Author + information
- Received February 3, 2015
- Revision received May 5, 2015
- Accepted June 4, 2015
- Published online September 1, 2015.
- Jean-Michel Paradis, MD∗,†∗ (, )
- Hersh S. Maniar, MD‡,
- John M. Lasala, MD‡,
- Susheel Kodali, MD†,§,
- Mathew Williams, MD‖,
- Brian R. Lindman, MD, MSCI‡,
- Ralph J. Damiano Jr., MD‡,
- Marc R. Moon, MD‡,
- Raj R. Makkar, MD¶,
- Vinod H. Thourani, MD#,
- Vasilis Babaliaros, MD#,
- Ke Xu, PhD†,
- Girma Minalu Ayele, PhD†,
- Lars Svensson, MD, PhD∗∗,
- Martin B. Leon, MD†,§ and
- Alan Zajarias, MD‡
- ∗Quebec Heart and Lung Institute, Quebec, Canada
- †Cardiovascular Research Foundation, New York, New York
- ‡Washington University School of Medicine, St Louis, Missouri
- §Columbia University Medical Center, New York, New York
- ‖New York University Langone Medical Center, New York, New York
- ¶Cedars Sinai Heart Institute, Los Angeles, California
- #Emory University School of Medicine, Atlanta, Georgia
- ∗∗Cleveland Clinic Foundation, Cleveland, Ohio
- ↵∗Reprint requests and correspondence:
Dr. Jean-Michel Paradis, Quebec Heart and Lung Institute, 2725 Chemin Sainte-Foy, Quebec, Canada G1V 4G5.
Objectives This study sought to clarify the clinical and echocardiographic prognostic implication of myocardial injury after transcatheter aortic valve replacement (TAVR).
Background The clinical significance of cardiac biomarker elevation after TAVR remains unclear.
Methods Patients treated with TAVR in the PARTNER (Placement of Aortic Transcatheter Valves) trial were divided into tertiles (T1, T2, T3) based on the difference between the values on post-procedure day 1 and the baseline values of 2 cardiac biomarkers: cardiac troponin I (ΔcTnI); and creatine kinase-myocardial band (ΔCK-MB) fraction. Patients were stratified according to their access route: transfemoral (TF) (n = 1,840) or transapical (TA) (n = 1,173).
Results At 30 days after TF-TAVR, patients in the highest tertile (T3) of cardiac biomarker elevation had a higher rate of all-cause mortality (ΔcTnI: T3: 5.4% vs. T1: 0.5%, p = 0.006; ΔCK-MB: T3: 5.7% vs. T1: 0.9%, p = 0.006) and cardiovascular mortality (ΔcTnI: T3: 4.9% vs. T1: 0.5%, p = 0.01; ΔCK-MB: T3: 3.9% vs. T1: 0.5%, p = 0.02). At 1 year, only patients in the highest CK-MB tertile had higher rates of all-cause (25.4% vs. 16.8%, p = 0.02) and cardiovascular (10.3% vs. 5.0%) mortality. Multivariable analysis demonstrated that greater release of cardiac biomarkers was independently associated with increased mortality in the TF population. After TA-TAVR, being in the highest tertile of cardiac biomarker elevation had no influence on clinical and echocardiographic outcomes at 30 days and 1 year.
Conclusions After TF-TAVR, a greater degree of myocardial injury was associated with higher rates of 30-day all-cause and cardiovascular mortality. At 1 year, being in the highest tertile of ΔCK-MB was correlated with a higher rate of all-cause and cardiac mortality. Finally, the level of myocardial injury after TA-TAVR had no impact on clinical and echocardiographic outcomes.
Transcatheter aortic valve replacement (TAVR) has become the standard treatment option for inoperable patients with severe symptomatic aortic stenosis (1,2) and has been shown to be noninferior to surgical AVR in terms of survival among selected high-risk patients (3,4). Recent studies have shown that a transapical (TA) approach to TAVR is associated with some degree of myocardial injury, which is exacerbated by renal dysfunction (5–7).
Myocardial injury after TAVR could be influenced by procedural or patient-specific factors. Myocardial damage following cardiac surgery or percutaneous coronary intervention has been strongly associated with cardiovascular morbidity and mortality (8–10); however, the clinical significance of cardiac biomarker elevation after TAVR remains uncertain. Accordingly, we sought to better characterize the clinical and echocardiographic impact of myocardial damage after transfemoral (TF) and TA TAVR using data from the multicenter PARTNER (Placement of Aortic Transcatheter Valves) trial.
