Author + information
- Received February 5, 2018
- Revision received March 14, 2018
- Accepted March 26, 2018
- Published online July 16, 2018.
- Gilbert H.L. Tang, MD, MSc, MBAa,∗∗ (, )
- Syed Zaid, MDb,∗,
- Isaac George, MDc,
- Omar K. Khalique, MDc,
- Yigal Abramowitz, MDd,
- Yoshio Maeno, MDd,
- Raj R. Makkar, MDd,
- Hasan Jilaihawi, MDe,
- Norihiko Kamioka, MDf,
- Vinod H. Thourani, MDg,
- Vasilis Babaliaros, MDf,
- John G. Webb, MDh,
- Nay M. Htun, MDh,
- Adrian Attinger-Toller, MDh,
- Hasan Ahmad, MDb,
- Ryan Kaple, MDb,
- Kapil Sharma, MDi,
- Joseph A. Kozina, MDi,
- Tsuyoshi Kaneko, MDj,
- Pinak Shah, MDj,
- Sameer A. Hirji, MDj,
- Nimesh D. Desai, MDk,
- Saif Anwaruddin, MDk,
- Dinesh Jagasia, MDk,
- Howard C. Herrmann, MDk,
- Sukhdeep S. Basra, MDl,
- Molly A. Szerlip, MDl,
- Michael J. Mack, MDl,
- Moses Mathur, MDm,
- Christina W. Tan, MDm,
- Creighton W. Don, MDm,
- Rahul Sharma, MDn,
- Sameer Gafoor, MDn,
- Ming Zhang, MDn,
- Samir R. Kapadia, MDo,
- Stephanie L. Mick, MDo,
- Amar Krishnaswamy, MDo,
- Nicholas Amoroso, MDe,
- Arash Salemi, MDp,
- S. Chiu Wong, MDp,
- Annapoorna S. Kini, MDa,
- Josep Rodés-Cabau, MDq,
- Martin B. Leon, MDc and
- Susheel K. Kodali, MDc
- aMount Sinai Medical Center, New York, New York
- bWestchester Medical Center, Valhalla, New York
- cColumbia University Medical Center, New York, New York
- dCedars-Sinai Medical Center, Los Angeles, California
- eNew York University Langone Medical Center, New York, New York
- fEmory University School of Medicine, Atlanta, Georgia
- gMedstar Washington Hospital Center, Washington, District of Columbia
- hSt. Paul’s Hospital, Vancouver, British Columbia, Canada
- iMercy General Hospital, Sacramento, California
- jBrigham and Women’s Hospital, Boston, Massachusetts
- kHospitals of the University of Pennsylvania System, Philadelphia, Pennsylvania
- lBaylor, Scott and White Health System, Plano, Texas
- mUniversity of Washington Medical Center, Seattle, Washington
- nSwedish Medical Center, Seattle, Washington
- oCleveland Clinic, Cleveland, Ohio
- pWeill Cornell Medical Center, New York, New York
- qLaval Heart and Lung Institute, Laval, Quebec, Canada
- ↵∗Address for correspondence:
Dr. Gilbert H. L. Tang, Mount Sinai Health System, Icahn School of Medicine at Mount Sinai, 1190 Fifth Avenue, GP2W, Box 1028, New York, New York 10029.
Objectives The aim of this study was to determine factors affecting paravalvular leak (PVL) in transcatheter aortic valve replacement (TAVR) with the Edwards SAPIEN 3 (S3) valve in extremely large annuli.
Background The largest recommended annular area for the 29-mm S3 is 683 mm2. However, experience with S3 TAVR in annuli >683 mm2 has not been widely reported.
Methods From December 2013 to July 2017, 74 patients across 16 centers with mean area 721 ± 38 mm2 (range: 684 to 852 mm2) underwent S3 TAVR. The transfemoral approach was used in 95%, and 39% were under conscious sedation. Patient, anatomic, and procedural characteristics were retrospectively analyzed. Valve Academic Research Consortium–2 outcomes were reported.
