Author + information
- Received January 21, 2014
- Revision received May 20, 2014
- Accepted June 2, 2014
- Published online December 1, 2014.
- Yoshinobu Onuma, MD∗,
- Patrick W. Serruys, MD, PhD∗∗ (, )
- Takashi Muramatsu, MD, PhD∗,
- Shimpei Nakatani, MD∗,
- Robert-Jan van Geuns, MD, PhD∗,
- Bernard de Bruyne, MD, PhD†,
- Dariusz Dudek, MD‡,
- Evald Christiansen, MD§,
- Pieter C. Smits, MD, PhD‖,
- Bernard Chevalier, MD¶,
- Dougal McClean, MD#,
- Jacques Koolen, MD, PhD∗∗,
- Stephan Windecker, MD††,
- Robert Whitbourn, MD‡‡,
- Ian Meredith, MD, PhD§§,
- Hector M. Garcia-Garcia, MD, PhD‖‖,
- Susan Veldhof, RN¶¶,
- Richard Rapoza, PhD## and
- John A. Ormiston, MBChB, PhD∗∗∗
- ∗Department of Interventional Cardiology, ThoraxCenter, Erasmus Medical Center, Rotterdam, the Netherlands
- †Department of Interventional Cardiology, Cardiovascular Center, Aalst, Belgium
- ‡Department of Cardiology and Cardiovascular Interventions, Jagiellonian University, Krakow, Poland
- §Department of Cardiology, Skejby Sygehus University Hospital, Aarhus, Denmark
- ‖Department of Interventional Cardiology, Maasstad Hospital, Rotterdam, the Netherlands
- ¶Institut Cardiovasculaire Paris Sud, Institut Jacques Cartier, Massy, France
- #Department of Interventional Cardiology, Christchurch Hospital, Christchurch, New Zealand
- ∗∗Department of Interventional Cardiology, Catharina Hospital, Eindhoven, the Netherlands
- ††Department of Interventional Cardiology, Bern University Hospital, Bern, Switzerland
- ‡‡Cardiac Investigation Unit, St. Vincents Hospital, Fitzroy, Australia
- §§Department of Medicine, Cardiology, Monash Cardiovascular Research Centre, Melbourne, Australia
- ‖‖Department of Interventional Cardiology, Cardialysis, Rotterdam, the Netherlands
- ¶¶Department of Clinical Research, Abbott Vascular, Diegem, Belgium
- ##Research and Development, Abbott Vascular, Santa Clara, California
- ∗∗∗Department of Interventional Cardiology, Auckland City Hospital, Auckland, New Zealand
- ↵∗Reprint requests and correspondence:
Prof. Patrick W. Serruys, ThoraxCenter, Ba-583, ‘s Gravendijkwal 230, 3015 CE Rotterdam, the Netherlands.
Objectives This study sought to describe the frequency and clinical impact of acute scaffold disruption and late strut discontinuity of the second-generation Absorb bioresorbable polymeric vascular scaffolds (Absorb BVS, Abbott Vascular, Santa Clara, California) in the ABSORB (A Clinical Evaluation of the Bioabsorbable Everolimus Eluting Coronary Stent System in the Treatment of Patients With De Novo Native Coronary Artery Lesions) cohort B study by optical coherence tomography (OCT) post-procedure and at 6, 12, 24, and 36 months.
Background Fully bioresorbable scaffolds are a novel approach to treatment for coronary narrowing that provides transient vessel support with drug delivery capability without the long-term limitations of metallic drug-eluting stents. However, a potential drawback of the bioresorbable scaffold is the potential for disruption of the strut network when overexpanded. Conversely, the structural discontinuity of the polymeric struts at a late stage is a biologically programmed fate of the scaffold during the course of bioresorption.
Methods The ABSORB cohort B trial is a multicenter single-arm trial assessing the safety and performance of the Absorb BVS in the treatment of 101 patients with de novo native coronary artery lesions. The current analysis included 51 patients with 143 OCT pullbacks who underwent OCT at baseline and follow-up. The presence of acute disruption or late discontinuities was diagnosed by the presence on OCT of stacked, overhung struts or isolated intraluminal struts disconnected from the expected circularity of the device.
