Author + information
- Received January 16, 2014
- Accepted February 13, 2014
- Published online June 1, 2014.
- Brian R. Lindman, MD, MSCI∗∗ (, )
- William J. Stewart, MD†,
- Philippe Pibarot, DVM, PhD‡,
- Rebecca T. Hahn, MD§,
- Catherine M. Otto, MD‖,
- Ke Xu, PhD¶,
- Richard B. Devereux, MD#,
- Neil J. Weissman, MD∗∗,
- Maurice Enriquez-Sarano, MD††,
- Wilson Y. Szeto, MD‡‡,
- Raj Makkar, MD§§,
- D. Craig Miller, MD‖‖,
- Stamatios Lerakis, MD¶¶,
- Samir Kapadia, MD†,
- Bruce Bowers, MD##,
- Kevin L. Greason, MD††,
- Thomas C. McAndrew, MS¶,
- Yang Lei, MS∗∗∗,
- Martin B. Leon, MD§,¶ and
- Pamela S. Douglas, MD†††
- ∗Washington University School of Medicine, St. Louis, Missouri
- †Cleveland Clinic Foundation, Cleveland, Ohio
- ‡Québec Heart and Lung Institute, Laval University, Québec, Québec, Canada
- §Columbia University Medical Center/New York Presbyterian Hospital, New York, New York
- ‖University of Washington School of Medicine, Seattle, Washington
- ¶Cardiovascular Research Foundation, New York, New York
- #Weill Medical College, Cornell University, New York, New York
- ∗∗Medstar Health Research Institute, Washington, DC
- ††Mayo Clinic, Rochester, Minnesota
- ‡‡University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania
- §§Cedars-Sinai Medical Center, Los Angeles, California
- ‖‖Stanford University School of Medicine, Stanford, California
- ¶¶Emory University School of Medicine, Atlanta, Georgia
- ##Medical City Dallas, Dallas, Texas
- ∗∗∗Saint Luke's Mid-America Heart Institute, Kansas City, Missouri
- †††Duke University Medical Center and Duke Clinical Research Institute, Durham, North Carolina
- ↵∗Reprint requests and correspondence:
Dr. Brian R. Lindman, Washington University School of Medicine, Cardiovascular Division, Campus Box 8086, 660 South Euclid Avenue, St. Louis, Missouri 63110.
Objectives This study sought to examine the relationship between left ventricular mass (LVM) regression and clinical outcomes after transcatheter aortic valve replacement (TAVR).
Background LVM regression after valve replacement for aortic stenosis is assumed to be a favorable effect of LV unloading, but its relationship to improved clinical outcomes is unclear.
Methods Of 2,115 patients with symptomatic aortic stenosis at high surgical risk receiving TAVR in the PARTNER (Placement of Aortic Transcatheter Valves) randomized trial or continued access registry, 690 had both severe LV hypertrophy (left ventricular mass index [LVMi] ≥149 g/m2 men, ≥122 g/m2 women) at baseline and an LVMi measurement at 30-day post-TAVR follow-up. Clinical outcomes were compared for patients with greater than versus lesser than median percentage change in LVMi between baseline and 30 days using Cox proportional hazard models to evaluate event rates from 30 to 365 days.
Results Compared with patients with lesser regression, patients with greater LVMi regression had a similar rate of all-cause mortality (14.1% vs. 14.3%, p = 0.99), but a lower rate of rehospitalization (9.5% vs. 18.5%, hazard ratio [HR]: 0.50, 95% confidence interval [CI]: 0.32 to 0.78; p = 0.002) and a lower rate of rehospitalization specifically for heart failure (7.3% vs. 13.6%, p = 0.01). The association with a lower rate of rehospitalization was consistent across subgroups and remained significant after multivariable adjustment (HR: 0.53, 95% CI: 0.34 to 0.84; p = 0.007). Patients with greater LVMi regression had lower B-type natriuretic peptide (p = 0.002) and a trend toward better quality of life (p = 0.06) at 1-year follow-up than did those with lesser regression.
Conclusions In high-risk patients with severe aortic stenosis and severe LV hypertrophy undergoing TAVR, those with greater early LVM regression had one-half the rate of rehospitalization over the subsequent year compared to those with lesser regression.