Results Procedural success was 100%, with 2 deaths, 1 stroke, and 2 major vascular complications at 30 days. Post-dilatation occurred in 32%, with final balloon overfilling (1 to 5 ml extra) in 70% of patients. Implantation depth averaged 22.3 ± 12.4% at the noncoronary cusp and 20.7 ± 9.9% at the left coronary cusp. New left bundle branch block occurred in 17%, and 6.3% required new permanent pacemakers. Thirty-day echocardiography showed mild PVL in 22.3%, 6.9% moderate, and none severe. There was no annular rupture or coronary obstruction. Mild or greater PVL was associated with larger maximum annular and left ventricular outflow tract (LVOT) diameters, larger LVOT area and perimeter, LVOT area greater than annular area, and higher annular eccentricity.
Conclusions TAVR with the 29-mm S3 valve beyond the recommended range by overexpansion is safe, with acceptable PVL and pacemaker rates. Larger LVOTs and more eccentric annuli were associated with more PVL. Longer term follow-up will be needed to determine durability of S3 TAVR in this population.
Transcatheter aortic valve replacement (TAVR) has become the preferred treatment of symptomatic severe aortic stenosis in patients who are at high or prohibitive risk for surgery (1–6). TAVR is also recently approved in intermediate-risk patients, and randomized trials comparing surgical aortic valve replacement with TAVR in low-risk patients have recently completed enrollment (7,8). The manufacturer-recommended maximum annular area for the 29-mm Edwards SAPIEN 3 (S3, Edwards Lifesciences, Irvine, California) is 683 mm2 (perimeter 92.6 mm) (9). S3 TAVR in extremely large annuli has been previously reported in small case series (10,11), but larger experience has not been described. The aim of our study was to report a multicenter experience of TAVR with the 29-mm S3 valve in annuli >683 mm2 and identify factors associated with paravalvular leak (PVL) in this population.
From December 2013 to July 2017, 74 patients with intermediate or greater surgical risk across 16 centers in North America underwent commercial S3 TAVR for symptomatic severe aortic stenosis. All patients had annular area >683 mm2 (mean 721 ± 38 mm2; range: 684 to 852 mm2). Patient data were prospectively collected in the American College of Cardiology/Society of Thoracic Surgeons U.S. TVT (Transcatheter Valve Therapy) registry and retrospectively analyzed. Our study was approved by each site’s Institutional Review Board, and the requirement to obtain patient consent was waived.
All patients underwent transthoracic echocardiography (TTE), and aortic root dimensions were determined at end-systole using multidetector computed tomography in 68, transesophageal echocardiography in 4 patients and cardiac magnetic resonance imaging in 2 patients. Locations and the severity of annular, left ventricular outflow tract (LVOT), and leaflet calcifications were evaluated on a semiquantitative scale (12). S3 prosthesis sizing to the annulus was calculated as: [(prosthesis area/annular area) − 1] × 100%, and sizing to the LVOT was calculated as: [(prosthesis area/LVOT area) − 1] × 100%. Annular and LVOT eccentricities were defined as: [1 − (minimum diameter/maximum diameter)] × 100%. The LVOT was measured at 5 mm below the annulus, which was within the seal zone of an optimally implanted 29-mm S3 valve.
S3 implantation technique and follow-up
S3 TAVR was performed using standard technique, under conscious sedation with TTE or general anesthesia with transesophageal echocardiographic monitoring. In brief, balloon aortic valvuloplasty using the recommended Edwards balloon was performed at the discretion of the operator. Valve balloon volume for S3 deployment was based on the degree of undersizing and the presence and severity of annular and LVOT calcification. Valve positioning was based on the top of the S3 frame relative to the sinotubular junction and the position of the bottom of center balloon marker. The severity of intraprocedural PVL and transvalvular aortic regurgitation (AR) were determined by a combination of TTE or transesophageal echocardiography using the Valve Academic Research Consortium–2 criteria (13), invasive hemodynamic assessment, and aortography. Balloon post-dilatation was performed at the operator’s discretion, generally if the PVL was mild or greater identified by at least 2 of the aforementioned 3 methods, with consideration of anatomic risk factors for annular injury. Implantation depth was analyzed by off-line evaluation of the pre- and post-implantation aortography using a previously described technique (14). Procedural success was defined as device success (13), no aortic root complications (e.g., coronary obstruction, annular injury), valve migration or embolization, severe PVL or transvalvular AR, and need for a second prosthesis. Pre-discharge TTE was performed in all patients. Thirty-day follow-up was 100% complete, with 2 deaths before 30 days. Mean follow-up was 7.6 ± 7.0 months (range 0.1 to 37.9 months) and 100% complete. Outcomes were reported using the Valve Academic Research Consortium–2 and U.S. TVT registry definitions.
