Author + information
- Received February 16, 2014
- Revision received April 3, 2014
- Accepted April 11, 2014
- Published online October 1, 2014.
- Josep Rodés-Cabau, MD∗∗ (, )
- Philip Kahlert, MD†,
- Franz-Josef Neumann, MD‡,
- Gerhard Schymik, MD§,
- John G. Webb, MD‖,
- Pierre Amarenco, MD¶,
- Thomas Brott, MD#,
- Zsolt Garami, MD∗∗,
- Gino Gerosa, MD††,
- Thierry Lefèvre, MD‡‡,
- Bjoern Plicht, MD†,
- Stuart J. Pocock, PhD§§,
- Marc Schlamann, MD†,
- Martyn Thomas, MD‖‖,
- Beverly Diamond, PhD¶¶,
- Ihsen Merioua, MD¶¶,
- Friedhelm Beyersdorf, MD## and
- Alec Vahanian, MD¶
- ∗Quebec Heart and Lung Institute, Quebec City, Quebec, Canada
- †University Hospital of Essen, Essen, Germany
- ‡Universtäts Herzzentrum Bad Krozingen, Krozingen, Germany
- §Universtäts Klinikum Karslruhe, Karslruhe, Germany
- ‖St. Paul’s Hospital, Vancouver, British Columbia, Canada
- ¶Hôpital Bichat, Paris, France
- #Mayo Clinic, Rochester, Minnesota
- ∗∗Methodist DeBakey Heart and Vascular Center, Houston, Texas
- ††Division of Cardiac Surgery, University of Padova, Padova, Italy
- ‡‡Hôpital Privé Jacques Cartier, Massy, France
- §§London School of Hygiene and Tropical Medicine, London, United Kingdom
- ‖‖St. Thomas Hospital, London, United Kingdom
- ¶¶Edwards Lifesciences, Irvine, California
- ##Freiburg Universitats Bad Krozingen, Krozingen, Germany
- ↵∗Reprint requests and correspondence:
Dr. Josep Rodés-Cabau, Quebec Heart and Lung Institute, Laval University, 2725 chemin Ste-Foy, G1V 4G5 Quebec City, Quebec, Canada.
Objectives This study sought to determine the feasibility, safety, and exploratory efficacy of the Embrella Embolic Deflector (EED) system (Edwards Lifesciences, Irvine, California) in patients undergoing transcatheter aortic valve replacement (TAVR).
Background Few data exist on the value of using embolic protection devices during TAVR.
Methods This pilot study included 52 patients who underwent transfemoral TAVR. The EED system was used in 41 patients, whereas 11 patients underwent TAVR without embolic protection (control group). Cerebral diffusion-weighted magnetic resonance imaging (DW-MRI) was performed at baseline and within 7 days and 30 days after TAVR.
Results The EED system was successfully deployed at the level of the aortic arch in all patients with no complications. The deployment of the EED system was associated with high-intensity transient signals (HITS) as evaluated by transcranial Doppler (median: 48 [interquartile range: 17 to 198] HITS), and a higher total number of HITS was observed in the EED group (p < 0.001 vs. control group). DW-MRI performed within 7 days after TAVR showed the presence of new ischemic lesions in all patients in both groups, with a median number of 7 (interquartile range: 3 to 13) lesions per patient. The use of the EED system was associated with a lower lesion volume compared with the control group (p = 0.003). All new cerebral lesions had disappeared on the DW-MRI performed at 30 days after TAVR. Two strokes unrelated to the EED system occurred 2 and 29 days after TAVR.
Conclusions This study showed the feasibility and safety of using the EED system in TAVR procedures. The EED system did not prevent the occurrence of cerebral microemboli during TAVR or new transient ischemic lesions as evaluated by DW-MRI, but it was associated with a reduction in lesion volume. Further studies are warranted to determine the efficacy of using the EED system during TAVR procedures.
