Author + information
- Received May 18, 2016
- Revision received August 4, 2016
- Accepted August 9, 2016
- Published online November 8, 2016.
- Nicolaj C. Hansson, MDa,∗ (, )
- Erik L. Grove, MD, PhDa,b,
- Henning R. Andersen, MD, DMSca,
- Jonathon Leipsic, MDc,
- Ole N. Mathiassen, MD, PhDa,
- Jesper M. Jensen, MD, PhDa,
- Kaare T. Jensen, MD, PhDa,
- Philipp Blanke, MDc,
- Tina Leetmaa, MDa,
- Mariann Tang, MDd,
- Lars R. Krusell, MDa,
- Kaj E. Klaaborg, MDd,
- Evald H. Christiansen, MD, PhDa,
- Kim Terp, MDd,
- Christian J. Terkelsen, MD, DMSca,
- Steen H. Poulsen, MD, DMSca,
- John Webb, MDc,
- Hans Erik Bøtker, MD, DMSca,b and
- Bjarne L. Nørgaard, MD, PhDa
- aDepartment of Cardiology, Aarhus University Hospital, Aarhus, Denmark
- bInstitute of Clinical Medicine, Faculty of Health, Aarhus University, Aarhus, Denmark
- cDepartment of Medical Imaging and Division of Cardiology, St. Paul’s Hospital, University of British Columbia, Vancouver, British Columbia, Canada
- dDepartment of Cardiothoracic Surgery, Aarhus University Hospital, Aarhus, Denmark
- ↵∗Reprint requests and correspondence:
Dr. Nicolaj C. Hansson, Department of Cardiology, Aarhus University Hospital Skejby, Palle Juul-Jensens Boulevard 99, 8200 Aarhus N, Denmark.
Background There are limited data on the incidence, clinical implications, and predisposing factors of transcatheter heart valve (THV) thrombosis following transcatheter aortic valve replacement (TAVR).
Objectives The authors assessed the incidence, potential predictors, and clinical implications of THV thrombosis as determined by contrast-enhanced multidetector computed tomography (MDCT) after TAVR.
Methods Among 460 consecutive patients who underwent TAVR with the Edwards Sapien XT or Sapien 3 (Edwards Lifesciences, Irvine, California) THV, 405 (88%) underwent MDCT in addition to transthoracic and transesophageal echocardiography 1 to 3 months post-TAVR. MDCT scans were evaluated for hypoattenuated leaflet thickening that indicated THV thrombosis.
Results MDCT verified THV thrombosis in 28 of 405 (7%) patients. A total of 23 patients had subclinical THV thrombosis, whereas 5 (18%) patients experienced clinically overt obstructive THV thrombosis. THV thrombosis risk did not differ among different generations of THVs (8% vs. 6%; p = 0.42). The risk of THV thrombosis in patients who did not receive warfarin was higher compared with patients who received warfarin (10.7% vs. 1.8%; risk ratio [RR]: 6.09; 95% confidence interval [CI]: 1.86 to 19.84). A larger THV was associated with an increased risk of THV thrombosis (p = 0.03). In multivariable analysis, a 29-mm THV (RR: 2.89; 95% CI: 1.44 to 5.80) and no post-TAVR warfarin treatment (RR: 5.46; 95% CI: 1.68 to 17.7) independently predicted THV thrombosis. Treatment with warfarin effectively reverted THV thrombosis and normalized THV function in 85% of patients as documented by follow-up transesophageal echocardiography and MDCT.
Conclusions Incidence of THV thrombosis in this large study was 7%. A larger THV size may predispose to THV thrombosis, whereas treatment with warfarin appears to have a protective effect. Although often subclinical, THV thrombosis may have important clinical implications.
- aortic stenosis
- multidetector computed tomography
- platelet aggregation inhibitors
- transcatheter aortic valve replacement
Transcatheter aortic valve replacement (TAVR) is a well-established treatment of severe aortic stenosis. Because of technical improvements, increased operator experience, and refined pre-procedural imaging, it is an increasingly safe and successful procedure (1,2). However, there is an increasing awareness of prosthesis valve thrombosis after TAVR (3–6). Accordingly, recent reports have demonstrated that conventional post-TAVR transthoracic echocardiography (TTE) follow-up is inferior for the detection of transcatheter heart valve (THV) thrombosis compared with contrast-enhanced multidetector computed tomography (MDCT). In fact, post-TAVR MDCT has the ability to detect THV thrombosis in asymptomatic patients with no evidence of THV obstruction on TTE (3–5). Although often subclinical, THV thrombosis may potentially lead to an increased risk of stroke, THV obstruction with heart failure, or reduced long-term THV durability, which makes early detection pivotal to guiding treatment. Current evidence regarding THV thrombosis mainly builds on case series and small studies of nonconsecutive patients with a short follow-up time (3–6). Consequently, the incidence, clinical implications, and predisposing factors of THV thrombosis remain to be fully understood. The aim of this study was to assess the incidence, potential predictors, and clinical implications of THV thrombosis after TAVR with a balloon-expandable THV.