Clinical, anatomic, and procedural characteristics of patients with overall mild or greater PVL on TTE were compared with those with none or trace PVL. Continuous variables are reported as mean ± SD, while categorical variables are reported as proportions. Differences were detected using the independent Student's t-test for normally distributed continuous variables, Wilcoxon rank sum test for nonparametric variables, and chi-square or Fisher exact test for categorical variables, depending on sample size. Univariate predictors of mild or greater PVL were identified. Because of the small sample size and low event rate, a multivariate analysis could not be performed. All statistical tests were 2 tailed, with p values <0.05 considered to indicate statistical significance. Statistical analyses were performed using SAS version 9.3 (SAS Institute, Cary, North Carolina).
Patient characteristics are listed in Table 1. The mean age was 77 ± 10 years, and 4.1% were women. Society of Thoracic Surgeons predicted risk for mortality averaged 5.5 ± 3.5%. Eleven patients (14.9%) had bicuspid aortic valves, and 22 (29.7%) had left ventricular ejection fractions <35%. There were no baseline clinical differences between the none or trace and mild or moderate PVL groups.
Anatomic and calcification characteristics between patients with none or trace and mild or moderate PVL are shown in Table 2. The largest annular and LVOT areas in our cohort were 852 and 1,043 mm2, with corresponding perimeters of 105 and 115 mm, respectively. Distribution of annular and LVOT areas and perimeters are depicted in Figure 1. There were no significant differences in annular area and perimeter between the PVL groups (Figure 2A). However, the mild or moderate PVL group had greater mean LVOT area (775.7 ± 110.9 mm2 vs. 725.9 ± 83.6 mm2; p = 0.043) (Figure 2A) and LVOT perimeter (100.7 ± 7.1 mm vs. 97.2 ± 5.7 mm; p = 0.033) (Figure 2B) than the none or trace PVL group. Almost half (45.8%) of all patients had annular area greater than LVOT area. Compared with patients with annular area greater than LVOT area, those with annular area smaller than LVOT area had a higher incidence of mild or moderate PVL (38.5% vs. 15.2%; p = 0.036) (Figure 3).
Maximal diameters averaged 33.6 ± 1.6 mm (range: 31.1 to 38.7 mm) at the annulus and 34.7 ± 2.7 mm (range 30.4 to 43.2 mm) at the LVOT. The mild or moderate PVL group had larger maximal diameters at the annulus (34.2 ± 2.0 mm vs. 33.3 ± 1.3 mm; p = 0.029) and LVOT (35.8 ± 2.8 mm vs. 34.2 ± 2.5 mm; p = 0.020) (Figure 2C). Patients in the mild or moderate PVL group also had higher annular eccentricity (20.6 ± 7.0% vs. 17.1 ± 6.2%; p = 0.038) (Figure 2D), but there were no differences in LVOT eccentricity (19.8 ± 9.1% vs. 18.2 ± 8.0%; p = 0.49). No differences in S3 sizing by area to the annulus (−10.9 ± 6.0% vs. −9.2 ± 3.3%; p = 0.13) and the LVOT (−14.7 ± 12.2% vs. −9.5 ± 10.1%; p = 0.07) were observed (Figure 4). Three-leaflet calcification was noted in 64%, with severe 3-leaflet calcification in 44.6% and moderate to severe calcification at the annulus in 44.6% and the LVOT in 20.3%. No significant differences were found in the location and severity of leaflet, annular, and LVOT calcifications between the 2 PVL groups.