Results Of 51 patients with OCT imaging post-procedure, acute scaffold disruption was observed in 2 patients (3.9%), which could be related to overexpansion of the scaffold at the time of implantation. One patient had a target lesion revascularization that was presumably related to the disruption. Of 49 patients without acute disruption, late discontinuities were observed in 21 patients. There were no major adverse cardiac events associated with this finding except for 1 patient who had a non-ischemia-driven target lesion revascularization.
Conclusions Acute scaffold disruption is a rare iatrogenic phenomenon that has been anecdotally associated with anginal symptoms, whereas late strut discontinuity is observed in approximately 40% of patients and could be viewed as a serendipitous OCT finding of a normal bioresorption process without clinical implications. (ABSORB Clinical Investigation, Cohort B [ABSORB B]; NCT00856856)
Fully bioresorbable scaffolds are a novel approach for treatment of coronary narrowing that provides transient vessel support with drug delivery capability without the long-term limitations of metallic drug-eluting stents, such as permanent caging with either outward bulging (evagination) of the luminal wall outside of the “cage,” or intracage neoatherosclerosis (1,2). By freeing the coronary artery from metallic caging, the vessel thereby recovers its pulsatility, and vasomotion becomes again responsive without any constraint to the biochemical milieu, the endothelial shear stress, and the physiological cyclic strain (3,4). The technology has the potential to overcome many of the safety concerns associated with metallic drug-eluting stents and could possibly even provide further clinical benefit (5).
In the ABSORB (A Clinical Evaluation of the Bioabsorbable Everolimus Eluting Coronary Stent System in the Treatment of Patients With De Novo Native Coronary Artery Lesions) cohort A trial, the first generation of the Absorb everolimus-eluting fully bioresorbable polymeric vascular scaffolds (Absorb BVS, Abbott Vascular, Santa Clara, California) showed a low event rate with a late lumen enlargement from 6 months to 2 years. At 5 years, the absence of metallic material allowed the noninvasive anatomical as well as functional assessment by multislice computed tomography of arteries previously treated with a bioresorbable scaffold (4,6,7). In the subsequent ABSORB cohort B trial, the second generation of the Absorb BVS showed a low late loss of 0.19 mm without any reduction of the scaffold area at 6 months by intravascular ultrasound (IVUS) and optical coherence tomography (OCT) (8,9). At 12-month follow-up, the angiographic late loss was 0.27 ± 0.32 mm, with an unchanged scaffold area. In addition, vasomotion induced by ergonovine and acetylcholine followed by intracoronary nitrate became detectable again, suggesting that the scaffolds mechanical integrity had subsided. At 24-month follow-up, the angiographic late loss remained stable (0.27 ± 0.20 mm) with a late enlargement of the scaffold that compensated for the neointimal growth as detected by OCT (10–12).
However, a potential drawback of this new technology is the risk for disruption of the strut network when it is overexpanded. Historically, the phenomenon was documented for the first time in an anecdotal case from the ABSORB cohort A trial. A 3.0-mm scaffold was overexpanded with a 3.5-mm balloon, resulting in scaffold disruption as documented by OCT (7). Due to the recurrence of anginal symptoms at 40 days, this patient underwent repeat revascularization despite an angiographically nonsignificant stenosis by quantitative coronary angiography (QCA) (diameter stenosis of 42%) (13). It is important that this acute mechanical disruption, is distinguished from the structural discontinuity of the polymeric struts at a later stage, a biologically programmed process during the course of bioresorption (13–15).
The purpose of the present report therefore is to describe the frequency and clinical impact of acute scaffold disruption and late strut discontinuity of the second-generation Absorb BVS in the ABSORB cohort B study. The frequency and impact are documented in a serial or nonserial manner by OCT post-procedure and at 6, 12, 24, and 36 months.
