Author + information
- Received March 6, 2015
- Revision received May 7, 2015
- Accepted May 8, 2015
- Published online October 1, 2015.
- Dean J. Kereiakes, MD∗,
- Robert W. Yeh, MD, MSc†,‡,
- Joseph M. Massaro, PhD†,§,
- Priscilla Driscoll-Shempp, MBA†,
- Donald E. Cutlip, MD†,‖,
- P. Gabriel Steg, MD¶,#∗∗,
- Anthony H. Gershlick, MBBS††,
- Harald Darius, MD, PhD‡‡,
- Ian T. Meredith, MD, PhD§§,
- John Ormiston, Mb, Chb‖‖,
- Jean-François Tanguay, MD¶¶,
- Stephan Windecker, MD##,
- Kirk N. Garratt, MD, MSc∗∗∗,
- David E. Kandzari, MD†††,
- David P. Lee, MD‡‡‡,
- Daniel I. Simon, MD§§§,
- Adrian Corneliu Iancu, MD‖‖‖,
- Jaroslaw Trebacz, MD, PhD¶¶¶,
- Laura Mauri, MD, MSc†,###∗ (, )
- DAPT Study Investigators
- ∗Christ Hospital Heart and Vascular Center and The Lindner Center for Research and Education, Cincinnati, Ohio
- †Harvard Clinical Research Institute, Boston, Massachusetts
- ‡Massachusetts General Hospital, Boston, Massachusetts
- §Boston University School of Public Health, Boston, Massachusetts
- ‖Beth Israel Deaconess Medical Center, Department of Medicine, Cardiology Division, Boston, Massachusetts
- ¶Université Paris-Diderot, Paris, France, INSERM U-1148, Paris, France
- #Hôpital Bichat, Département Hospitalo-Universitaire FIRE, Assistance Publique–Hôpitaux de Paris, Paris, France
- ∗∗NHLI, Imperial College, Royal Brompton Hospital, London, United Kingdom
- ††Department of Cardiovascular Sciences, University of Leicester and National Institute of Health Research Leicester Cardiovascular Biomedical Research Unit, University Hospitals of Leicester, Leicester, United Kingdom
- ‡‡Vivantes Neukoelln Medical Center, Department of Cardiology, Angiology, Nephrology and Intensive Care Medicine, Berlin, Germany
- §§Monash Heart, Monash Health, Monash University, Victoria, Australia
- ‖‖Mercy Hospital, Auckland, New Zealand
- ¶¶Montreal Heart Institute, Department of Medicine/Division of Interventional Cardiology, Université de Montréal, Department of Medicine, Montreal, Canada
- ##Bern University Hospital, Department of Cardiology, Bern, Switzerland
- ∗∗∗Center for Heart and Vascular Health, Christiana Care, Wilmington, Delaware
- †††Piedmont Heart Institute, Atlanta, Georgia
- ‡‡‡Stanford University, Department of Medicine, Division of Cardiovascular Medicine, Stanford, California
- §§§University Hospitals Case Medical Center, Harrington Heart and Vascular Institute, Cleveland, Ohio
- ‖‖‖Heart Institute, University of Medicine Iuliu Hatieganu, Cluj Napoca, Romania
- ¶¶¶Jan Pawel II Hospital Krakow, Krakow, Poland
- ###Brigham and Women’s Hospital, Division of Cardiovascular Medicine, Boston, Massachusetts
- ↵∗Reprint requests and correspondence:
Dr. Laura Mauri, Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women’s Hospital, 75 Francis Street, Boston, Massachusetts 02115.
Objectives This study sought to compare rates of stent thrombosis and major adverse cardiac and cerebrovascular events (MACCE) (composite of death, myocardial infarction, or stroke) after coronary stenting with drug-eluting stents (DES) versus bare-metal stents (BMS) in patients who participated in the DAPT (Dual Antiplatelet Therapy) study, an international multicenter randomized trial comparing 30 versus 12 months of dual antiplatelet therapy in subjects undergoing coronary stenting with either DES or BMS.