All procedures were successful, with the transfemoral approach in 70, the transapical approach in 2, the transaortic approach in 1, and the subclavian approach in 1 patient (Table 3). Thirty-nine percent of cases were performed under conscious sedation, with no difference between PVL groups. The bottom of the balloon marker was positioned at the annulus in 47.8%, with positioning above the annulus in 32.8% and below in 19.4%. In 57% of cases, the 29-mm S3 valve was overexpanded by adding volume (1 to 5 ml extra) during initial deployment, with nominal filling in the remaining 43%. Post-dilatation occurred in 32% of cases, resulting in 70% of patients’ having balloon overfilling (1 to 5 ml extra), and the remaining 30% had nominal filling. No differences in balloon center marker position, post-dilatation, valve balloon filling, and contrast use were observed between PVL groups. In patients with balloon overfilling, the implantation depth on average, at the noncoronary and left coronary cusps, respectively, was not different from those without balloon overfilling (20.0 ± 11.0% vs. 23.9 ± 7.1% average, 22.4 ± 12.7% vs. 27.7 ± 10.5% noncoronary cusp, 21.7 ± 10.7% vs. 22.6 ± 7.3% left coronary cusp; p = 0.54, p = 0.15, and p = 0.76, respectively).
Immediate intraprocedural echocardiography after valve deployment showed 12 (16.2%) mild and no moderate or severe PVLs, with 3 (4.0%) mild, 4 (5.4%) moderate, and no severe transvalvular AR. Implantation depth averaged 22.3 ± 12.4% (range 5.0% to 60.7%) at the noncoronary cusp and 20.7 ± 9.9% (range 3.1% to 48.4%) at the left coronary cusp. There were no differences in mean S3 implantation depth and depth at the noncoronary and left coronary cusps, respectively, between the PVL groups (Figure 5). There was no annular rupture or coronary obstruction. The Valve Academic Research Consortium–2 device success rate was 70 of 74 (94.6%) after the procedure and 68 of 74 (91.9%) at 30 days, because of moderate PVL or AR. No procedural mortality occurred.
Clinical and echocardiographic outcomes
In-hospital and 30-day outcomes are listed in Table 4. Median intensive care unit stay was 24.0 hours, and total length of stay after TAVR was 3.0 days, with no differences between PVL groups. There was 1 in-hospital death due to cardiogenic shock and multiorgan failure and 2 30-day deaths overall. One stroke and 2 major vascular complications occurred in the entire group. New persistent left bundle branch block occurred in 10 of 60 patients (16.7%) without prior conduction abnormalities and 4 of 63 patients (6.3%) without prior permanent pacemakers (PPMs) required new PPMs. Thirty-day TTE showed 16 (22.3%) mild, 5 (6.9%) moderate, and no severe PVLs and 1 (1.4%) mild, 4 (5.4%) moderate, and no severe transvalvular AR. The incidence of none or trace transvalvular AR was significantly less in the mild or moderate PVL group (80.9% vs. 98.0%, p = 0.031). All surviving patients had New York Heart Association class improvements.
Predictors of mild or moderate PVL
Univariate predictors of mild or moderate PVL are listed in Table 5. Mild or moderate PVL was associated with larger annular and LVOT maximal diameters, larger LVOT area and perimeter, LVOT area greater than annular area, and higher annular eccentricity.
Our study had several notable findings: 1) TAVR with the 29-mm S3 in annuli >683 mm2 is feasible and safe; 2) despite significant undersizing and valve overexpansion, the rate of PVL was acceptable and comparable with those reported in published studies (15–19); 3) transvalvular AR and PPM rates were low; and 4) larger LVOT was associated with more PVL, suggesting its important role when considering implanting the 29-mm S3 in this group.