- aortic stenosis
- heart failure
- hypertrophic left ventricular remodeling
- transcatheter aortic valve replacement
Left ventricular hypertrophy (LVH), defined by increased left ventricular mass (LVM), is associated with increased mortality and morbidity in a broad spectrum of disorders, including patients with severe calcific aortic stenosis (AS) who are undergoing valve replacement surgery (1–3). LVM regression after valve replacement for AS is presumed to be a favorable effect of LV unloading (4). A number of studies have evaluated the extent and timing of LVM regression after surgical valve replacement, and it is often used as a criterion by which to compare the performance of prosthetic valves (5–9). However, the widely held axiom of a relationship between greater LVM regression and improved clinical outcomes has not been clearly established, and some findings undercut it (10). In addition, these issues have not been studied extensively in patients undergoing transcatheter aortic valve replacement (TAVR).
Accordingly, we examined the clinical outcomes of patients with severe symptomatic AS at high risk for surgery (Cohort A) enrolled in the PARTNER (Placement of Aortic Transcatheter Valves) randomized trial and those in the continued access registry to evaluate whether outcomes varied according to the amount of LVM regression after treatment with TAVR (11). Because the presence of more marked LVH prior to valve replacement portends worse clinical outcomes, we evaluated patients with severe LVH on their baseline pre-procedure echocardiogram.
The design, inclusion and exclusion criteria, and primary results of the high-risk cohort (Cohort A) of the PARTNER randomized clinical trial have been reported (11). The inclusion and exclusion criteria for patients enrolled in the high-risk continued access registry were the same as those enrolled in the Cohort A randomized trial. These patients had severe AS with an aortic valve area <0.8 cm2 (or indexed aortic valve area <0.5 cm2/m2) and either resting or inducible mean gradient >40 mm Hg or peak jet velocity >4 m/s. They were symptomatic from AS (New York Heart Association functional class II or higher) and were at high surgical risk as defined by a predicted risk of death of 15% or higher by 30 days after conventional surgery. After evaluation of vascular anatomy, patients were included in either the transfemoral cohort or transapical cohort, and if enrolled in the trial, randomized to transcatheter therapy with the Edwards Sapien heart valve system (Edwards Lifesciences, Irvine, California) or surgical aortic valve replacement. For this analysis, we included only patients who received treatment with TAVR (the “as treated” population) who also had: 1) severe LVH on the baseline echocardiogram (American Society of Echocardiography sex-specific cutoffs of left ventricular mass index [LVMi] ≥149 g/m2 for men, ≥122 g/m2 for women); and 2) echocardiograms performed at baseline and 30 days post-TAVR with LVMi measured. Clinical characteristics were determined by the enrolling sites. The study protocol was approved by the institutional review board at each enrolling site and all patients provided written informed consent.
An independent core laboratory analyzed all echocardiograms as previously described (12,13). LV mass was calculated using the formula recommended by the American Society of Echocardiography and indexed to body surface area (12,14,15). Relative wall thickness was calculated in 2 ways: [(posterior wall thickness × 2)/LV end-diastolic dimension] and [(posterior wall thickness + septal wall thickness)/LV end-diastolic dimension], in which the septal wall thickness was measured at the basal septal bulge. Stroke volume was calculated as the LV outflow tract area multiplied by the pulsed-wave Doppler LV outflow tract velocity-time integral and indexed to body surface area. Moderate prosthesis-patient mismatch was defined as an effective orifice area index of 0.65 to 0.85 cm2/m2 and severe prosthesis-patient mismatch as an effective orifice area index of <0.65 cm2/m2. The presence and severity of post-procedural aortic regurgitation were determined according to Valve Academic Research Consortium-2 criteria (16). Per protocol, echocardiograms were obtained at baseline (within 45 days of TAVR), and post-TAVR at discharge (or 7 days), 30 days, 6 months, and 1 year (12).
Clinical events including all-cause death, cardiac death, repeat hospitalizations, stroke, renal failure, major bleeding, and myocardial infarction; vascular complications were adjudicated by a clinical events committee (11). Repeat hospitalizations were defined as hospitalization for complications from TAVR (e.g., renal failure, infection) or symptoms of heart failure, angina, or syncope due to aortic valve disease requiring aortic valve intervention or intensified medical management. Stroke was defined as a focal neurologic deficit lasting ≥24 h or a focal neurologic deficit lasting <24 h with imaging findings of acute infarction or hemorrhage. Renal failure events were defined as the need for dialysis of any sort. The Kansas City Cardiomyopathy Questionnaire, a heart failure disease-specific health status measure, was used to assess health status (17,18).