- embolic protection
- Embrella Embolic Deflector
- magnetic resonance imaging
- transcatheter aortic valve implantation
- transcranial Doppler
The occurrence of cerebrovascular ischemic events remains one of the most worrisome complications of transcatheter aortic valve replacement (TAVR). The periprocedural stroke rate associated with TAVR is ∼3% and the PARTNER (Placement of AoRtic TraNscathetER Valves) trial showed a higher incidence of early cerebrovascular events in patients undergoing TAVR compared with those who received medical treatment or standard surgical aortic valve replacement (1–3). Furthermore, several studies have shown a very high incidence (∼70%) of new cerebral ischemic defects as evaluated by diffusion-weighted magnetic resonance imaging (DW-MRI) after TAVR (4–8). It is, therefore, of the utmost clinical importance to implement additional preventive measures for reducing cerebral emboli during TAVR procedures.
The use of embolic protection devices in carotid interventions has been shown to be effective in reducing the rate of new cerebral ischemic defects as evaluated by DW-MRI (9), but very few (and preliminary) data are available on the use of embolic protection devices in the TAVR field (1). The Embrella Embolic Deflector (EED) system (Edwards Lifesciences, Irvine, California) consists of an oval-shaped nitinol frame covered with a porous polyurethane membrane that is positioned at the level of the aortic arch with the purpose of deflecting embolic debris generated during TAVR procedures. Nietlispach et al. (10) reported the first in-human experience with the EED device showing the feasibility and safety of device implantation in a preliminary series of 4 patients (1 aortic valvuloplasty, 3 TAVR procedures). The objectives of this study were as follows: 1) to determine the procedural safety, technical feasibility, and exploratory efficacy of the EED system in patients undergoing TAVR; and 2) to evaluate the mechanisms and temporal patterns of embolic events during TAVR procedures.
Patients with severe symptomatic aortic stenosis considered to be candidates for TAVR by the heart team at 6 centers in Europe and Canada were eligible for the study. The study had a prospective and nonrandomized design that empirically pre-established the inclusion of 54 patients (9 patients per center), with 42 patients receiving the EED device (the first 7 patients at each center) and 12 patients (the last 2 patients at each center) not receiving it (control group). The main exclusion criteria were the following: history of cerebrovascular event within the previous 12 months, carotid artery stenosis >70%, left ventricular ejection fraction <20%, serum creatinine >2.5 mg/dl, known or suspected right subclavian artery or brachiocephalic artery stenosis, and any contraindication to undergoing a DW-MRI examination. The study protocol was approved by the Ethics Committee of each center, and all patients had to provide signed informed consent to participate in the study.
The TAVR procedures were performed according to the standards of each participating center. The SAPIEN XT transcatheter valve (Edwards Lifesciences) implanted via the transfemoral approach was the only valve/approach permitted. All patients received dual-antiplatelet treatment (aspirin + clopidogrel) before and after the procedure, and intravenous heparin was administered during the procedure with the goal of obtaining an activated clotting time of >300 s. All procedural and 30-day events were defined according to the Valve Academic Research Consortium criteria (11) and adjudicated by an independent clinical events committee.
The EED system
The EED system consists of an oval-shaped nitinol frame (length, 59 mm; width, 25.5 mm) covered with a porous polyurethane membrane (100-μm pore size) (Figure 1A). The device is inserted via the right radial or brachial approach using a 6-French delivery system. The frame of the device has 2 opposing petals that are positioned along the greater curvature of the aorta, covering the ostia of both the brachiocephalic and the left common carotid arteries (Figure 1B). The EED system was to be deployed (as per protocol) at the beginning of the TAVR procedure just before any attempt to cross the native aortic valve. The system was retrieved at the end of the procedure and visually inspected by the physician responsible for the procedure to evaluate potential tears or fractures of the nitinol frame and/or polyurethane membrane.
Transcranial doppler examinations
Simultaneous Transcranial Doppler (TCD) examinations of both middle cerebral arteries were performed during the entire TAVR procedure. Details of TCD examinations are provided elsewhere (12). All centers received TCD training and quality supervision by an expert on TCD (Z.G.), and the same TCD machine was used at all centers (Multi-Dop T digital system, DWL Compumedics, Singen, Germany). Time-stamped signal recording and procedure protocol were used for offline analysis to exclude artifacts from patient movement, catheter flushing, or contrast injections. The presence and number of high-intensity transient signals (HITS) at each step of the TAVR procedure were recorded and measured offline in a central core laboratory at the Universitäts Klinikum Essen, Essen, Germany.