Background Despite antirestenotic efficacy of coronary DES compared with BMS, the relative risk of stent thrombosis and adverse cardiovascular events is unclear. Many clinicians perceive BMS to be associated with fewer adverse ischemic events and to require shorter-duration dual antiplatelet therapy than DES.
Methods Prospective propensity-matched analysis of subjects enrolled into a randomized trial of dual antiplatelet therapy duration was performed. DES- and BMS-treated subjects were propensity-score matched in a many-to-one fashion. The study design was observational for all subjects 0 to 12 months following stenting. A subset of eligible subjects without major ischemic or bleeding events were randomized at 12 months to continued thienopyridine versus placebo; all subjects were followed through 33 months.
Results Among 10,026 propensity-matched subjects, DES-treated subjects (n = 8,308) had a lower rate of stent thrombosis through 33 months compared with BMS-treated subjects (n = 1,718, 1.7% vs. 2.6%; weighted risk difference −1.1%, p = 0.01) and a noninferior rate of MACCE (11.4% vs. 13.2%, respectively, weighted risk difference −1.8%, p = 0.053, noninferiority p < 0.001).
Conclusions DES-treated subjects have long-term rates of stent thrombosis that are lower than BMS-treated subjects. (The Dual Antiplatelet Therapy Study [DAPT study]; NCT00977938)
Although drug-eluting stents (DES) have reduced restenosis when compared with bare-metal stents (BMS) for percutaneous coronary intervention (PCI), the relative hazard for stent thrombosis, a potentially catastrophic event, is uncertain. Previous randomized data indicated a higher risk of stent thrombosis after 1 year with DES (1,2), yet more recent studies suggest a lower risk when compared with BMS (3–5). Whether these findings are applicable to a broader range of clinical indications is unknown.
Although current clinical practice guidelines recommend a minimum of only 1 month of dual antiplatelet therapy after BMS placement following elective PCI (compared with 6 to 12 months for DES) (6,7), patients with acute coronary syndromes (ACS) benefit from 12 months of therapy whether or not PCI with stenting is performed (8). A recent randomized trial (DAPT [Dual Antiplatelet Therapy]) demonstrated a reduction in stent thrombosis and non–stent-related myocardial infarction with thienopyridine therapy beyond 12 months following DES placement (9), and consistent findings among a smaller cohort of BMS-treated subjects, which included an increase in bleeding (10). Because BMS remain a commonly used alternative treatment strategy to DES, particularly for patients who present with ACS or in whom dual antiplatelet therapy has a perceived increased bleeding risk (11,12), we aimed to determine whether the risks of stent thrombosis and non–stent-related adverse cardiovascular events differ for BMS and DES in a powered, prospective, comparative analysis.
The DAPT study design has previously been described (13). This double-blind, international randomized controlled trial (NCT00977938) compared the risks and benefits of continued thienopyridine (clopidogrel or prasugrel) versus placebo, when given in addition to aspirin for the prevention of stent thrombosis or major adverse cardiovascular and cerebrovascular events (MACCE) following coronary stenting with either DES or BMS. The results comparing continued thienopyridine versus placebo (randomized treatment) in each of the DES- and BMS-treated cohorts have been reported separately (9,10). Choice of stent type (DES or BMS) was not randomly assigned, although study inclusion/exclusion criteria (including lack of contraindication to DAPT therapy) were similar for both stent types. A prospective secondary analysis was designed to compare rates of stent thrombosis and MACCE between DES- and BMS-treated subjects who were both eligible to receive DAPT for at least 1 year after the index procedure.
All institutions received approval from their institutional review boards, and each subject provided written informed consent for study participation.
Study objectives and hypothesis
We hypothesized that DES-treated subjects would have stent thrombosis and MACCE (composite of death, myocardial infarction, or stroke) rates that were noninferior to those of BMS-treated subjects through 33 months following the index stent procedure.