The ABSORB cohort B trial is a multicenter single-arm trial assessing the safety and performance of the second-generation Absorb BVS in the treatment of 101 patients with a maximum of 2 de novo native coronary artery lesions. The inclusion and exclusion criteria have been described previously (8,12). The first 45 patients (B1) had an invasive imaging follow-up at 6 and 24 months, whereas the latter 56 patients (B2) had an imaging follow-up at 12 months and at 36 months.
The current analysis included 51 patients who underwent OCT at baseline as an optional investigation. The details of the follow-up are presented in Online Figure 1. In total, the analysis included 143 OCT pullbacks performed at baseline and follow-up. The details of the study device and study procedure are described in the Online Appendix.
Optical coherence tomography
As an optional investigation, intravascular OCT imaging using either time-domain OCT (M3 system, LightLab Imaging, Westford, Massachusetts) or frequency-domain OCT (C7XR system, LightLab Imaging) was performed at baseline and at follow-up (15–19). The OCT measurements were performed with proprietary software for offline analysis (LightLab Imaging). To search for the presence of scaffold disruption, the analysis of continuous cross sections was performed in all frames within the treated segment. The main quantitative measurements (strut core area, strut area, lumen area, scaffold area, incomplete scaffold apposition area, and neointimal area) required different analysis rules than metallic stents (8,9,12,20). The thickness of the neointimal coverage was measured for every strut between the abluminal side of the strut core and the lumen. Because the strut thickness is approximately 150 μm, the strut was considered as covered whenever the thickness of the coverage was above this threshold value (8,12).
Definition of acute scaffold disruption or late discontinuity on OCT
Ex vivo experiments were performed to identify OCT findings of disrupted struts. In a silicon phantom with a diameter of 3.5 mm, a 3.0-mm Absorb BVS (maximal labeled diameter expansion of 3.5 mm) was deployed and expanded with a 4.0-mm compliant balloon (21). After disrupting the scaffold, OCT pullback was performed and analyzed (Figure 1). Acute (peri-procedural) structural scaffold disruption or late strut discontinuities were diagnosed by at least 1 of the following: 1) if 2 struts overhung each other in the same angular sector of the lumen perimeter, without close contact (overhung strut) or with contact (stacked strut) in at least 1 cross section; or 2) if there was isolated (malapposed) struts that could not be integrated in the expected circularity of the device in at least 1 cross section. “Isolated strut” was defined as a strut located at a distance from the vessel wall (>1/3 of span between the center of gravity and the luminal border) (8,12,21).
If acute scaffold disruption was persistently observed at follow-up, the case was classified as persistent scaffold disruption. Late discontinuity at follow-up was diagnosed when no initial procedural scaffold disruption could be documented post-procedure. In the case of iterative follow-up, late discontinuities could be classified as resolved or persistent (Table 1). Using the new criteria, the OCT image was reanalyzed for the presence of acute disruption or late discontinuities. The details of 3-dimensional OCT analysis, IVUS grayscale analysis, and definition of clinical events are described in the Online Appendix.
Continuous variables are presented as mean ± SD, whereas categorical variables are expressed as percent. Categorical variables were compared using Pearson chi-square test or Fisher exact test and continuous variables were compared using F test for analysis of variance. As no formal hypothesis testing was planned for assessing the success of the study, no statistical adjustment was applied. The p values presented are exploratory analyses only and therefore should be interpreted cautiously. Statistical analysis was performed with SPSS (version 20 for Macintosh, SPSS Inc., Chicago, Illinois).
Baseline characteristics are presented in Online Table 1. All patients received 1 Absorb scaffold except for 1 patient who received 2. Post-dilation was performed in 57% of lesions.
Acute procedural scaffold disruption at baseline
Of 51 patients with OCT imaging post-procedure (52 scaffolded lesions), acute scaffold disruption was observed in 2 patients (3.9%). Table 2 tabulates the details of the procedures and imaging by OCT, IVUS, and QCA. Scaffold disruption at baseline was detectable on IVUS in 1 of these 2 cases.