The effect of LVMi regression was evaluated by comparing patients with severe LVH at baseline with greater versus lesser decrease in LVMi between baseline and 30 days post-TAVR. The groups were determined based on the median percentage decrease for each sex, so that women with greater than the median sex-specific percentage decrease in LVMi were combined with the men with greater than the median sex-specific percentage decrease in LVMi into a combined greater LVMi regression group. Continuous variables were summarized as mean ± SD or medians and quartiles and were compared using the Student t-test or Mann-Whitney rank sum test as appropriate. Categorical variables were compared with the chi-square or Fisher exact test. Changes in LVMi over time were evaluated by an overall F test to examine trends, and a paired t test was used to compare individual time points. A Student 2-sample t test was used to compare changes in LVMi between groups. Receiver-operating characteristic analysis was performed using Youden index criterion to determine the optimal cutpoint for percentage of LVMi regression for predicting repeat hospitalizations. Survival curves for time-to-event variables, based on all available follow-up data, were performed with the use of Kaplan-Meier estimates and were compared between groups with the use of the log-rank test. Cox proportional hazards models were used to calculate hazard ratios and to test for interactions. Stepwise Cox models (entry/stay criteria 0.10/0.10) evaluated the relationship between greater versus lesser LVMi regression (from baseline to 30 days) and repeat hospitalizations (from 30 days to 1 year) after adjustment for clinical and echocardiographic variables that had a univariable association (p ≤ 0.10) with repeat hospitalizations. Linear regression models evaluated clinical and echocardiographic predictors of percentage of change in LVMi from baseline to 30 days. The Kansas City Cardiomyopathy Questionnaire's overall summary scores were compared using analysis of covariance to adjust for baseline differences in the questionnaire's scores between groups. All statistical analyses were performed with SAS software (version 9.2, SAS Institute, Cary, North Carolina).
Among the 2,115 patients with symptomatic AS at high surgical risk receiving TAVR in the PARTNER randomized trial or continued access registry, 1,852 (48% women) had LVMi measured at baseline and 887 (40% of men and 57% of women with LVMi measured at baseline) had severe LVH (Fig. 1). Of those with severe LVH at baseline, 690 patients (n = 137 randomized; n = 553 registry) also had LVMi measured on the echocardiogram obtained 30 days after TAVR, which formed the population for this study; 197 patients did not have LVMi measured 30 days after TAVR for the following reasons: death (n = 45); no echocardiogram obtained (n = 85); or LVMi was not measured due to poor image quality (n = 67). A transfemoral approach was used in 55% of patients, and the remainder were treated via a transapical approach. The study population had a mean age of 85 ± 7 years, aortic valve area of 0.65 ± 0.20 cm2, Society of Thoracic Surgeons score of 11.0 (interquartile range: 9.7, 13.0), and 56% were women.
Regression of LVMi
Among patients with severe LVH at baseline who survived 1 year after TAVR, LVMi decreased from 166 ± 31 g/m2 (baseline) to 137 ± 35 g/m2 (1 year) (p < 0.001) (Fig. 2A). LVMi regression over the first year post-TAVR occurred in both men and women (p < 0.001 for each) with a similar pattern of incremental regression, but the overall percentage of LVMi regression was greater among women (p = 0.004). Over one-half of the LVMi regression observed in this population occurred by 30 days (Fig. 2A). Compared with those with lesser LVMi regression at 30 days, those with greater LVMi regression had a higher baseline LVMi, but lower LVMi at 30 days, 6 months, and 1 year (p < 0.05 for each comparison) (Fig. 2B). Those with greater LVMi regression at 30 days had no change in LVMi during the remainder of the year (p = 0.22), whereas those with lesser LVMi regression at 30 days had significant regression during the remainder of the year (p < 0.001) (Fig. 2B).
Patients with greater early LVMi regression had lower baseline prevalences of obesity (p = 0.05) and permanent pacemaker implantation (p = 0.01) than did those with lesser regression (Table 1). Baseline echocardiographic variables were also significantly different between groups (Table 2). In the greater LVMi regression group, there was greater midwall fractional shortening (p < 0.001), a thicker posterior wall (p = 0.02) resulting in greater relative wall thickness by the posterior wall thickness calculation (p = 0.04), and a strong trend toward a higher mean transvalvular gradient (p = 0.057). There was no baseline difference in LV dimensions, ejection fraction, or stroke volume index. Following TAVR, the greater LVMi regression group had smaller LV dimensions (p < 0.01), wall thickness (p < 0.001), and relative wall thickness (p < 0.01). There was also significantly less moderate or severe prosthesis-patient mismatch in the greater LVMi regression group (p = 0.04). Greater early LVMi regression was associated with increased relative wall thickness at baseline, but decreased relative wall thickness on the 30-day post-TAVR echocardiogram, suggesting that the mass regression resulted from a relatively greater decrease in wall thickness than from a decrease in LV cavity dimension. In multivariable analysis including clinical and echocardiographic variables (at baseline and 30 days post-TAVR), female sex, absence of a pacemaker, higher LVMi, greater midwall fractional shortening at baseline, and lower transvalvular mean gradient 30 days post-TAVR were independently associated with greater early LVMi regression (Table 3).