Study population and procedures
In brief, subjects who were candidates for dual antiplatelet therapy and who received treatment with either DES or BMS were recruited. Stent treatment was performed according to site standards of care using only Food and Drug Administration–approved DES and BMS devices. DES types included Cypher sirolimus-eluting stent (Cordis, Warren, New Jersey), Endeavor zotarolimus-eluting stent (Medtronic, Santa Rosa, California), TAXUS paclitaxel-eluting stent (Boston Scientific, Marlborough, Massachusetts), and Xience/Promus everolimus-eluting stents (Abbott Vascular, Santa Clara, California, or Boston Scientific). DES-treated subjects were those who received DES at the index procedure, regardless of any other type of stent received at or after the index procedure. BMS-treated subjects were those treated with BMS only, during the index procedure or the following 6 weeks. All subjects signed the consent and were enrolled into the trial within 3 days of the index procedure, and all received open-label aspirin plus thienopyridine (either clopidogrel or prasugrel) for the first 12 months. At 12 months, subjects who were alive and free from myocardial infarction, stroke, repeat coronary revascularization, stent thrombosis, and moderate or severe bleeding and who demonstrated compliance with thienopyridine treatment (defined as having taken 80% to 120% of the drug without an interruption of longer than 14 days) were then eligible for randomization to continued thienopyridine or placebo, and all continued aspirin.
Propensity analysis cohort
Because DES use was more prevalent than BMS use during the time of enrollment, we employed a propensity-matched study design for DES–BMS comparisons rather than randomization to stent type, but required the same inclusion criteria for DES- and BMS-treated subjects (13). The propensity analysis cohort included enrolled subjects (randomized or not). The DAPT study utilized uniform enrollment and randomization criteria, and central endpoint adjudication, yet allowed enrollment via 5 contributing studies (13). Although all randomized subjects were to be followed for 33 months regardless of the study source, in 2 contributing studies subjects who were not randomized were not followed beyond 12 months (Xience V USA DAPT [XIENCE V USA Dual Antiplatelet Therapy (DAPT) Cohort], NCT01106534; EDUCATE [EDUCATE: The MEDTRONIC Endeavor Drug Eluting Stenting: Understanding Care, Antiplatelet Agents and Thrombotic Events], NCT01069003), and in 3 of the contributing studies, subjects were consented for follow-up through 33 months regardless of randomization status (TAXUS Libertē Post Approval Study, NCT00997503; CYPRESS [CYPHER for Evaluating Sustained Safety], NCT00954707; The Dual Antiplatelet Therapy [DAPT] Study, NCT00977938). Subjects enrolled in the latter 3 studies were therefore considered eligible for propensity-matched analysis and evaluation of 0- to 33-month data. The present analysis is restricted to those subjects who reached at least the 30-month follow-up visit window (30 months ± 30 days), or those who had experienced a stent thrombosis or MACCE event before that time, in order to ensure comparable follow-up duration between analysis groups.
The effectiveness endpoints were cumulative incidence of definite/probable stent thrombosis (14) and incidence of MACCE at 0 to 33 months in the propensity-matched DES versus BMS comparison. These events were adjudicated by an independent clinical events committee blinded to treatment assignment and administered by Harvard Clinical Research Institute. An unblinded independent central data monitoring committee oversaw the safety of all subjects.
Due to the nonrandomized nature of DES versus BMS comparisons, differences between DES- and BMS-treated subjects with respect to distribution of baseline characteristics were expected (11,12). To account for this, the primary analysis was conducted on a subsample created by matching BMS- to DES-treated subjects exactly on prevalence of ST-segment elevation myocardial infarction (STEMI) and then matching on remaining baseline characteristics via propensity score, using a caliper width of 0.10. A BMS-treated subject was matched to a variable number of DES-treated subjects without replacement, up to a maximum of 8 (15). The 55 variables used in propensity score matching are listed in Online Figure 1. To assess the adequacy of the match, weighted standardized differences in clinical characteristics between groups were calculated, with absolute differences of <10% considered evidence of balance. Additional secondary events not expected to differ between DES after match and BMS were compared to assess for residual confounding. These included moderate or severe bleeding (GUSTO [Global Utilization of Streptokinase and TPA for Occluded Arteries] classification) (16) at 12 to 30 months, stroke, and non-stent thrombosis–related myocardial infarction.