Notably, 1 patient had a target lesion revascularization (TLR) presumably associated with the acute disruption and its worsening at 1 month. In this case (Figure 2), an Absorb BVS 3.0 mm × 18 mm scaffold was implanted in an obtuse marginal branch with a reference diameter of 3.26 mm (13). After post-dilation with a 3.25-mm noncompliant balloon at 24 atm, malapposition remained at the proximal part of the scaffold on OCT. To correct the malapposition, an additional post-dilation was performed with a compliant 3.5-mm balloon at 16 atm (expected diameter, approximately 4.0 mm). The repeat OCT and IVUS demonstrated acute scaffold disruption in the scaffolded segment. At 1 month, the patient experienced 5 episodes of recurrent angina at rest. Despite the fact that the exercise tolerance test was negative, the patient underwent recatheterization because of persisting symptoms. The angiography revealed a patent scaffold segment with a TIMI (Thrombolysis In Myocardial Infarction) flow grade 3; however, OCT, compared with baseline images, showed a deterioration of scaffold disruption. There was no tissue observed around the struts. A metallic Xience V stent (Abbott Vascular) was placed inside the Absorb scaffold, which eliminated the symptoms. After this nonischemic TLR, there was a rise in troponin (0.09 μl/g with an upper limit of normal of 0.03 μl/g), which would be adjudicated as a non–Q-wave myocardial infarction according to the Academic Research Consortium definition.
In the second case, a 3.0-mm scaffold was implanted in a small vessel with a reference vessel diameter of 2.24 mm followed by a post-dilation with a 3.0-mm noncompliant balloon at 24 atm. Immediately after procedure, overhung struts were observed on OCT at baseline in 5 cross sections (Figure 3). According to the protocol, this asymptomatic patient underwent repeat angiography at 6 months with IVUS and OCT imaging. After the IVUS acquisition, the operator experienced difficulty recrossing the scaffold segment with the OCT catheter. After rewiring the scaffolded vessel, OCT was successfully acquired, which demonstrated extremely malapposed struts close to the OCT catheter (see the noncircularity of struts). The irregularity of the strut structure might have been caused by advancing the wire outside of the scaffold and pushing the OCT catheter under the abluminal side of the struts. At 2-year imaging follow-up, OCT revealed detached struts densely encapsulated with homogeneous tissue, forming an arch attached proximally and distally to the vessel wall. On IVUS, it was documented as a dissection in the scaffold segment. Despite the abnormal imaging findings, the patient remains asymptomatic to date.
Late strut discontinuities at follow-up
Follow-up OCT images were obtained in all but 2 patients (at 6 months, 1 year, 2 years, or 3 years) (Online Figure 1). Of 50 scaffolded lesions (49 patients) without acute scaffold disruption, late acquired structural discontinuity was observed in 21 scaffolds (n = 21, 42%). The cases are detailed in Online Table 2 and Figure 4. There were no differences in baseline characteristics between patients with or without late discontinuities except for the pre-procedural minimal lumen diameter and diameter stenosis, which could be a play of chance. On IVUS, late discontinuities were detected only in 3 cases.
In the series with 6- and 24-month follow-up, late discontinuities were observed in 3 cases at 6 months and were persistently observed at the second follow-up at 24 months (Online Figure 2). In 8 cases, late discontinuities were observed only at 2 years.
In the series with 1- and 3-year follow-up, late structural discontinuities were observed at 1 year in 8 cases. Two discontinuities were persistently observed in serial OCT images at 3 years, whereas in 3 cases, discontinuities were resolved at 3 years. In 2 cases, no follow-up was performed after 1 year, so the outcomes of these discontinuities remained unknown. One patient underwent unscheduled OCT at 2 years, revealing persistent discontinuities. Two scaffolds had late structural discontinuities only at 3 years. Figure 4 illustrates the complex timing and outcome of these serial or nonserial investigations.