Compared with patients with lesser regression, patients with greater LVMi regression 30 days after TAVR had a similar rate of all-cause mortality between 30 days and 1 year (14.1% vs. 14.3%, p = 0.99), but a lower rate of rehospitalization (9.5% vs. 18.5%, hazard ratio [HR]: 0.50; 95% confidence interval [CI]: 0.32 to 0.78; p = 0.002) and the composite endpoint of death or rehospitalization (19.4% vs. 27.1%, HR: 0.70, 95% CI: 0.51 to 0.97; p = 0.03) (Table 4, Fig. 3). In particular, greater early LVMi regression was associated with a lower rate of repeat hospitalizations for heart failure (7.3% vs. 13.6%, HR: 0.53, 95% CI 0.32 to 0.88, p = 0.01), which was the most common reason for repeat hospitalization in these patients (Table 4, Fig. 3C). The strong association of greater early LVMi regression with a lower rate of repeat hospitalizations was consistent across several subgroups with no significant interactions (Table 5) and remained essentially unchanged after extensive multivariable adjustment for clinical and echocardiographic factors associated with repeat hospitalizations (Table 6, Online Table 1). Receiver-operating characteristic analysis demonstrated that an early LVMi regression of 10% was the optimal cutoff for predicting repeat hospitalizations (area under the curve: 0.60, 95% CI: 0.53 to 0.66). Greater early LVMi regression was also associated with a lower rate of repeat hospitalization between 30 days and 1 year when we evaluated patients with moderate or severe baseline LVH (11.5% vs. 18.4%, HR: 0.62, 95% CI: 0.43 to 0.88, p = 0.007) or patients with any degree of baseline LVH (12.6% vs. 16.8%, HR: 0.75, 95% CI: 0.55 to 1.03; p = 0.07) (Online Tables 2 and 3).
B-type natriuretic peptide, quality of life, and functional status
Although similar at baseline, B-type natriuretic peptide levels were lower at 1 year in patients with greater early LVMi regression than in those with lesser regression (p = 0.002) (Table 7). New York Heart Association functional class was similar between the groups as was the ability to perform a 6-minute walk and the distance walked. After adjustment for baseline differences, there was a trend toward better quality of life at 1 year in patients with greater, compared with lesser, early regression of severe LVH (p = 0.06) (Table 7).
We found that among patients with severe symptomatic AS at high surgical risk, approximately one-half of the population had severe LVH at baseline (40% of the men and 57% of the women), and that those with greater LVMi regression 30 days after TAVR had one-half the rate of repeat hospitalizations from 30 days to 1 year. This was primarily due to a significant decrease in repeat hospitalizations due to heart failure. This association of greater early LVMi regression with fewer hospitalizations was consistent across subgroups and remained significant after adjustment for clinical and echocardiographic factors associated with repeat hospitalizations. Whereas previous studies have either been inconclusive or have undercut the existing dogma, these findings support the assumption that LVH regression after valve replacement for AS is associated with a clinical benefit.
There are several novel aspects to our evaluation of LVMi regression after valve replacement in comparison to previous studies. We looked at a large number of patients, all of whom were enrolled in a multicenter clinical trial and were treated with TAVR instead of surgical AVR. Echocardiograms were performed at pre-specified consistent intervals for all patients before TAVR (baseline study) and during follow-up, and were all analyzed in a uniform manner by a core laboratory. Given the large number of patients, we were able to focus our analysis on those with severe LVH in whom the issues of LVMi regression after AVR would presumably be most important. We also had systematic echocardiographic follow-up at 30 days and were, therefore, able to evaluate the impact of early LVMi regression. Finally, a particular strength was our use of adjudicated clinical events, specifically hospitalizations, in all patients, whereas previous similar studies have been limited to mortality as the only outcome (10).