BMS and weighted DES event rates were calculated, where the DES subject weight was the inverse of the number of DES subjects matched to the same BMS subject. Noninferiority was assessed via risk differences (RDs) using the Nam and Kwon (17) method to account for sample size and for correlation of subjects within each matched cohort (this RD does not necessarily equal the difference between BMS and weighted DES event rates). Noninferiority margins of 0.97% for stent thrombosis and 2.28% for MACCE were used. After noninferiority was met, we subsequently conducted a 2-sided test for difference at the 0.05 significance level. As a secondary analysis, the crude rates of events between groups and propensity-adjusted noninferiority analysis were performed on all eligible DES- and BMS-treated subjects (Online Table 1, Online Methods Section 2.3).
Also, given recent randomized data indicating lower rates of stent thrombosis with newer (everolimus- and zotarolimus-eluting) compared with older (paclitaxel- and sirolimus-eluting) DES, we examined the consistency of the stent thrombosis comparison to BMS by individual DES type (18,19). Finally, we estimated the effect of a possible unmeasured confounder using a Bayesian probabilistic approach based on Monte Carlo (Markov Chain Monte Carlo) sampling (20), and convergence of the Markov Chain Monte Carlo sampler using the Brooks-Gelman-Rubin method (21) assuming: 1) independence of the possible confounder from all measured covariates; 2) an odds ratio on each outcome that could range from one-third to 3; and 3) with prevalence of 30% versus 70% between the 2 treatment groups. All analyses presented were pre-specified except this sensitivity analysis evaluation of consistency of treatment effect across DES types (vs. BMS), and comparison of 12-month outcomes between DES and BMS.
All statistical analyses were conducted at Harvard Clinical Research Institute with SAS software, version 9.2. (SAS Institute, Cary, North Carolina), and for Markov Chain Monte Carlo sampling, JAGS Software version 3.4.0. Noninferiority p values are 1-sided and are considered significant at the 0.025 level; all other p values are 2-sided and considered significant at the 0.05 level.
Enrollment in the DAPT study was conducted between August 2009 and July 2011. A total of 13,257 DES-treated and 2,056 BMS-treated subjects were eligible for propensity matching, with a median follow-up of 990 and 990 days, respectively (Figure 1). Results comparing only randomized subjects (continued thienopyridine or placebo) have been reported separately (9,10).
Although the same inclusion and exclusion criteria were applied to all enrolled subjects, DES- and BMS-treated subjects differed according to clinical and procedural characteristics (Table 1). DES-treated subjects were more likely to have a history of diabetes mellitus, hypertension, previous PCI, and to have longer lesions, with smaller reference vessel diameter, whereas BMS-treated subjects were more likely to present with STEMI, or non-STEMI, and have evidence of thrombus in the treated lesion.
Propensity match DES versus BMS cohort
Propensity-matched cohorts were similar with respect to clinical- and lesion-related variables, with standardized differences within 10% for all match variables (Table 1, Online Figure 1). Importantly, pre-specified risk factors for stent thrombosis were similar between matched DES- and BMS-treated subjects with at least 1 risk factor present in 64.0% and 63.9% respectively (Table 2). Thienopyridine therapy adherence did not differ between matched DES and BMS groups (94.5% vs. 94.4%, p = 0.86) at 12 months follow-up. Among subjects in the propensity-matched sample, 61.4% of DES and 76.0% of BMS were also randomized.