Study population and TAVR procedure
Among 460 consecutive patients who underwent TAVR (Edwards Sapien XT or Sapien 3, Edwards Lifesciences, Irvine, California) at Aarhus University Hospital between January 2011 and January 2016, a total of 405 patients (88%) underwent MDCT in addition to TTE and transesophageal echocardiography (TEE) 1 to 3 months after the TAVR procedure (routine follow-up visit 1) (Figure 1). These 405 patients form the basis of the present study. In the remaining 55 patients who underwent TAVR, MDCT was not performed because of death before follow-up (n = 19), severely impaired renal function (n = 7), or patient refusal and/or frailty (n = 29). Clinical and TTE assessment were performed in our outpatient clinic 12 months post-TAVR (routine follow-up visit 2). All procedures were performed as part of standard clinical care.
Standard post-TAVR antithrombotic treatment included dual antiplatelet therapy with aspirin (75 mg/day) and clopidogrel (75 mg/day) for 12 months, followed by lifelong aspirin (75 mg/day) (3). In patients with atrial fibrillation, the decision for treatment with warfarin alone or in combination with 1 platelet inhibitor was at the discretion of the treating physician.
TTE was performed before discharge and at routine follow-up visits 1 and 2. THV function was assessed by the mean trans-THV gradient and the effective orifice area (EOATHV). Paravalvular regurgitation was graded as mild, moderate, or severe according to the Valve Academic Research Consortium-2 criteria (10). Furthermore, at routine follow-up visit 1 and after THV thrombosis treatment, TEE was performed to further delineate the aortic root, THV anatomy, and THV leaflet mobility (3).
Pre- and post-TAVR contrast-enhanced MDCT examinations were performed using a second-generation dual-source CT system (Siemens Somatom Definition Flash, Siemens Healthcare, Erlangen, Germany) as previously described (3). Post-TAVR MDCT scans were performed using a prospectively electrocardiographically gated sequential acquisition protocol in all patients.
MDCT examinations were analyzed using commercially available software (syngo.via and Multimodality Workplace, Siemens Healthcare, Forchheim, Germany). On pre-TAVR MDCT scans, aortic root dimensions and degree of calcification were determined as previously described (7). Post-TAVR MDCT scans were evaluated for hypoattenuated leaflet thickening that indicated THV thrombosis (3). Leaflet thrombus was defined as diffuse thickening of 1 or more THV leaflets or a more focal hypo-attenuating abnormality attached to the THV leaflet. The finding had to be identifiable on ≥2 reconstructed planes (double-oblique axial and multiplanar reformatted reconstructions). In the event of THV thrombosis, the number of leaflets involved and the maximal leaflet thickening was assessed. THV dimensions, eccentricity, and expansion were assessed as previously described (3). THV underexpansion was defined as an expansion ratio of ≤90% at both the inflow, midportion, and outflow. The THV was deemed noncircular if eccentricity was >10% at the inflow, midportion, and outflow.
THV thrombosis diagnosis, treatment, and follow-up
Follow-up MDCT and echocardiography were performed by separate operators, but all imaging and clinical information were available to the treating physician. As per institutional policy, initiation of warfarin alone or in combination with antiplatelet therapy was recommended in patients with MDCT evidence of THV thrombosis, but the final decision was at the discretion of the treating physician, which took into account the patient’s bleeding risk and preferences. Additional TTE, TEE, and MDCT was performed 3 months after the diagnosis of THV thrombosis.