There were no events associated with these late discontinuities observed on OCT at follow-up except for 1 patient who underwent a non-ischemia-driven repeat TLR (Online Figure 3). The 45-year-old man received a 3.0 mm × 18 mm Absorb BVS scaffold in the mid–left anterior descending artery. Post-procedural OCT did not show malapposition. At 1 year, the patient underwent a planned repeat angiography, which showed an enlargement of the lumen. OCT showed late discontinuity with malapposed overhanging struts over a length of 4 mm. Due to the pronounced malapposition, clopidogrel treatment was continued after 1 year. The patient had stable angina of Canadian Cardiovascular Society class 2 to 3 and underwent a repeat angiography on day 722. On angiography, the lumen was found to become ectatic (QCA maximal diameter: 3.6 mm) without any significant stenosis in the scaffolded segment, whereas on OCT, 1 ring of scaffold showed persistent discontinuity with malapposition. Despite the absence of evidence of ischemia, it was thought that the anginal symptoms were somewhat related to the malapposition. A 3.0 mm × 28 mm metallic Xience Prime stent was placed in the scaffolded segment. After post-dilation with a 3.5-mm balloon, retention of angiographic contrast medium was observed along the new stent and diagnosed as malapposed struts on OCT. The segment was further dilated with a 4.5-mm balloon. Following the dilation, contrast retention was resolved.
The main findings of the current analysis are the following: 1) acute disruption induced by the procedure was observed in 2 of 51 patients (52 pullbacks, 3.9%), with 1 patient, it was presumably related to the TLR; 2) late resorption-related discontinuity was observed in 21 patients with 1, presumably nonrelated, non-ischemia-driven TLR; 3) QCA was unable to detect these structural changes, whereas IVUS was able to detect some of the major acute disruptions/late discontinuities (4 of 23 cases).
Acute scaffold disruption and sizing
Although both acute scaffold disruption and late discontinuity can be diagnosed as stacked/overhung struts or isolated struts on OCT, the 2 phenomena should be categorized differently: 1 as an accidental occurrence; and 1 as a programmed biological process. At the time of implantation, the bioresorption process does not influence the mechanical integrity of the scaffold at all, so that any disrupted struts observed immediately after the procedure are the result of a mechanical disruption caused by extreme overexpansion of the scaffold. The radial force of the polymeric device is comparable with a metallic scaffold as long as the device is expanded within certain restricted limits; however, the mechanical force yields quickly if expanded over the pre-determined boundary of expansion.
The tensile strength of the poly-l-lactide is 50 to 70 MPa, whereas that of cobalt-chrome alloy or stainless steel is in the range of 668 to 1,449 MPa. Percent of elongation at break is 2% to 10 % for poly-l-lactide, whereas it is more than 40% for cobalt chromium or stainless steel. The expansion range of the polymeric device is therefore inherently limited (12).
The relationship between the diameter of expansion and likelihood of device disruption was investigated ex vivo in 30,000 scaffolds. After inflating a 3.0-mm balloon in a phantom, the presence of acute scaffold disruption was examined. Up to a size of 3.65 mm, no scaffold disruption was observed. However, when a 3.0-mm scaffold was expanded to 3.70, 3.76, 3.83, and 3.92 mm in diameter, the likelihood of acute disruption increased by 3%, 24%, 58%, and 80%. The expansion capability is, however, one of multiple attributes related to the performance of the scaffold, such as radial strength, vessel support time, flexibility, fatigue, and acute recoil. To ensure an optimal performance of the drug-eluting scaffold, the scaffold should be expanded within its indicated range, so that the scaffold will not become disrupted and will still perform as expected. This expansion capacity should also be maintained during the entire shelf life of the device. The manufacturer accordingly recommends the maximal limits of expansion of the 3.0-mm device examined in this study as 3.5 mm.