The design and results of the PARTNER trial (cohorts A and B) have been previously published (1–4). Briefly, the randomized portion of the trial enrolled patients with severe symptomatic aortic stenosis who were either at high risk for surgical AVR (cohort A) or deemed inoperable (cohort B). In cohort A, after assessment of vascular anatomy, patients were allocated to a TF or TA placement cohort and randomized to TAVR with the Edwards Sapien heart valve system (Edwards Lifesciences, Irvine, California) or surgical valve replacement. In cohort B, patients were randomized to standard therapy or TAVR via a TF approach if vascular access was adequate. After completion of the randomized trial, the NRCA (Non-Randomized Continued Access) registry allowed treatment of both cohort A and cohort B patients with TAVR. Inclusion and exclusion criteria, data collection, and monitoring were the same in both the randomized trial and the NRCA registry. All patients were presented and adjudicated as appropriate candidates during conference calls with the executive committee and other investigators.
For the current analysis, we included only patients who were randomized to and treated with TAVR in the randomized trial and those treated with TAVR in the NRCA registry (as-treated population) who had cardiac biomarkers—cardiac troponin I (cTnI) and creatinine kinase-myocardial band (CK-MB) fraction—measured at baseline and on the first day after the procedure. Many centers used several different immunoassays for measurements of troponin and CK-MB. In order to have the largest study group possible, but to limit variability and to allow each patient to become his/her own control, we elected to exclude patients with troponin T measurements (because a minority of centers were using this specific immunoassay). The PARTNER study was approved by the institutional review board at each participating site, and all patients provided written informed consent.
Patients were stratified according to their access route (TF or TA). Cardiac biomarkers were measured at baseline and on post-procedure day 1. As biomarker measurements were not performed in a central laboratory, in order to control for the potential differences in reference values, patients in each group were divided into tertiles (T1, T2, T3) based on the difference between the post-procedure day 1 value and the baseline values of each cardiac marker (ΔcTnI and ΔCK-MB).
Study endpoints were reported according to Valve Academic Research Consortium definitions (11) or according to the definitions established in the PARTNER 1 protocol. All adverse events were adjudicated by an independent clinical events committee. Independent core laboratory analysis was performed on all echocardiograms and electrocardiograms. All data were sent for analysis to an independent academic biostatistics group.
Periprocedural myocardial infarction (MI) was defined according to a modified version of the Valve Academic Research Consortium criteria (12) as described in the PARTNER trial protocol (1–4). Any of the following criteria met the definition of MI: 1) acute MI demonstrated by autopsy; 2) emergent percutaneous coronary intervention performed for acute ST-segment elevation myocardial infarction; 3) administration of thrombolytics for acute MI; 4) clinical periprocedural MI (up through 7 complete days post–index procedure) defined as follows:
a. periprocedural Q-wave MI: development of new pathologic Q waves in 2 or more contiguous leads with elevation of CK-MB or CK (in absence of CK-MB data). New Q waves in the absence of symptoms or elevated markers were not considered an MI; and
b. periprocedural non–Q-wave MI: documented signs or symptoms of ischemia and/or new ischemic changes on electrocardiography and CK-MB elevation >10× the upper limit of normal. In the absence of CK-MB data, CK was used with the same >10× the upper limit of normal criteria.
Continuous variables were analyzed via mean ± SD or medians and quartiles, as appropriate, and were compared using Student t test. If data were not normally distributed, the Mann-Whitney U test was used instead. Categorical variables were analyzed with the chi-square test or Fisher exact test where asymptotic validity was not met. For each access route (TF vs. TA), clinical and echocardiographic outcomes were compared across tertiles and between the highest and lowest tertiles (T3 and T1). Kaplan-Meier estimates were used to construct survival curves for time-to-event variables, which were compared using the log-rank test. Statistical significance was defined as a p value <0.05. Univariable analysis and multivariable logistic regression were performed to identify independent predictors of 30-day and 1-year all-cause mortality and cardiovascular mortality, respectively. To avoid overfitting, variables included in the multivariable model were selected only if they were of clinical interest and/or fulfilled the entry criterion of p < 0.1 in the univariable analysis. We also used cubic spline plots to display the estimated cubic spline function relating ΔcTnI and ΔCK-MB to the 30-day and 1-year all-cause mortality for a Cox model (Online Appendix). Data are based on an extract date of March 11, 2014. All statistical analyses were performed with the use of SAS software (version 9.2, SAS Institute, Cary, North Carolina).