The risk ratio (RR) with 95% confidence intervals (CIs) and the chi-square were calculated to compare THV thrombosis risks (Tables 1 to 3⇓⇓). A left ventricular ejection fraction (LVEF) ≤35% at hospital discharge, use of a 29-mm THV, and no post-TAVR warfarin treatment were entered into a log-linear model for binary data to estimate adjusted RRs for THV thrombosis (3–5). Clinical implications of THV thrombosis were studied by comparing the distribution of various factors between THV thrombosis and non-THV thrombosis patients (Tables 4 and 5⇓⇓). Continuous normally distributed variables are presented as mean ± SD and compared using the unpaired or paired Student t-test. Other distributed continuous variables are presented as median (interquartile range [IQR]) and compared using the Mann-Whitney U test. Categorical variables are presented as frequencies (percentages) and compared using the Fisher exact test or the chi-square test as appropriate. A 2-tailed p value <0.05 was considered statistically significant. All analyses were performed using Stata 12 (StataCorp LP, College Station, Texas).
Predictors of THV thrombosis
Table 1 depicts the risk of THV thrombosis in relation to pre-TAVR clinical characteristics, whereas THV thrombosis risk in relation to pre-TAVR echocardiographic and MDCT characteristics are shown in Online Table 1. Median age of the study cohort was 83 years (IQR: 78 to 86 years), 54% were women, and the median Society of Thoracic Surgeons predicted risk of mortality was 5.3 (IQR: 3.6 to 7.1). THV thrombosis risk was higher in patients without atrial fibrillation and an estimated glomerular filtration rate of ≤30 ml/min, and tended to be higher in men.
Procedural data, THV, and pre-discharge echocardiographic characteristics
Information on THV thrombosis risk related to procedural data and pre-discharge echocardiographic characteristics are provided in Table 2. A larger THV was associated with THV thrombosis (p = 0.03). Otherwise, there were no differences in THV thrombosis risk in relation to procedural characteristics or THV function between groups. THV oversizing (≤17% vs. >17%) did not affect THV thrombosis risk significantly. The risk of THV thrombosis did not differ between the 2 generations of THVs.
Post-procedural antithrombotic regimen
Antithrombotic regimens from the TAVR procedure until routine follow-up visit 1 are outlined in Table 3. The risk of THV thrombosis in patients who did not receive warfarin was higher compared with patients who received warfarin (10.7% vs. 1.8%; RR: 6.09; 95% CI: 1.86 to 19.84). In patients who received antiplatelet therapy alone, the risk of THV thrombosis was 18.8% (6 of 32).
Multivariable analysis of predictors of THV thrombosis
In multivariable analysis, a 29-mm THV (RR: 2.89; 95% CI: 1.44 to 5.80) and no post-TAVR warfarin treatment (RR: 5.46; 95% CI: 1.68 to 17.70), but not a LVEF ≤35% at discharge (RR: 2.21; 95% CI: 0.93 to 5.26), independently predicted THV thrombosis.
Incidence and clinical implications of THV thrombosis
Routine follow-up visit 1
There was no difference in the median (IQR) interval from the TAVR procedure to follow-up in the non-THV thrombosis group versus the THV thrombosis group (42 days [25 to 59] vs. 43 days [28 to 57]; p = 0.55). The post-TAVR MDCT effective radiation dose was similar in the non-THV thrombosis group versus the THV thrombosis group (3.1 ± 1.6 mSv vs. 2.9 ± 1.7 mSv; p = 0.63).
There was no difference between the mean trans-THV gradient at pre-discharge and at routine follow-up visit 1 in the THV thrombosis group (10 ± 5 mm Hg vs. 10 ± 4 mm Hg; p = 1.00). The trans-THV mean gradient was higher among THV thrombosis patients (Table 4). A LVEF ≤35% was twice as frequent among THV thrombosis patients compared to those without THV thrombosis (n = 5 [18%] vs. n = 30 [8%]; p = 0.08). There was no difference in 30-day complication rates between the 2 groups.
Follow-up and treatment of THV thrombosis
At routine follow-up visit 1, post-TAVR MDCT demonstrated THV thrombosis in 24 patients. In addition, 4 patients presented with THV thrombosis before or after routine follow-up visit 1. Thus, the THV thrombosis group included 28 of 405 (7%) patients. TEE demonstrated leaflet thickening and/or restrictive leaflet movement in 24 (86%) patients. In 2 (7%) patients, there were no abnormal findings on TEE, whereas 2 (7%) patients did not undergo TEE. No patients without THV thrombosis determined by MDCT had compromised leaflet motility as assessed by TEE.
Warfarin alone or in addition to antiplatelet therapy was prescribed in 4 (14%) and 17 (61%) patients, respectively. In the 3 (11%) patients already receiving warfarin, the target international normalized ratio level was raised from 2.5 to 3.0. In 4 (14%) patients, routine antithrombotic therapy without warfarin was maintained, and additional further follow-up TEE and MDCT imaging were planned. Of these 4 patients, 2 experienced spontaneous THV thrombus regression, whereas 2 had THV thrombosis progression, and warfarin was initiated. TEE and MDCT follow-up after 3 months of treatment showed complete thrombus resolution in 85% of cases (Figures 2 and 3⇓⇓).