Undersizing and overexpansion with the earlier generation SAPIEN XT was feasible but had more PVL than the S3 (17). The SAPIEN XT, with its shorter stent frame and shorter leaflets, has the potential limitation of central leaflet malcoaptation from overexpansion causing transvalvular AR. Also, the 29-mm XT balloon is less distensible than the S3 balloon, limiting its ability to overexpand the SAPIEN XT. The S3, with its taller stent frame and taller leaflets with more central coaptation, can potentially better tolerate overexpansion while maintaining sufficient leaflet coaptation to minimize risk for transvalvular AR (10,11). This improvement is due to the design of the stent frame whereby ventricular foreshortening during valve deployment allows further expansion beyond manufacturer recommendations. Shivaraju et al. (10) first reported the addition of 4 ml to enable successful implantation of the S3 in an annular area of 742 mm2 measured in diastole. The investigators recommended that instead of significant oversizing with a larger prosthesis and risking annular injury, undersizing with overexpansion of a smaller prosthesis may be a safer alternative. However, specific data on the 29-mm S3 subgroup were not reported in their study, including the range of annular area that was treated by an overexpanded 29-mm S3. Mathur et al. (11) detailed their 3 successful cases of 29-mm S3 TAVR in annuli 748.1, 793, and 787 mm2, respectively, with an extra 4 ml added to the balloon during deployment. Intraprocedural PVLs were trace, mild, and mild to moderate, respectively, with angiography demonstrating significant ventricular foreshortening in 2 cases (frame heights 17 to 18 mm vs. 22.5 mm, per manufacturer’s specification) with variable inflow flaring.
Annular undersizing in TAVR with the S3, however, has been shown to increase PVL (17–19). Yang et al. (17) found among 61 S3 patients that those with annular undersizing had 27.8% mild or greater PVL. The 1-year mild or greater PVL rate in the PARTNER (Placement of Aortic Transcatheter Valve) 2 S3 high- and extreme-risk cohort was 30.8% (15), while the rate in the intermediate-risk cohort was 40% (16). Blanke et al. (18) reported among 835 intermediate-risk patients in a multicenter, nonrandomized registry that those with <−5% oversized by area had 34% mild or greater PVL. Undersizing was also associated with more PVL and balloon post-dilatation in the PARTNER 2 S3 trial (19). Although only moderate or greater PVL was associated with adverse 1-year outcomes with the S3 (15,16,19), clearly this can be a potential limitation in very large annuli with significant undersizing. Despite our patients having annuli 5% to 24% undersized, it was possible to achieve the same acceptable proportion of mild or greater PVL (29.8%) in this group as in published studies (17–19), although slightly higher rates of moderate PVL and transvalvular AR may be seen. This observation could be due to a greater need for balloon overfilling (70.0%) and post-dilatation (32.4%) to overexpand the S3 valve in order to increase sealing against the LVOT.
Our study identified an association of larger LVOT with mild or greater PVL. To the best of our knowledge, this is the first study that systematically looked at LVOT dimensions and sizing and their impact on PVL in balloon-expandable valves. Specifically, mild or greater PVL was associated with both maximum LVOT diameter and LVOT area (and perimeter), with a higher incidence in patients with LVOT area larger than annular area. We hypothesize that the mechanism of larger LVOT affecting PVL in S3 TAVR in our patient group is due to a reduced LVOT seal zone (Figure 6). Sealing of a transcatheter valve against PVL occurs at the annulus and LVOT level. In patients with extremely large annuli in whom the S3 valve is already undersized beyond the manufacturer’s recommendations, valve overexpansion can further foreshorten and flare the inflow portion to increase sealing at the LVOT. However, greater LVOT dimensions, particularly when larger than the annulus, may reduce the amount of potential sealing available below the annulus. Given that the LVOT is where the S3 sealing cuff is located after deployment, an LVOT larger than the annulus reduces the amount of contact between the S3 sealing cuff, S3 frame, and LVOT, reduces the LVOT seal zone, and increases the possibility of PVL. This hypothesis was supported by our annulus less than LVOT group having overall more mild or greater PVL, despite 3 moderate PVL in the annulus greater than LVOT group (38.5% vs. 15.2%; p = 0.036), which could be due to variance in PVL severity grading across institutions (Figure 3).