Cerebral DW-MRI examinations
Cerebral DW-MRI examinations were performed at baseline (before TAVR) and within 7 days (1 to 7 days) and at 30 days (−7 to +14 days) after the procedure. Details about performing and evaluating cerebral DW-MRI examinations are provided elsewhere (4). Briefly, the DW-MRI protocol included 3 sequences: 1) transversal fluid-attenuated inversion recovery; 2) transversal DW-MRI with apparent diffusion coefficient maps (T2 if susceptibility-weighted imaging [SWI] was not available); and 3) transversal SWI (T2 if SWI was not available). All DW-MRI exams were analyzed offline in a central core laboratory at the Universitäts Klinikum of Essen, Essen, Germany. The presence, number, size, and location of all new focal diffusion abnormalities were evaluated in each patient at the examinations performed within 7 days and at 30 days after the procedure.
Neurological and cognitive function assessment
Assessment of neurological and cognitive status was obtained pre-procedure and at 30 days (−7 to 14 days) after the procedure. The following examinations were performed at each time point: 1) the National Institutes of Health Stroke Scale (NIHSS) questionnaire (13); 2) the modified Rankin Scale score (14); 3) the Barthel Index (15); 4) the Mini-Mental State Examination (MMSE) (16); and 5) the Montreal Cognitive Assessment (MoCA) (17). Changes in neurological (NIHSS, modified Rankin Scale score, Barthel Index) and cognitive (MMSE, MoCA) status over time were determined by changes in the mean/median values for each test over time.
Continuous variables are expressed as mean ± SD or median (25th to 75th interquartile range) depending on variable distribution. Comparisons between 2 groups were performed using the Student t test or Wilcoxon test for continuous variables, and the Fisher exact test for categorical data. Differences were considered statistically significant at p values <0.05. The data were analyzed with SAS statistical software version 9.1.3 (SAS Institute, Cary, North Carolina).
A total of 54 patients were included in the study: 42 patients in the EED group and 12 patients in the control group. One TAVR procedure in each (EED and control) group was aborted due to failure to obtain femoral access; those patients were subsequently excluded from the study, leading to a final study population of 52 patients. The main baseline and procedural characteristics of the EED and control groups are shown in Table 1. There were no significant differences in baseline and procedural characteristics between groups except for transcatheter valve size. The EED system was successfully deployed at the level of the greater curvature of the aortic arch in all patients. The radial approach was the access site in most (68%) patients, and the median time from obtaining access to complete deployment of the EED system was 2 min (interquartile range, 1 to 3 min). Two devices were used in 2 patients due to excessive tortuosity of the subclavian artery, which made advancement and deployment of the first device difficult. Damage of the first device was suspected (but not confirmed after device withdrawal and visual inspection), and a second device was used. The device covered both the brachiocephalic trunk and left carotid artery ostia in all cases but 1 due to anatomic reasons (anomalous origin of the left carotid artery from the ascending aorta). There were no cases of ruptures or tears of the membrane of the device as evaluated by visual inspection at the end of the procedure.
The main 30-day events of the study population are summarized in Table 2. There were 2 complications related to the EED device: 1 radial thrombosis with no clinical consequences and 1 pseudoaneurysm of the brachial artery that required surgical repair. There were 3 cerebrovascular events (2 strokes, 1 transient ischemic attack [TIA]), all of which occurred in the EED group, but none of which was related to the EED system. One patient in whom new-onset atrial fibrillation developed within the hours after the procedure had a minor stroke 48 h after the procedure, and another patient had a major stroke on day 29. One additional patient had a TIA 9 days after the procedure.