After matching, DES-treated subjects had an incidence of stent thrombosis over the 0- to 33-month period that was lower than that of BMS-treated subjects (1.7% vs. 2.6%, weighted RD: −1.1%, 1-sided upper 97.5% confidence limit −0.27%, noninferiority p < 0.001, p for difference = 0.01) (Table 3, Figure 2A) In addition, DES-treated subjects had an incidence of MACCE that was noninferior to that of BMS-treated subjects (11.4% vs. 13.2%, weighted RD −1.8%, 1-sided upper 97.5% confidence limit 0.03%, noninferiority p < 0.001; p for difference = 0.053). For both stent thrombosis and MACCE, the major portions of this RD were observed within the first 12 months (0 to 12 months, weighted RD: −1.0%, p for difference = 0.002 for stent thrombosis; −1.8% weighted RD, p for difference = 0.011 for MACCE) (Figure 3). A secondary analysis using propensity score adjustment was consistent with the primary analysis (Online Table 1).
Moderate or severe bleeding events were similar for matched DES and BMS (4.0% vs. 3.7% weighted RD: 0.5%, p = 0.32) (Figure 2B) as was the incidence of stroke (1.8% vs. 2.1%, weighted RD: −0.2%, p = 0.49) (Table 3, Figure 2B), and myocardial infarction not related to stent thrombosis (6.0% vs. 6.5%, weighted RD: −0.2%; p = 0.76) (Figure 2B).
Although the RD favoring DES (vs. BMS) for MACCE was similar for each of the 4 separate DES types, the RD favoring DES (vs. BMS) for stent thrombosis was evident for all DES types except the TAXUS paclitaxel-eluting stent (PES) (Figure 4). In a Bayesian sensitivity analysis examining the impact of a plausible unmeasured confounder, we found that the primary conclusions remained robust.
We found that propensity-matched BMS-treated subjects had higher rates of stent thrombosis compared with DES-treated subjects, with the largest portion of RD accrued during the first year after stent treatment. In addition, rates of MACCE were noninferior among DES- versus BMS-treated subjects through 33 months and were significantly lower following DES at 1 year.
Previous randomized trials comparing outcomes following DES or BMS have either utilized older-generation DES (1,2) or, more recently, been limited to subjects with acute myocardial infarction (5). Unfortunately, dual antiplatelet therapy duration and adherence have not been uniform across stent types in many of these studies. Similarly, in retrospective observational studies, important variables related to dual antiplatelet therapy adherence and/or previous bleeding history are often not included and may confound comparisons between stent types. In this regard, the DAPT study was designed to include a prospective propensity-matched comparison of DES- and BMS-treated subjects with uniform inclusion criteria (specifically requiring subjects to be eligible for continued thienopyridine therapy), uniform clinical follow-up, and blinded adjudication of endpoints by a central independent clinical events committee (13). Furthermore, among both DES and BMS propensity-matched subjects who were randomized, study medication adherence was identical. Indeed, the similarities in bleeding events, stroke rates, and rates of myocardial infarction not related to stent thrombosis (DES vs. BMS) in the propensity-matched analysis suggest lack of residual confounding. Lastly, the analysis of individual DES types with their matched BMS-treated cohorts provides unique insights into a differential risk of stent thrombosis. Although DES are often aggregated for purpose of analysis, a differential risk for stent thrombosis (lack of RD favoring DES) was evident only for the PES. All other DES included in analysis had lower rates of stent thrombosis compared with BMS. Of note, a higher rate of stent thrombosis has been observed following PES in pooled patient-level data from randomized comparative trials with BMS and appears consistent with the present observation (22). Additionally, the present observation is supported by the facts that: 1) stent thrombosis rates for the sirolimus- and PES and BMS included in propensity match analysis are similar to those reported for similar stent types in previous randomized trials (1,2); and 2) the current results are consistent with recent randomized trial data comparing DES with BMS in subjects with acute myocardial infarction that demonstrate a reduction in stent thrombosis risk for newer DES (5). The observation that all 4 DES types (including PES) have a lower risk for MACCE than their matched BMS cohorts suggests that stent thrombosis is not the sole or main driver of MACCE and that restenosis benefit, common to all 4 DES types (vs. BMS), may be operative. Indeed, BMS-treated subjects accrue both target lesion (stent) related events in ≥2%/year (23) and non-target lesion/vessel events in ≥5% per year following stent deployment (24,25). Atherothrombotic events following BMS may be due to lack of healing/uncovered stent struts, neoatherosclerosis (26), restenosis (27), or disease progression outside the stent, in other regions or vessels. The fact that the major portion of RD between DES and BMS is accrued early, within 12 months, would be consistent both with the known differential occurrence of restenosis between DES and BMS in this time frame as well as the premise that restenosis may not be benign (27).