To prevent overexpansion, it is important to implant the scaffold in a properly sized vessel using angiography or intravascular imaging in order to avoid severe mismatch between the device and vessel size. In a previously published study, QCA was used to detect the maximal diameter (Dmax) of the vessel in the landing zone proximal or distal to the stenosis. Three vessel-size groups according to Dmax (small: <2.5 mm, middle: 2.5 to 3.3 mm, large: >3.3 mm) were investigated by OCT post-procedure. The small vessel group presented with a higher percent of lesions with any degree of edge dissections visually detected on OCT (small: 61.5% vs. middle: 33.3% vs. large: 11.1%; p = 0.05). Lesions with >5% of incomplete scaffold apposition were significantly higher in the large vessel group with a Dmax >3.3 mm (7.7% vs. 36.7% vs. 66.7%; p = 0.02). Thus, sizing according to Dmax seems to be useful in optimizing the acute OCT outcomes (22).
Although the incidence of acute scaffold disruption is low (2 cases, 3.9%), 1 of these 2 cases was associated with a clinical event of non-ischemia-driven TLR at 1 month, followed by a rise of troponin after repeat intervention. On OCT, from baseline to 1 month, more struts became malapposed and isolated toward the lumen center, suggesting that the degree of scaffold disruption may have become worse over time. Although the presence of ischemia was not proven, the fact that chest pain vanished after repeat intervention suggests a relationship between the acute disruption and the symptoms. This could be due to the vasomotion disturbance triggered by the intraluminal presence of struts, or due to small thrombus formation around the malapposed struts with subsequent embolization. Both explanations are hypothetical as objective proof was not observed. Although ex vivo analysis showed that the thrombogenicity of polymeric struts is less than that of bare-metal struts, the possibility exists that a small thrombus could form around the isolated and malapposed struts. This is also suggested by 1 of the cases of acute disruption in cohort A of the ABSORB trial. The patient presented with chest pain at rest with OCT showing intraluminal masses with irregular contour around the disrupted strut (7).
Late, resorption-related structural discontinuities
The hydrolysis of polymeric strut starts immediately after the device comes in contact with water, whereas the decrease in mechanical support of the scaffold starts approximately 6 months after implantation. The process of restenosis is a time-limited phenomenon due to negative remodeling of the vessel and neointimal hyperplasia inside of the stent, which occurs 3 to 6 months after implantation in the coronary artery. During this time, the maintenance of the mechanical structure as well as the elution of everolimus is critical to prevent restenosis. Beyond this critical period, however, the mechanical support of the scaffold, as well as the active neointimal inhibition are no longer necessary, because the restenosis process is no longer ongoing. In fact, after 6 months, the polymeric scaffold starts losing its mechanical integrity and that can lead to expected late discontinuity. Figure 5 shows the progression of structural disintegration over time due to bioresorption. The spread-out view showed that post-procedure, the scaffold consisted of 19 rings connected to each other with 3 links, as manufactured. As shown in Figure 5, at 1 year, mechanical integrity had partially subsided and the distal part of the scaffold has started to dismantle, which corresponds to late discontinuities of individual struts. This phenomenon is considered benign because the struts are mostly covered at 1 and 3 years.
Among the 21 cases with late strut discontinuity, 20 cases had no clinical consequences during the entire follow-up. In 1 case, non-ischemia-driven- TLR with a metallic stent was performed at 2 years to remediate an abnormal outward bulging of the vessel wall, resulting in major malapposition and late strut discontinuities already detected by OCT at 1-year follow-up. Although a huge malapposition could increase a risk of scaffold thrombosis, the microscopic resolution of OCT imaging may have triggered a new kind of “occulo-OCT” reflex because, on angiography, this was inconspicuous.
Single or serial observation
In the current analysis, post-procedural OCT was available in all cases, which enabled us to distinguish the persistent acute disruption from late discontinuities. Whenever OCT was not available post-procedure, differentiation of persistent acute disruption from late discontinuities was speculative (Table 1). Stacked, overhung, or isolated malapposed struts with circular structure that were observed later than 6 months, especially when covered and apposed, could likely be attributed to late resorption-related discontinuities.
OCT and IVUS
The current analysis showed that IVUS is less sensitive than OCT in the detection of acute strut disruption or late strut discontinuity. IVUS was able to detect major disruptions or discontinuities, but overlooked some disruptions or could not differentiate them from malapposition (23). Because acute scaffold disruption could be associated with anginal symptoms, OCT might be recommended as an additional diagnostic technique when the scaffolded vessel angiographically appears patent, and oversizing and/or overexpansion is suspected.