TCD imaging was performed during the TAVR procedure in all patients, and TCD data were interpretable in all of them. The results of TCD examinations in the EED and control groups are shown in Figure 2. The presence of HITS was detected at every step of the TAVR procedure in both groups, and crossing the native aortic valve and positioning the transcatheter valve were the procedural steps associated with the highest number of HITS (243 [interquartile range: 124 to 318] HITS and 87 [interquartile range: 0 to 238] HITS in the EED and control groups, respectively, p = 0.04), followed by the deployment of the transcatheter valve (56 [interquartile range: 18 to 87] HITS and 29 [interquartile range: 0 to 57] HITS in the EED and control groups, respectively, p = 0.05), and the insertion of the EED device (48 [interquartile range: 17 to 198] HITS). The total number of HITS during the TAVR procedure was higher in the EED group than in the control group (632 [interquartile range: 347 to 893] HITS vs. 279 [interquartile range: 0 to 505] HITS, p < 0.001).
The timing and patients undergoing DW-MRI examinations at each time point in the study are shown in Figure 3. The main results of the DW-MRI examinations performed within 7 days (median, 3 [interquartile range: 2 to 5] days) after TAVR are shown in Table 3. All patients (100%) in the 2 groups had new ischemic defects at the first DW-MRI performed after the TAVR procedure. The vast majority of patients in both groups had multiple defects, with a median number of defects per patient in the EED and control groups of 8 (interquartile range: 3 to 13) and 4 (interquartile range: 2 to 8), respectively, p = 0.41. No differences (p = 0.58) in total lesion volume per patient were observed between groups, but patients in the EED group had a smaller lesion volume per lesion compared with the control group (30 [interquartile range: 20 to 50] mm3 vs. 50 [interquartile range: 30 to 70] mm3, p = 0.003).
A total of 31 patients (26 and 5 patients in the EED and control groups, respectively) had a second DW-MRI examination performed at 36 (interquartile range: 29 to 42) days after the procedure. All new cerebral lesions present on the first DW-MRI had disappeared in the second DW-MRI (Table 4, Figure 4). Two patients with cerebrovascular events (1 stroke, 1 TIA) did not undergo DW-MRI at 30 days due to the implantation of a pacemaker after TAVR. Another patient had a stroke at day 29 post-TAVR.
The relationship between baseline and procedural factors and the number and size of new ischemic defects as evaluated by DW-MRI within 7 days after the procedure are shown in Table 5. A history of peripheral vascular disease was associated with a higher number of new ischemic lesions (21 [interquartile range: 18 to 26] vs. 4 [interquartile range: 2 to 9], p = 0.006). A history of stroke/TIA (p = 0.004) was associated with a greater lesion volume, whereas the use of the EED system (p = 0.003) was associated with a lower lesion volume.
Neurological and cognitive function assessment
The results of neurological and cognitive function assessment are summarized in Table 6. Post-procedural neurological evaluation with the NIHSS scale, the modified Rankin Scale and the Barthel Index showed no differences in the median scores compared with baseline examinations (p > 0.15 for all of them in the EED and control groups). The post-procedural cognitive assessment with the MMSE exhibited median values similar to those with the examinations performed at baseline (p > 0.2 for both examinations in the EED and control groups). The cognitive status as evaluated by the MoCA showed a mild improvement (p < 0.001) at 30 days compared with baseline in the EED group, and no differences over time (p = 0.678) in the control group.
The present study showed the feasibility and safety of using the EED system during TAVR procedures. The device was successfully implanted in all patients, and the only complications were related to access site. However, the EED system did not prevent the occurrence of cerebral microemboli during TAVR procedures as evaluated by TCD. Indeed, the burden of procedural cerebral microemboli was higher compared with patients who had TAVR with no embolic protection, partially due to the microemboli occurring during the insertion of the EED system. The use of the EED system had no effect on the occurrence and number of new silent cerebral ischemic lesions as evaluated by DW-MRI within the 7 days after TAVR. All patients exhibited new ischemic lesions, which were multiple in the vast majority of them. However, the volume of cerebral lesions was smaller in those patients who underwent the TAVR procedure with the EED system in place. A history of peripheral vascular disease was the only factor associated with a higher number, but not volume, of new cerebral lesions. The occurrence of new cerebral lesions was not associated with any significant early neurological or cognitive impairment, and all lesions had disappeared at 30 days after the procedure.