Regression of LVH after valve replacement for AS and its clinical implications
LV hypertrophy commonly occurs in patients with chronic LV pressure overload from severe AS. It regresses over months to years after valve replacement (6–8), and some studies have shown that significant LVM regression occurs even earlier (19,20). We showed that in patients with severe LVH treated with TAVR, more than 50% of the 1-year LVMi regression occurred by 30 days. This pattern was consistent for men and women and highlights the remarkable plasticity of the heart, even in this elderly cohort with many comorbidities (21). It was also interesting that those with greater LVMi regression at 30 days did not regress further over the remainder of the year. In contrast, those who had less or no LVMi regression by 30 days experienced LVMi regression between 30 days and 1 year, although they failed to achieve an equivalent degree of regression over the year. LVM is a function of chamber dimensions and wall thickness. We observed that whereas those with more early regression had smaller LV chamber dimensions and thinner walls at 30 days, the relative wall thickness measurements at baseline and 30 days indicate that there was a greater reduction in the muscle (wall thickness) than in the LV chamber dimensions in those patients. After adjusting for baseline LVMi, clinical and echocardiographic variables associated with greater early LVMi regression included female sex, absence of a pacemaker pre-operatively, increased pre-operative midwall fractional shortening, and lower transvalvular mean gradient at 30 days.
Many studies have evaluated LVMi regression after AVR, using it as a surrogate endpoint to compare different valve prostheses; this attests to the widespread assumption that LVMi regression after AVR is a clinically beneficial effect of valve replacement (4,5,9). A few studies suggest clinical benefit from greater post-operative LVMi regression, but significant methodological flaws or small sample size led to inconclusive findings (22,23). In contrast, some studies have reported that greater LVMi regression after AVR is not associated with improved outcome, thus questioning the prevailing dogma (10). For hypertensive patients with LVH, regression of LVH with antihypertensive medical therapy has been associated with improved clinical outcomes (24,25). However, such an association has not previously been demonstrated for patients with AS experiencing LVM regression after valve replacement. As such, our finding that greater early LVMi regression is associated with one-half the rate of repeat hospitalization during the first year after TAVR provides a novel and important insight into the connection between regression of LVH and clinical outcomes after valve replacement for AS.
Potential mechanisms for the relationship between LVMi regression and hospitalizations
Greater LVMi regression was associated with a lower rate of repeat hospitalization, and the majority of these hospitalizations were related to heart failure. B-type natriuretic peptide levels were lower at 180 and 365 days in patients who had greater early LVMi regression, which is consistent with improved LV function and less heart failure in these patients. We hypothesize that more mass regression might have caused improved diastolic function (26,27), but assessment of diastolic function was not included in the core laboratory echocardiographic measurements (12). Related to this, we speculate that more early LVMi regression might result from less myocardial fibrosis, as suggested by greater midwall fractional shortening at baseline in these patients. LV fibrosis has been associated with impaired systolic function in patients with AS and associated with increased mortality and less symptomatic improvement and LV functional recovery after AVR (28,29).
The event rates for repeat hospitalizations between patients with greater versus lesser early LVMi regression continued to separate during the entire period from 30 days to 1 year (Fig. 1B), suggesting that greater early LVMi regression is associated with ongoing and accumulating clinical benefits. Whether early (30 days) versus intermediate (6 months) LVMi regression has differential associations with clinical outcomes requires further study. Despite the association between greater LVM regression and fewer hospitalizations, there was no association with cardiac or all-cause mortality. This may be because a 1-year follow-up time frame is too short to detect differences in mortality, but further studies with longer term follow-up are needed to evaluate this relationship.
Repeat hospitalizations are a major contributor to healthcare costs and a particular focus of efforts to reduce spending. Our findings demonstrate that greater LVMi regression after valve replacement has important clinical and economic implications. Because of its favorable impact on clinical outcomes, we need to better understand what predicts LVMi regression as well as what may augment it. Our findings suggest that LVMi regression after valve replacement may be a therapeutic target and provide a rationale for identifying adjunctive medical therapy that, in addition to valvular unloading, could accentuate LVMi regression after valve replacement. It is also important to note that in addition to decreasing repeat hospitalizations, greater early LVMi regression was associated with a trend toward improved quality of life at 1 year, an important patient-centered metric of the clinical benefit of TAVR. To our knowledge, this is also the first analysis that specifically evaluates clinical and echocardiographic factors associated with repeat hospitalizations after TAVR and offers insights into other potentially modifiable factors.
