards Lifesciences. Dr Meier holds a grant from Medtronic/Edwards Lifesciences. Dr Windecker holds a grant from Medtronic and reports honoraria from Medtronic and Edwards Lifesciences. Dr Wenaweser reports proctor fees and honoraria from Medtronic CoreValve and Edwards Lifesciences.
Manuscript submitted March 29, 2012, provisional acceptance given April 17, 2012, final version accepted June 11, 2012.
Address for correspondence: Peter Wenaweser, MD, Professor of Cardiology, Swiss Cardiovascular Center, University Hospital Bern, CH-3010 Bern Switzerland. Email: peter.wenaweser@insel.ch