Obstructive THV thrombosis
Five (18%) patients developed obstructive THV thrombosis with heart failure symptoms during the 12-month follow-up. Details regarding these cases are presented in Online Table 2. In 1 patient, obstructive THV thrombosis was diagnosed at routine follow-up visit 1, whereas 1 patient presented with symptoms of heart failure before and 3 patients 3 to 8 months after routine follow-up visit 1. Four (80%) of these patients received antiplatelet therapy alone. No cases of THV obstruction were observed among patients without THV thrombosis.
Selected clinical characteristics, THV thrombus characteristics, and outcomes in patients with nonobstructive versus obstructive THV thrombosis are presented in Online Table 3. No patients with obstructive THV thrombosis received warfarin as part of post-TAVR antithrombotic therapy. Patients with obstructive THV thrombosis had involvement of more THV leaflets than patients with nonobstructive thrombus (1.3 ± 0.5 vs. 2.4 ± 0.5; p = 0.0001), and the mean maximal leaflet thickness was significantly higher (4.2 ± 1.8 mm vs. 7.5 ± 1.3 mm; p = 0.0007).
Routine follow-up visit 2
The median time from the TAVR procedure to routine follow-up visit 2 in the non-THV thrombosis group versus the THV thrombus group was 360 days (IQR: 341 to 383 days) versus 363 days (IQR: 348 to 375 days) (p = 0.45).
As shown in Figure 1, routine follow-up visit 2 data, including clinical and echocardiographic assessment, as well as mortality status were available in 335 (83%) patients. Twelve-month all-cause mortality was 17% (54 of 316) in the non-THV thrombosis group versus 11% (2 of 19) among patients with THV thrombosis (p = 0.75). Twelve-month follow-up data with echocardiography and information on stroke were available for 229 patients in the control group and 17 patients with THV thrombosis (Table 5). In patients with THV thrombosis, the mean trans-THV gradient was lower at routine follow-up visit 2 versus routine follow-up visit 1 (9 ± 4 mm Hg vs. 11 ± 4 mm Hg; p = 0.03). Antithrombotic regimens at follow-up visit 2 are outlined in Online Table 4.
In this study, which is the largest to date and the first consecutive cohort with MDCT performed following TAVR with the Edwards XT or Edwards S3 THVs, the incidence of THV thrombosis was 7% (Central Illustration). Although in most cases, there were no signs of THV obstruction on TTE, 18% of patients with THV thrombosis formation developed clinically overt obstructive THV thrombosis. Other main findings were that the use of a 29-mm THV and no warfarin post-TAVR treatment were independently associated with an increased risk of THV thrombosis. Treatment with warfarin effectively reversed THV thrombosis findings and normalized THV function.
Two recent smaller studies assessed the presence of THV thrombosis with MDCT as the diagnostic modality. Makkar et al. (5) and Pache et al. (4) performed retrospective electrocardiographically gated MDCT scans that allowed assessment of THV leaflet morphology and leaflet mobility throughout the cardiac cycle. In contrast, the present study evaluated THV leaflet morphology by performing low-radiation dose prospective electrocardigraphically gated MDCT imaging, whereas THV leaflet mobility was assessed by TEE. THV leaflet mobility assessment by TEE is most likely improved compared with MDCT due to the superior temporal resolution. In addition, TEE is a valuable supplement to TTE for evaluation of paravalvular regurgitation. We found that the agreement between MDCT-verified THV thrombosis and restricted THV leaflet mobility on TEE was high, and importantly, no patients without THV thrombosis on MDCT had restricted THV leaflet mobility on TEE. Taken together, these findings suggest that a front-line diagnostic strategy for THV thrombosis may consist of TTE and THV leaflet morphology assessment by MDCT with supplementary TEE in cases of equivocal MDCT findings or contraindications to MDCT. In our experience, MDCT offers several potential advantages over TEE with regard to detection of THV thrombosis; for example, it is less invasive, less operator-dependent, and it detected a few more cases of THV thrombosis in this study.