Imaging procedure at follow-up
The anecdotal cases presented in this report highlight the fact that imaging procedures at follow-up can worsen pre-existing scaffold disruptions at late follow-up. The mechanical strength of the device starts to subside 6 months after implantation so that intravascular imaging follow-up occurring later than 6 months post-implantation has to be performed cautiously. Introducing a guidewire into the scaffolded segment should be carried out carefully in cases of known malapposition post-procedure. The operator should not reinvestigate the vessel if any resistance in advancing the imaging device into the scaffolded segment is experienced.
The current study has a limited number of patients who underwent OCT at the different time points. However, it is the largest series of patients investigated with serial OCT over a follow-up period of 3 years. The “snapshot” nature of the OCT investigations precludes any dynamic interpretation of the ongoing and intended mechanical dismantling of the scaffold. For instance, the longitudinal polymeric links rather than the rings may be the first structures to degrade and the longitudinal mechanical stress might be more intense along the outer epicardial border of the vessel rather than at the inner myocardial side. These speculations should be the focus of further preclinical investigations involving other techniques such as a permanently implanted sono-micrometer. The OCT criteria used in this analysis (stacked struts or overhung struts) will not be applicable to the overlapped segment, because these strut dispositions are normally seen in such segments.
Acute scaffold disruptions are rare procedural phenomena that have been anecdotally associated with angina symptoms, although pathological correlation between disrupted struts and angina remain elusive. They can be generally avoided by respecting the stated expansion limits for each scaffold diameter. In case of recurrent angina without angiographic stenosis, OCT might be recommended as an additional diagnostic technique, whereas the imaging follow-up later than 6 months needs a careful advance of the imaging device. Late discontinuities as a result of the expected resorption process are observed in approximately 40% of patients who experienced, at the time of follow-up, the struts fully covered or embedded in tissue and should be viewed as a serendipitous OCT finding of a normal bioresorption process without clinical implication.
This study was sponsored by Abbott Vascular. Dr. van Geuns has consulted for Abbott Vascular. Dr. Dudek has received consulting and lecture fees from Abbott, Adamed, Adyton Medical Polska, Abiomed Europe, AstraZeneca, Biotronik, Balton, Bayer, BBraun, BioMatrix, Boston Scientific, Boehringer Ingleheim, Bracco, Bristol-Myers Squibb, Comesa Polska, Cordis, Cook, Covidien Polska Sp. z o. o., DRG MedTek, Eli Lilly, EuroCor, Hammermed, GE Healthcare, GlaxoSmithKline, Inspire-MD, Iroko Cardio International, Medianet Sp. z o. o., Medtronic, Medicines Company, Meril Life Sciences, MSD, Orbus-Neich, Pfizer Inc., Possis, ProCardia Medical, Promed, REVA Medical, Sanofi-Aventis, Siemens, Solvay, Stentys, St. Jude Medical, Terumo, Tyco, and Volcano. Dr. Smits has received speaking and travel fees from Abbott Vascular; and research grants from Abbott Vascular, St. Jude Medical, and Terumo. Dr. Chevalier has consulted for Abbott Vascular. Dr. Whitbourn has been awarded institutional grants from Abbott Vascular. Ms. Veldhof and Dr. Rapoza are full-time employees of Abbott Vascular. Dr. Ormiston has served on the advisory boards of Abbott Vascular and Boston Scientific; and has received honoraria from Abbott Vascular and Boston Scientific. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose. Drs. Ormiston and Serruys are coprincipal and principal investigators. The other investigators are listed as coauthors according to the recruitment of their respective centers.
- Abbreviations and Acronyms
- bioresorbable polymeric vascular scaffolds
- maximum diameter
- intravascular ultrasound
- optical coherence tomography
- quantitative coronary angiography
- target lesion revascularization
- Received January 21, 2014.
- Revision received May 20, 2014.
- Accepted June 2, 2014.
- American College of Cardiology Foundation
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