The PARTNER trial was funded by Edwards Lifesciences and designed collaboratively by the steering committee and the sponsor. The present analysis was carried out mainly by investigators at the Cardiovascular Research Foundation, Columbia University Medical Center, and Washington University School of Medicine. The authors had unrestricted access to the study data, drafted the manuscript, made the decision to submit for publication, and guarantee the completeness and accuracy of its content.
Patients and baseline characteristics
Among the 3,013 patients enrolled in the as-treated population of the PARTNER trial, 1,840 were treated with TAVR via the TF approach and 1,173 by a TA approach. In the TF population, 557 patients had cTnI measurements at the 2 specified time points. Among these patients, the ΔcTnI had the following distribution: T1 (n = 187), −82.81 to 0.30 ng/ml; T2 (n = 184), 0.31 to 0.88 ng/ml; and T3 (n = 186), 0.89 to 402.38 ng/ml. ΔCK-MB data were available in 632 patients with the following distribution: T1 (n = 211), −80.00 to 0.80 U/l; T2 (n = 212), 0.90 to 2.90 U/l; and T3 (n = 209), 3.00 to 85.90 U/l. In the TA population, ΔcTnI was available in 340 patients: T1 (n = 113), −5.62 to 4.41 ng/ml; T2 (n = 114), 4.42 to 8.09 ng/ml; and T3 (n = 113), 8.10 to 348.87 ng/ml. Also, among the TA population, 416 were included in the ΔCK-MB analysis with the following distribution: T1 (n = 138), −27.00 to 9.40 U/l; T2 (n = 139), 9.41 to 21.60 U/l; and T3 (n = 139), 21.61 to 4,027.00 U/l. Baseline and periprocedural characteristics of patients stratified by approach and further divided by tertiles for each cardiac biomarker are shown in Table 1. Patients in the highest tertiles of both biomarkers were more commonly women and had a lower prevalence of previous coronary artery bypass graft irrespective of approach. The hemodynamic and echocardiographic data are summarized in Table 2.
Clinical and echocardiographic outcomes
When compared with the lowest tertile (T1), patients in the highest tertile (T3) of cardiac biomarker elevation who underwent a TF approach had a higher rate of all-cause mortality (ΔcTnI: T3: 5.4% vs. T1: 0.5%, p = 0.006; ΔCK-MB: T3: 5.7% vs. T1: 0.9%, p = 0.006) and cardiovascular mortality (ΔcTnI: T3: 4.9% vs. T1: 0.5%, p = 0.01; ΔCK-MB: T3: 3.9% vs. T1: 0.5%, p = 0.02) at 30 days (Figure 1A). At 1 year, there was still a significant difference in rates of all-cause mortality (25.4% vs. 16.8%, p = 0.02) and cardiovascular mortality (10.3% vs. 5.0%) between the highest and the lowest CK-MB tertiles (Figure 1B). However, there was no longer a significant association between a larger periprocedural cTnI release and higher 1-year all-cause (ΔcTnI: T3: 23.2% vs. T1: 18.9%, p = 0.22) and cardiovascular (ΔcTnI: T3: 13.0% vs. T1: 7.8%, p = 0.09) mortality. The rates of MI were very low and were similar across tertiles for both markers (ΔcTnI: p = 0.60, ΔCK-MB: p = 0.37) (Table 3).
Functional assessment and echocardiography
At 1 year, the proportion of patients with an improvement of more than 1 class in the New York Heart Association (NYHA) classification system was similar across the tertiles for both cTnI and CK-MB (ΔcTnI: T3: 67.4% vs. T1: 61.1%, p = 0.28; ΔCK-MB: T3: 57.4% vs. T1: 65.2%, p = 0.16). Additionally, no significant differences were noted across the tertiles in the 6-min walk performed at 1 year (ΔcTnI: T3: 216.9 m vs. T1: 224.5 m, p = 0.64; ΔCK-MB: T3: 218.1 m vs. T1: 236.2 m, p = 0.30).