In addition, larger maximum annular and LVOT diameters may result in more foreshortening of the long axis of the annular-LVOT region during S3 deployment, reducing the amount of contact with the S3 frame and sealing cuff and risking more PVL. To improve sealing in undersized annuli, placing the balloon center marker more ventricular can help increase the proportion of the S3 frame in the LVOT. Doing so would also leave room for more inflow foreshortening when balloon overfilling is performed, to reduce the risk for valve embolization or insufficient sealing at the LVOT and consequently more PVL. Additional factors including location and severity of aortic root calcification, and stiff wire position may affect S3 frame flaring and foreshortening (Online Figure 1). Post-procedural multidetector computed tomography would further evaluate our hypothesis of LVOT seal zone and association with PVL in S3 TAVR in our study population.
Our study also demonstrated the association of annular eccentricity with PVL. A previous study by Willson et al. (20) did not find annular eccentricity associated with PVL, but it was studied on older generation balloon-expandable valves. We recently reported annular and LVOT eccentricity as predictors of PVL in S3 TAVR (21,22). The mechanism of this observation is unclear but can potentially be due to incomplete circularization of the annulus and LVOT against the S3 frame, reducing the LVOT seal zone in extremely large annulus and LVOT as in our cohort, and increasing PVL. Previous studies have identified annular and LVOT calcification as predictors of PVL in S3 TAVR (23,24). We did not observe such an association, likely because of our small sample size. Our overall PPM rate of 6.3% was lower than those reported in the S3 clinical trials (17–19). This could be due to valve undersizing to the annulus and LVOT in our patients, reducing the contact between the S3 frame and interventricular septum, with lower risk for new conduction abnormalities.
The 34-mm Evolut R XL (Medtronic, Galway, Ireland) is approved for a mean annular diameter up to 30 mm and perimeter up to 94.2 mm and can be an alternative in patients with extremely large annuli. Yet 65 of 74 (88%) of the same patients in our study, when sized to the 34-mm Evolut R, would have been outside the manufacturer’s recommendations (Online Figure 2). As shown in our study, the 29-mm S3 valve is an excellent alternative to a self-expanding prosthesis in these cases.
There were several limitations in our study, the first of which was a small sample size. Given that the incidence of extremely large annuli evaluated for TAVR is relatively low, our multicenter study represents the largest series reported to date using the 29-mm S3 valve. Our small sample size and low event rate also precluded us from performing a multivariate analysis to determine independent predictors of PVL in our group. Annular dimensions were evaluated at each site and not at a core laboratory, so overestimation could be possible. Our series nonetheless represents the largest reported dimensions treated with the 29-mm S3 valve. Intraprocedural, pre-discharge, and 30-day echocardiography were not adjudicated by a core laboratory and were therefore subject to institutional variance. Post-dilatation was left to the discretion of the site operator, and it is conceivable that a more aggressive approach could have led to fewer PVL in our study cohort.
TAVR with the 29-mm S3 valve beyond the manufacturer-recommended range is safe, with acceptable PVL and pacemaker rates. Overexpansion of the S3 frame can be achieved by adding balloon volume before valve deployment or post-dilatation with additional volume. A larger LVOT and a more eccentric annulus, however, were associated with more PVL. Longer term follow-up will be needed to determine the durability of S3 TAVR in this population.
WHAT IS KNOWN? The largest recommended annular area for 29-mm S3 TAVR is 683 mm2. However, experience with S3 TAVR in annuli >683 mm2 has not been widely reported.
WHAT IS NEW? We demonstrated the feasibility of S3 TAVR in annuli >683 mm2 with acceptable PVL and pacemaker rates. LVOT dimensions and annular eccentricity were associated with PVL in this patient group.
WHAT IS NEXT? Longer follow-up will determine valve durability, and post-procedural multidetector computed tomography will help identify potential mechanisms of PVL in patients with extremely large annuli who undergo S3 TAVR.