The successful implantation of the EED system in all patients included in this multicenter study provides important data on the feasibility of using this embolic protection system in TAVR procedures. Indeed, most participating centers had no previous experience with the device, and the rapidity of device deployment (median of 2 min after obtaining access) reflects both its simplicity of use and a very short learning curve. Importantly, there were no complications related to the deployment of the device, and no significant interaction with the transcatheter valve system was observed in any case. In fact, all complications related to the device occurred at the level of the access site with no major clinical consequences except for 1 case of brachial aneurysm that required surgical repair. Also, no significant increase in the incidence of acute kidney injury or new for dialysis was observed in the EED group compared with the control group or historical data (18). In addition to the EED system, 2 other embolic protection devices, the Triguard embolic deflection device (Keystone Heart Inc., Tel Aviv, Israel) and the Montage dual-filter system (Claret Medical Inc., Santa Rosa, California) have reported feasibility data in patients undergoing TAVR. Also in accordance with the results of the present study, no major safety issues were observed with the use of such devices (19–23).
Previous TAVR studies using TCD monitoring during the procedure have shown that cerebral microemboli occur in each of the procedural steps and are more frequent during valve positioning and implantation of the transcatheter valve (12,24). In accordance with these studies, cerebral microemboli were detected by TCD in all steps of the TAVR procedure in the present study, and the highest number was observed during native valve crossing and positioning of the transcatheter valve system. The use of the EED system did not prevent the occurrence of cerebral microemboli in any of the procedural steps, suggesting that most microemboli occurring during the TAVR procedure are smaller than 100 μm, which is the size of the porous membrane of the system. However, the presence of larger debris (from 0.15 to 4 mm) has also been shown in a recent study using the Montage dual-filter device (Claret Medical Inc.) (21), and these are probably the debris that are deflected by the EED system. Furthermore, although good apposition of the device against the greater curvature of the aortic arch was verified by angiography at the beginning of the procedure, the occurrence of cerebral microemboli due to inadequate apposition of the device during the procedure cannot be ruled out and should be further evaluated in future studies. Of note, the deployment of the EED system was also associated with a significant number of cerebral microemboli. We hypothesize that most of these microemboli were probably of gaseous origin, generated during the opening of the device within the lumen of the aortic arch, but the occurrence of solid microemboli due to the interaction of the device with the wall of the aortic arch cannot be ruled out. Unfortunately, differentiation between solid and gaseous microemboli is impossible with current conventional TCD systems like the one used in the present study.
TAVR has been systematically associated with a very high rate (∼70%) of new silent cerebral lesions as evaluated by DW-MRI (Online Table 1) (4–8). The presence of new lesions is usually multiple, with new lesions equally distributed in the 2 cerebral hemispheres and vascular territories. The present study shows that the use of the EED system failed to reduce the presence and number of new ischemic lesions compared with a control group and with historical data. However, the lesion volume was reduced by about half compared with the control group and by more than one-half compared with historical data (Online Table 1). These results are consistent with those associated with the use of another embolic deflector device, the Triguard device (Claret Medical Inc.), which also showed a potential beneficial effect on lesion volume with no effect on the presence and number of lesions (20). In fact, lesion volume has been identified as an important prognostic factor in patients experiencing a stroke (25,26), and recent studies have shown that smaller lesions have a much greater likelihood of being transient than do larger lesions (27,28). Interestingly, the present study showed for the first time that all new lesions seen on DW-MRI that were detected within the first days after TAVR had disappeared 1 month after the procedure, only about 4 weeks after the first DW-MRI examination. This is in accordance with the results of the study of Kahlert et al. (4) showing the disappearance of new lesions seen on DW-MRI in 80% of the patients at 3 months and is probably related to the very small size of the vast majority of these new lesions observed after TAVR.