In paired analyses of baseline and 1-year left ventricular ejection fraction (LVEF) measurements, there was a significant improvement in the LVEF at 1 year in T1 and T2 ΔcTnI tertiles (ΔcTnI: T1: 3.10%, p = 0.002; T2: 2.72%, p = 0.006; T3:1.78, p = 0.17) and in each ΔCK-MB tertile (ΔCK-MB: T1:4.41%, p = 0.0001; T2: 2.58%, p = 0.01; T3: 2.35%, p = 0.02). The degree of cTnI or CK-MB elevation was not associated with LVEF change (ΔcTnI: T3:1.78% vs. T1:3.10%, p = 0.31, ΔCK-MB: T3: 2.35% vs. T1: 4.41%, p = 0.15).
There was no significant difference in all-cause or cardiovascular mortality at 30 days or 1 year when comparing patients in the lowest and highest tertiles (Figures 2A and 2B). The incidence of MI at 30 days was similar between the highest and lowest tertiles of both biomarkers (ΔcTnI: T3: 1.8% vs. T1: 0.9%, p = 0.56; ΔCK-MB: T3: 1.5% vs. T1: 0.7%, p = 0.56) (Table 3).
Functional assessment and echocardiography
At 1 year, the fraction of individuals with improvement of the NYHA functional classification by more than 1 class was similar between tertiles of both cardiac biomarkers (ΔcTnI: T3: 79.5% vs. T1: 71.4%, p = 0.25; ΔCK-MB: T3: 72.7% vs. T1: 79.8%, p = 0.26). The 6-min walk distance at 1 year was also similar between T3 and T1 for both biomarkers (ΔcTnI: T3: 214.6 m vs. T1: 245.5 m, p = 0.15; ΔCK-MB: T3: 187.7 m vs. T1: 201.1 m, p = 0.49).
In paired analyses, there was no significant change in LVEF from baseline to 1 year in any tertile of either cardiac biomarker (ΔcTnI: T1: 2.28%, p = 0.06; T2: 1.32%, p = 0.18; T3: -0.37%, p = 0.41; ΔCK-MB: T1: 2.27%, p = 0.09; T2: 1.74%, p = 0.23; T3: -0.03%, p = 0.90) after TA-TAVR at 1 year. The degree of myocardial injury across tertiles (T3 vs. T1) did not influence the change in LVEF 1 year after a TA procedure (ΔcTnI: p = 0.09, ΔCK-MB: p = 0.18).
Multivariable analyses were performed to evaluate the association between a greater release of cardiac biomarkers and increased mortality in the TF population. After adjusting for significant confounders (Table 4), the highest tertile of ΔcTnI and of ΔCK-MB remained independent predictors of 30-day all-cause and cardiovascular mortality. At 1 year, a higher CK-MB elevation (T3 vs. T1) was an independent predictor of all-cause death and of cardiac death. In the multivariable analysis, renal disease requiring dialysis was identified as a predictor of 1 year all-cause mortality, whereas the incidence of major vascular complication was linked to a higher rate of cardiovascular mortality at 12 months.
In patients with elevated surgical risk treated with TAVR in the PARTNER trial and reported in the NRCA registry, post-operative cardiac biomarker elevation was common after the procedure. Higher differences between pre- and post-procedural CK-MB values resulted in an increase in short-term all-cause and cardiac mortality rates in patients undergoing transfemoral TAVR. Also, in the multivariable analysis, the highest tertile of CK-MB persisted as an independent predictor of 1-year all-cause and cardiac mortality. The degree of myocardial injury did not influence the improvement of NYHA class, the performance on the 6-min walk test, or the change in LVEF at 1 year. There was no association of myocardial injury with 30-day or 1-year mortality in patients undergoing TA-TAVR as measured by changes in the cardiac biomarkers.
Larger cardiac biomarker elevation is seen after TA-TAVR due to instrumentation of the LV apex and the surgical repair of the ventriculotomy. A certain degree of myocardial injury is expected during this procedure, resulting in higher CK-MB and cTnI elevation, perhaps masking its prognostic value. Our findings are similar to those reported by Barbash et al. (7) who showed that an increase of cTnI or CK-MB had no prognostic accuracy to predict 30-day mortality among TA patients. In addition, there were no statistically significant differences between tertiles for NYHA functional class improvement, 6-min walk test distance, or LVEF recovery at 1 year after TA-TAVR, minimizing the importance of these laboratory findings.