The pooled data presented by Makkar et al. (5) demonstrated reduced leaflet motion and hypoattenuating opacities in 40% of 55 TAVR patients in a clinical trial and 13% of 132 patients (105 THVs, 27 bioprosthetic surgical valves) in 2 registries. Pache et al. (4) detected hypoattenuated leaflet thickening in 10.3% of 156 patients (from a cohort of 249 consecutive patients) who underwent TAVR with the Edwards S3 THV. Cases of THV obstruction attributable to THV thrombosis were not presented in any of these studies. The present study extended these findings in a larger cohort with more extensive follow-up, and further illustrated the important clinical implications of THV thrombosis. In addition, we included 88% of all patients who underwent TAVR at our institution, thus reducing the risk of selection bias compared with the aforementioned studies. The differences in THV thrombosis incidence among studies might result from major differences in crucial determinants of outcomes. First, the interval from the TAVR procedure to MDCT follow-up differed significantly among studies, ranging from 5 days to 3 months. Moreover, the proportion of patients who received post-TAVR anticoagulant therapy varied from 20% to 40%. Finally, different THV types were investigated (4,5). Of note, Latib et al. (11) recently reported an incidence of THV thrombosis of 0.61% in a multicenter retrospective registry that included >4,000 patients. However, most of these patients had progression of symptoms, and the diagnosis of THV thrombosis was based mainly on TTE; thus, the true incidence of THV thrombosis was likely underestimated (3).
There is limited evidence on optimal antithrombotic therapy following TAVR, and current recommendations regarding post-TAVR antithrombotic therapy have been empirically determined (12–14). In a recent meta-analysis that compared aspirin versus aspirin+clopidogrel following TAVR, there was no difference in the 30-day clinical and cerebrovascular adverse event rates; however, a trend toward more bleeding in the aspirin+clopidogrel group was demonstrated (15). In this context, it should be acknowledged that in this study, monotherapy with aspirin was associated with a THV thrombosis risk of 25%, and importantly, all patients who experienced obstructive THV thrombosis received antiplatelet therapy alone. Moreover, the present study indicated that a post-TAVR antithrombotic regimen without warfarin seems to predispose patients to THV thrombosis (5). In line with these findings are recent data from a multicenter registry that demonstrated that a lack of anticoagulant therapy following TAVR seems to be associated with THV dysfunction (16). The protective effect of anticoagulant therapy might explain the lower incidence of THV thrombosis among patients with atrial fibrillation in this study. Several ongoing randomized trials, such as GALILEO (NCT02556203; Global Study Comparing a Rivaroxaban-based Antithrombotic Strategy to an Antiplatelet-based Strategy After Transcatheter Aortic Valve Replacement to Optimize Clinical Outcomes) and POPular-TAVI (NCT02247128), will provide data on the use of non-vitamin K antagonist oral anticoagulants and antiplatelets after TAVR.
Currently, there is no consensus on how to treat THV thrombosis. As in previous studies, anticoagulation with warfarin was effective in most of the patients in the present study (4,5,11,17). We and others have observed recurrence of THV thrombosis after discontinuation of warfarin, thus indicating that short-term warfarin treatment of THV thrombosis might not be sufficient in patients who are prone to developing THV thrombosis (5). Furthermore, there is still uncertainty with regard to the natural history of THV thrombosis. Hypothetically, spontaneous THV thrombosis resolution might explain the discrepancy observed between the incidence of incidental THV thrombosis and clinically overt obstructive THV thrombosis. The data provided in this and previous studies suggest that follow-up MDCT in patients with THV thrombus will show either no regression or progression in most patients who continue antiplatelet therapy only (4,5). Moreover, we observed cases of incidental THV thrombosis progressing to clinically overt THV thrombosis with accompanying THV obstruction and symptoms of heart failure. These findings suggest that early detection and anticoagulation might be crucial to prevent deterioration of THV function. An alternative strategy to ours is “watchful waiting,” which includes serial clinical and imaging follow-up, with anticoagulation being initiated only in the event of clinical THV thrombosis. However, 1 of 5 patients with obstructive THV thrombosis in this study did deteriorate despite initiation of anticoagulation. Furthermore, the clinical consequences of nonobstructive THV thrombosis might also include decreased long-term THV durability and increased risk of stroke, although assessment of the latter association is challenging due to the potential multiple mechanisms underlying TAVR-related stroke (5,18). The safety of a watchful waiting strategy needs delineation in future studies.