Whereas the use of the EED device was the procedural variable associated with a lower lesion volume as evaluated by DW-MRI, a history of peripheral vascular disease and stroke/TIA were the baseline factors associated with a greater number and larger volume of new cerebral lesions, respectively. Peripheral vascular disease and previous cerebrovascular disease have been associated with a higher rate of late cerebrovascular events in previous TAVR studies (29,30), but this is the first report highlighting the potential role of these factors in cerebral embolisms occurring early after the procedure. The presence of these factors usually reflects the presence of a higher atherosclerotic burden including the ascending aorta/aortic arch, which indeed may increase the risk of cerebral emboli. In fact, Van Mieghem et al. (22) showed that atheroma accounted for a high proportion of the macroscopic debris captured by a dual carotid filter device during TAVR procedures. Finally, it is well-known that only ∼50% of cerebrovascular events after TAVR occur within the 24 h after the procedure (29), and the possibility of a higher atherosclerotic burden being involved in embolic events in the subacute period (between 24 h and the time of first DW-MRI) after TAVR cannot be excluded.
Several studies have shown the lack of a relationship between new cerebral lesions as assessed by DW-MRI and neurological or cognitive impairment after TAVR (4–8). The patients included in the present study had an extensive and systematic evaluation of neurological and cognitive status, and, as in previous studies, no early deterioration was detected by these examinations despite the presence of new cerebral lesions in all of them. The small size and transient behavior of these new lesions may partially explain these findings, but further studies with a longer follow-up are warranted. The mild improvement in the MoCA test results observed at 30 days after TAVR in the EED group may be related to a “learning effect” from the patients fulfilling the test and will have to be confirmed by future studies.
Although no major differences were observed between the control and EED groups, the results of the comparisons between groups should be interpreted with caution due to both the nonrandomized nature of the study and the small sample size of the control group. These results need to be confirmed by a larger randomized study.
The use of the EED system in TAVR procedures is feasible, easy to deploy, and safe, but is associated with a higher rate of cerebral microemboli as evaluated by TCD. The EED system did not prevent the occurrence and multiplicity of new cerebral lesions seen on DW-MRI, but seemed to be associated with a smaller lesion volume probably related to the deflection of the larger debris, which warrants further confirmation. Finally, all new lesions seen on the DW-MRI examination disappeared within a few weeks and were not associated with any early neurological or cognitive impairment. While waiting for the results of future randomized trials, no recommendation on the systematic use of embolic protection during TAVR procedures can be made on the basis of these findings.
The PROTAVI-C Pilot Study was supported by Edwards Lifesciences. Dr. Rodés-Cabau is a consultant for and has received research grants from Edwards Lifesciences. Dr. Kahlert is a clinical proctor and consultant for Edwards Lifesciences. Dr. Neumann has received institutional grants and speaker honoraria and travel support from Edwards Lifesciences. Dr. Schymik is a proctor for Edwards Lifesciences. Drs. Webb, Brott, and Garami are consultants for Edwards Lifesciences. Dr. Gerosa has received speaker honoraria from St. Jude Medical and HeartWare. Dr. Lefevre is a proctor for Edwards Lifesciences; and has received minor fees from Direct Flow Medical and Symetis. Dr. Plicht has received honoraria from Edwards Lifesciences; and travel support and speaker honoraria from Abbott Vascular Dr. Thomas is a proctor and consultant for Edwards Lifesciences. Dr. Vahanian has received speaker’s fees from Edwards Lifesciences; and is on the Advisory Boards of Abbott and Valtech. Drs. Merioua and Diamond are employees of Edwards Lifesciences. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Abbreviations and Acronyms
- diffusion-weighted magnetic resonance imaging
- Embrella Embolic Deflector
- high-intensity transient signal(s)
- Mini-Mental State Examination
- Montreal Cognitive Assessment
- National Institutes of Health Stroke Scale
- susceptibility-weighted imaging
- transcatheter aortic valve replacement
- transcranial Doppler
- transient ischemic attack
- Received February 16, 2014.
- Revision received April 3, 2014.
- Accepted April 11, 2014.
- American College of Cardiology Foundation
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