In the TF subset, cardiac biomarker elevation appears to play a role in predicting mortality. Elevation of cTnI or CKMB after TAVR may be associated to patient or procedural characteristics. Patients with a higher degree of cardiac enzymes elevation were older; more frequently female; had lower body mass index; and lower rates of coronary artery disease, chronic obstructive pulmonary disease, diabetes mellitus, and previous coronary artery bypass graft. Periprocedural biomarker elevation may be due to the presence of lower capillary density and a larger degree of LV hypertrophy in previously unscarred ventricles. Procedural characteristics such as procedural time; episodes of hypotension; duration of rapid ventricular pacing; injury by the guidewire or delivery system; coronary obstruction; or abnormal coronary perfusion due to elevated LV end-diastolic pressure, pre-existing unrevascularized coronary disease, and procedural hypotension are associated with episodes of ventricular ischemia. Yong et al. (13) identified procedural duration as an independent predictor of myocardial injury after TAVR with the Medtronic CoreValve device (Minneapolis, Minnesota). In our analysis with the Edwards Sapien transcatheter heart valve, procedural time was longer in the highest tertiles of ΔcTnI and ΔCK-MB after TF cases only. Longer cases are also associated with procedural complications that may further predispose to myocardial ischemia. Depth of implantation has also been identified as a risk factor for periprocedural myocardial damage in patients undergoing self-expanding TAVR, but this finding may apply to patients undergoing TAVR with a balloon-expanding prosthesis.
Numerous studies have demonstrated that the occurrence of myocardial injury after a cardiac procedure such as cardiac surgery or percutaneous coronary intervention is correlated with worse future cardiovascular outcomes (14,15). Nevertheless, there is a paucity of data on the impact of myocardial injury following TAVR. Following a TF procedure, Buellesfeld et al. (16) and Grube et al. (17) have reported an incidence of 1.5% to 1.8% of CK-MB elevation >2× the upper limit of normal. Using the definition of spontaneous myocardial infarction, Svensson et al. (18) demonstrated that periprocedural MI occurred in 17% of patients who underwent a TA procedure. The study by Rodés-Cabau et al. (5) showed that uncomplicated TAVR was associated with some degree of troponin elevation in 99% of patients. In our study, the presence of biomarker elevation was associated with mortality in the TF patients even in levels that were not considered diagnostic for MI. In these high-risk patients, the extent of comorbidities may suggest a lower threshold of injury required to be considered pathologic. Furthermore, it is possible that the degree of coronary reserve is lower in these patients, which may predispose to procedural myocardial damage.
In another study (5), the TA approach and baseline renal insufficiency were the main predictors of a greater increase in cardiac biomarkers levels. Indeed, cardiac mortality at 9-month follow-up was higher in patients with a larger rise in cardiac troponin level. A greater degree of myocardial injury was linked with a reduced improvement of LVEF. In our study, patients in the highest CK-MB tertile had a significantly higher cardiovascular mortality at 12 months and only patients in the highest tertile of delta troponin did not significantly improve their LVEF after TF-TAVR. On the contrary, all the patients who underwent a TA procedure had no significant modification of their LVEF at 1 year, regardless of the degree of cardiac biomarker elevation.
Renal dysfunction can be interrelated with higher levels of cardiac troponin even in the absence of clinically suspected myocardial ischemia (19). In the study by Carrabba et al. (6), TAVR was systematically associated with myocardial injury, occurring at a greater level in individuals who developed acute kidney injury. However, in our analysis, all tertiles of cTnI, after both TF and TA procedures, were associated with similar rates of 30-day need for dialysis. Nonetheless, in the multivariable analysis, post-procedural renal failure requiring dialysis was still identified as an independent predictor of 1-year all-cause mortality.
The PARTNER trial was performed using first-generation devices (22- and 24-F sheath introducer diameter for the TF approach and 29-F for the TA route) with operators and sites at the beginning of their learning curve. The evolution toward lower profile TAVR devices might affect the level of myocardial damage after TAVR, especially for TA cases. Moreover, different reference values of biomarkers measured created the need to analyze the data in tertiles using each patient as his/her own control. Furthermore, to decrease the variability associated with the use of multiple troponin assays, only patients with available TnI measurements have been included in our analysis. Consequently, the number of patients included was reduced, therefore affecting the power to detect significant differences between tertiles. Also, the delta was calculated only with the 24-h post-procedural value. Because troponin is known to peak around 48 h post-TAVR (5), the calculation used in our analysis might have underestimated the maximal delta in a certain number of patients. To establish the exact location and the precise amount of myocardial injury, cardiac magnetic resonance imaging after TAVR could have been a useful imaging modality. In addition, the small number of clinical adverse events allowed the adjustment for very few covariates, subsequently limiting the multivariable analysis. Finally, other potential, unmeasured confounders may still be present, and this post-hoc secondary analysis of data collected as part of a randomized trial should be considered hypothesis-generating rather than definitive.