For the first time, we demonstrated an association between larger THV size and THV thrombosis. Ex vivo data showed that local flow dynamics in the sinuses of Valsalva are modified upon THV implantation (19). Whether these local flow dynamics are further modified by THV size and/or type, and thus play a causative role in development of THV thrombosis could be speculated. Additional procedural manipulation of the THV (e.g., post-dilation), post-deployment THV geometry, and degree of THV oversizing did not affect the incidence of THV thrombosis in our study or in other studies (4,5,11). Whether the rate of THV thrombosis varies with different types of THVs remains unclear, but different designs (e.g., supra-annular vs. intra-annular) that lead to differences in local flow dynamics and variations in leaflet material (e.g., porcine vs. bovine) might potentially account for differences in thrombogenicity. Recently, it was shown that platelet activation appears to be less enhanced in the Sapien 3 valve compared with the Sapien XT valve, which is possibly due to the lower rate of post-TAVR aortic regurgitation. However, in the present study, the incidence of THV thrombosis did not differ between these 2 THVs (20). Studies that include a larger number of THV thrombosis cases are needed to further elucidate specific risk factors for THV thrombosis.
This study had the inherent limitations of an observational single-center design. The diagnosis of THV thrombosis was not confirmed by histology or autopsy; however, THV leaflet thickening and restricted mobility were rapidly reversible by anticoagulation as documented by follow-up TEE and MDCT, which strongly underlined the thrombotic nature of these findings. The selection of variables included in the multivariable model for prediction of THV thrombosis, although based on knowledge from previous studies, was post hoc in nature. The present study design did not allow for conclusions on the natural history and management of THV thrombosis. Data in this real-world observational study were collected in a nonselected cohort of patients and involved multiple MDCT, echocardiography, and TAVR operators who were unblinded to the test results. There was no established consensus on the interpretation and management of imaging findings indicative of THV thrombus. This diagnostic strategy was previously described in our center (3). It should be acknowledged that treatment decisions might have varied among observers, also taking into account clinical observations (e.g., symptoms, bleeding risk, and patient preferences). However, this study included all patients in a defined time period and represented consecutive data from a contemporary and relevant study cohort in a real-world setting. The impact of untreated THV thrombosis on clinical outcomes and structural valve degeneration was also not answered by our data. This study was confined to the first 12 months after THV; therefore, it did not provide data on the long-term impact or the occurrence of late THV thrombosis. Concerning warfarin-treated patients, the international normalized ratio levels from discharge to routine follow-up visit 1 were not available. Finally, our findings might not be generalizable to other types of THVs.
The incidence of THV thrombosis in this large study was 7%. Larger THV size might pre-dispose to THV thrombosis, whereas treatment with warfarin appears to have a protective effect. Although often subclinical, THV thrombosis might have important clinical implications. Future studies are warranted to assess whether tailored post-TAVR antithrombotic therapy can reduce the incidence of THV thrombosis.
COMPETENCY IN PATIENT CARE AND PROCEDURAL SKILLS: MDCT can identify thrombus formation on a substantial proportion of prosthetic aortic valves after transcatheter deployment (TAVR). These thrombi are usually subclinical but may cause overt valvular obstruction. Larger prostheses are more prone to this complication. Treatment with warfarin is associated with thrombosis resolution and restoration of prosthetic valve function.
TRANSLATIONAL OUTLOOK: Randomized trials are needed to establish the scope and clinical impact of prosthetic valve thrombosis following TAVR and to define optimum antithrombotic strategies to reduce the risk of valve thrombosis.
For supplemental tables, please see the online version of this article.
Dr. Grove has received speaker honoraria from AstraZeneca, Baxter, Bayer, Boehringer Ingelheim, and Pfizer; and has participated in advisory board meetings for AstraZeneca, Bayer, Boehringer Ingelheim, and Bristol-Myers Squibb. Dr. Leipsic has been a consultant for and provides the CT core laboratory for Edwards Lifesciences and Medtronic. Dr. J.M. Jensen has received speaker honorarium from Bracco Imaging. Dr. Blanke has been a consultant for Edwards Lifesciences, Neovasc, Tendyne, and Circle Imaging. Dr. Klaaborg has been a proctor for Edwards Lifesciences. Dr. Webb has been a consultant for Edwards Lifesciences. Dr. Nørgaard has received unrestricted institutional research grants from Edwards Lifesciences, Siemens, and HeartFlow. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Abbreviations and Acronyms
- confidence interval
- effective orifice area
- interquartile range
- left ventricular ejection fraction
- multidetector computed tomography
- risk ratio
- transcatheter aortic valve replacement
- transesophageal echocardiography
- transcatheter heart valve
- transthoracic echocardiography
- Received May 18, 2016.
- Revision received August 4, 2016.
- Accepted August 9, 2016.
- American College of Cardiology Foundation
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