↵∗ Drs. Tang and Zaid contributed equally to this work.
Dr. Tang is a physician proctor for Edwards Lifesciences and Medtronic. Dr. George is a consultant for Edwards Lifesciences and Medtronic. Dr. Khalique has served on the Speakers Bureau for Edwards Lifesciences and Boston Scientific; and as a reader for a core laboratory that has contracts with Edwards Lifesciences. Dr. Makkar has received grants from Edwards Lifesciences and St. Jude Medical; is a consultant for Abbott Vascular, Cordis, and Medtronic; and holds equity in Entourage Medical. Dr. Jilaihawi has served as a consultant for Edwards Lifesciences and Venus Medtech. Dr. Thourani is a member of the PARTNER Trial Steering Committee and a consultant for Edwards Lifesciences, Sorin Medical, St. Jude Medical, and DirectFlow. Dr. Babaliaros has received grant and research support from Medtronic, Abbott Vascular, and Edwards Lifesciences; and is a consultant for Abbott Vascular and Edwards Lifesciences. Dr. Webb has served as a consultant for Edwards Lifesciences. Dr. Kaneko has served as a proctor and educator for Edwards Lifesciences. Dr. Shah is a proctor and educator for Edwards Lifesciences; and is an educator for St. Jude Medical. Dr. Desai has been an investigator for Medtronic, Edwards Lifesciences, St. Jude Medical, Gore, and Cook Medical and has received speaking fees from Medtronic, Edwards Lifesciences, St. Jude Medical, and Gore. Dr. Anwaruddin serves as a consultant and speaker for Edwards Lifesciences and Medtronic. Dr. Herrmann has received grants from Edwards Lifesciences, St. Jude Medical, Medtronic, Boston Scientific, Abbott Vascular, Gore, Siemens, Cardiokinetix, and Mitraspan; has received consulting fees and honoraria from Edwards Lifesciences and Siemens; and holds equity in Microinterventional Devices. Dr. Szerlip has served as a speaker and proctor for Edwards Lifesciences; as a consultant and speaker for Medtronic; and as a speaker for Abbott Vascular. Dr. Mack is an uncompensated co–principal investigator of COAPT trial (Abbott Vascular); and serves on the Apollo Trial Executive Committee (Medtronic). Dr. Don is an investigator for Edwards Lifesciences; and a consultant to Medtronic. Dr. R. Sharma currently serves as a site subinvestigator for the Edwards EARLY TAVR trial; and in the past, he has served as a site subinvestigator for the Low Risk TAVR trial (Medtronic) and the REFLECT trial (Keystone Heart). Dr. Gafoor is a consultant for Medtronic, Boston Scientific, and Abbott Vascular. Dr. Zhang has served as proctor for Edwards Lifesciences, as a site principal investigator for the REPRISE trial (Boston Scientific), and as a site subinvestigator for the REFLECT trial (Keystone Heart) and TAVR Low Risk trial (Medtronic). Dr. Kapadia is an unpaid co–principal investigator of the SENTINEL trial, sponsored by Claret Medical. Dr. Salemi is a physician proctor for Edwards Lifesciences and Medtronic. Dr. Wong has served on the medical advisory board for Medtronic Vascular. Dr. Rodés-Cabau receives research grant support from Edwards Lifesciences. Dr. Leon has served as a nonpaid member of the scientific advisory board of Edwards Lifesciences; and consultant for Abbott Vascular and Boston Scientific. Dr. Kodali is on the steering committee for Edwards Lifesciences; is a consultant for Medtronic and Claret Medical; and is on the scientific advisory board for Thubrikar Aortic Valve. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Abbreviations and Acronyms
- aortic regurgitation
- left ventricular outflow tract
- permanent pacemaker
- paravalvular leak
- SAPIEN 3
- transcatheter aortic valve replacement
- transthoracic echocardiography
- Received February 5, 2018.
- Revision received March 14, 2018.
- Accepted March 26, 2018.
- 2018 American College of Cardiology Foundation
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