Our study, which is the largest published to date on the topic of cardiac biomarker elevation after TAVR, demonstrates that after TF-TAVR, a higher elevation of cTnI is associated with higher frequencies of 30-day all-cause and cardiovascular mortality. A greater rise of CK-MB after TF-TAVR is correlated with increased rates of 30-day and 1-year all-cause and cardiovascular mortality. The degree of myocardial injury after TA-TAVR had no influence on short- and long-term survival. Further studies are needed to elucidate the patient and procedural factors that contribute to greater myocardial injury during TAVR so that steps can be taken to address those that are modifiable.
WHAT IS KNOWN? TAVR has become the standard treatment option for inoperable patients with severe symptomatic aortic stenosis and has been shown to be noninferior to surgical AVR in terms of survival among selected high-risk patients. Recent studies have demonstrated that TAVR is systematically associated with some degree of myocardial injury. The exact clinical significance of cardiac biomarker elevation after TAVR remains uncertain.
WHAT IS NEW? Our study, which is the largest published to date on the topic of cardiac biomarker elevation after TAVR, demonstrates that after TF-TAVR, a higher elevation of cTnI is associated with higher rates of 30-day all-cause and cardiovascular mortality. A greater rise of CK-MB after TF-TAVR is correlated with increased frequencies of 30-day and 1-year all-cause and cardiovascular mortality. The degree of myocardial injury after TA-TAVR had no impact on short- and long-term survival.
WHAT IS NEXT? Further studies will be needed not only to substantiate the influence of cardiac biomarker elevation on outcomes after TAVR, especially with newer generation devices, but also to identify precautionary actions that could reduce the amount of myocardial injury after TAVR.
The PARTNER trial was funded by Edwards Lifesciences and designed collaboratively by the steering committee and the sponsor. Dr. Lasala has consulted for Boston Scientific and Direct Flow Medical; has received speaking fees from Boston Scientific and St. Jude; and has received stock options from Direct Flow Medical. Dr. Kodali has received consulting fees from Edwards Lifesciences; and is a member of the Scientific Advisory Board for Thubrikar Aortic Valve. Dr. Williams has received consulting fees from Edwards Lifesciences. Dr. Lindman was supported by grant no. K23 HL116660 from the National Institutes of Health; receives research support from and serves on the Scientific Advisory Board for Roche Diagnostics; and consults for Gerson Lehrman Group Research. Dr. Damiano consults for AtriCure; and receives speaking fees from Edwards Lifesciences. Dr. Makkar has received grant support from Edwards Lifesciences and St. Jude Medical; consults for Abbott Vascular, Cordis, and Medtronic; and holds equity in Entourage Medical. Dr. Thourani is a member of the PARTNER Trial Steering Committee; and consults for Edwards Lifesciences, Sorin Medical, St. Jude Medical, and DirectFlow. Dr. Babaliaros is an investigator for Edwards Lifesciences and Abbott Vascular; and a consultant for Direct Flow Medical, Edwards Lifesciences, and Abbott Vascular. Dr. Svensson is an unpaid member of the PARTNER Trial Executive Committee; holds equity in Cardiosolutions and ValvXchange; and has intellectual property rights/royalties from Posthorax. Dr. Leon is a nonpaid member of the PARTNER Trial Executive Committee. Dr. Zajarias has received consulting fees from Edwards Lifesciences. All other authors have reported that they have no relationships relevant to the contents of the paper to disclose.
- Abbreviations and Acronyms
- aortic valve replacement
- creatine kinase-myocardial band
- cardiac troponin I
- left ventricle
- left ventricular ejection fraction
- myocardial infarction
- New York Heart Association
- transcatheter aortic valve replacement
- Received February 3, 2015.
- Revision received May 5, 2015.
- Accepted June 4, 2015.
- American College of Cardiology Foundation
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