Echocardiography is not as accurate for assessment of LVM as magnetic resonance imaging, but magnetic resonance imaging is much more expensive and was not available in this randomized clinical trial. There may be minor problems with the accuracy of some of the echocardiographic measurements due to image quality or distortions in LV geometry, and evaluating the change in LVM may have a wider range of error than evaluating a single measurement does. However, these inaccuracies should affect all patients in the study, and all echocardiographic measurements were made by a core laboratory (12). Our findings apply to elderly patients at high surgical risk treated with TAVR; however, they may not apply to younger lower risk patients, those without severe LVH at baseline, or those treated with surgical valve replacement. Selection bias may also have influenced our results insofar as patients that did not survive 30 days or patients with poor image quality, which precluded measurement of LVMi, were not included in our analysis. Finally, the follow-up time was limited to 1 year because events were not adjudicated beyond this point, which may explain the lack of a relationship between LVMi regression and mortality.
In high-risk patients with severe LVH undergoing TAVR, those with greater early LVMi regression had one-half the rate of repeat hospitalizations, principally for heart failure, over the first post-procedure year. This association was consistent across subgroups and remained significant after multivariable adjustment. These findings support the dogma that LVMi regression after valve replacement is associated with clinical benefits, which had previously lacked supporting evidence. The strong association between LVMi regression and reduced hospitalizations has important economic and clinical implications. Further study is needed to elucidate factors associated with LVMi regression and to identify adjunctive medical therapies and other interventions that may optimize regression of LVH after valve replacement.
The authors thank Maria Alu for her contribution in the preparation of the manuscript.
For supplemental tables, please see the online version of this paper.
The PARTNER trial was funded by Edwards Lifesciences and the protocol was designed collaboratively by the Sponsor and the Steering Committee. The present analysis was carried out by academic investigators through the PARTNER Publications Office with no direct involvement of the sponsor in the analysis, the drafting of the manuscript, or the decision to publish. Dr. Lindman is supported by grant #K23 HL116660 and the Washington University Institute of Clinical and Translational Sciences grant (#UL1 TR000448, #KL2 TR000450) from the National Center for Advancing Translational Sciences of the National Institutes of Health. Dr. Miller is supported by grant #HL67025 from the National Heart, Lung, and Blood Institute, National Institutes of Health. Dr. Lindman is a site coinvestigator for the PARTNER Trial; consults for Gerson Lehrman Group Research; has received assay support from BG-Medicine and assay and research support from Roche Diagnostics. Dr. Pibarot has received an unrestricted research grant from Edwards Lifesciences. Dr. Hahn consults for Edwards Lifesciences; and has received grant support from Philips Healthcare. Dr. Devereux has received honoraria for training courses from Edwards Lifesciences; serves as a consultant for Merck; and serves on an advisory board of GE Medical. Dr. Weissman has received grant support from Edwards Lifesciences, Boston Scientific, Abbott, St. Jude Medical, Medtronic, Direct Flow, MitralAlign, and Sorin. Dr. Enriquez-Sarano has received grant support from Abbott Vascular; and consulting fees/honoraria from Valtech. Dr. Szeto is an investigator with the PARTNER trial; and has received consulting fees/honoraria from MicroInterventional Devices. Dr. Makkar has received grant support from Edwards Lifesciences and St. Jude Medical; is a consultant for Abbott Vascular, Cordis, and Medtronic; and holds equity in Entourage Medical. Dr. Miller has received travel reimbursements from Edwards Lifesciences related to his work as an unpaid member of the PARTNER Trial Executive Committee; has received consulting fees/honoraria from Abbott Vascular, St. Jude Medical, and Medtronic; and serves on the GenTAC Scientific Advisory Oversight Board. Dr. Lerakis has received consulting fees from Edwards Lifesciences. Dr. Bowers has received consulting fees/honoraria from Daiichi Sankyo/Eli Lilly and Edwards Lifesciences. Dr. Leon has received travel reimbursements from Edwards Lifesciences related to his activities as an unpaid member of the PARTNER Trial Executive Committee. Dr. Douglas has received institutional research support from Edwards Lifesciences. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Abbreviations and Acronyms
- aortic stenosis
- confidence interval
- hazard ratio
- left ventricular hypertrophy
- left ventricular mass
- left ventricular mass index
- transcatheter aortic valve replacement
- Received January 16, 2014.
- Accepted February 13, 2014.
- American College of Cardiology Foundation
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