Although MACCE is influenced by events outside of stent thrombosis, the rates of stent thrombosis and MACCE were both directionally consistent in favor of DES. Comparison of DES with BMS did conclude noninferiority on MACCE as primarily designed, yet did not reach statistical significant difference favoring DES. Nonetheless, the absolute reduction in rates of MACCE associated with DES compared with BMS (1.8 percentage point reduction) was similar or greater in magnitude to that of stent thrombosis (1.1 percentage point reduction). The lack of statistical significance on the MACCE is, therefore, a reflection that only 20% of the MACCE were stent related. Other, more common MACCE did not differ (and would not be expected to differ) between stent types (e.g., myocardial infarction not related to stent thrombosis).
There are several limitations of this propensity-matched analysis. First, although propensity score matching was used to overcome confounding related to measured factors, the potential presence of unrecognized confounders remains a limitation of this nonrandomized analysis. However, the lack of differences in bleeding (not expected to differ between stent types), stroke, and myocardial infarction not related to stent thrombosis provide reassurance that residual confounding is limited. Second, although propensity matching is a preferred method to reduce selection bias, inference is limited to the population selected for the match. Although the majority of enrolled BMS-treated subjects were used for the match (84%), a lesser proportion of DES-treated subjects (63%) were selected, and these appear to represent a group with lower lesion complexity and diabetes prevalence, but higher frequency of STEMI indication for revascularization than the overall DAPT study DES-treated population. Third, although we performed a sensitivity analysis to determine the consistency of the DES versus BMS comparison, we did not compare different types of DES to one another, as such comparisons were not randomized, pre-specified, or powered.
DES were associated with a lower long-term rate of stent thrombosis and a noninferior rate of MACCE compared with BMS, among subjects eligible for treatment with continued thienopyridine and aspirin for at least 1 year.
WHAT IS KNOWN? BMS are a commonly used alternative treatment strategy to DES, particularly for patients who present with acute coronary syndrome or in whom dual antiplatelet therapy has increased bleeding risk. BMS are perceived to be associated with fewer adverse ischemic events and to require shorter-duration dual antiplatelet therapy than DES.
WHAT IS NEW? A prospective, powered, propensity-match analysis comparing BMS and DES treated patients enrolled into the DAPT study demonstrated BMS to have increased risk for stent thrombosis during 0 to 33 months following stent deployment with the major portion of risk difference (vs. DES) being present in the first 12 months.
WHAT IS NEXT? This study contributes to the growing body of evidence regarding comparative rates of stent thrombosis and other adverse ischemic events (BMS vs. DES), which may inform future guidelines for both stent use as well as duration of dual antiplatelet therapy.
The authors thank the other investigators, the staff, and the participants of the DAPT study for their valuable contributions. They also wish to acknowledge Joanna Suomi for assistance editing and formatting the manuscript, and Wen-Hua Hsieh for assistance with statistical analysis.
This research was sponsored by Harvard Clinical Research Institute and funded by Abbott, Boston Scientific, Cordis, Medtronic, Bristol-Myers Squibb/Sanofi Pharmaceuticals Partnership, Eli Lilly and Company, and Daiichi Sankyo, and the U.S. Department of Health and Human Services (grant 1RO1FD003870-01). Dr. Yeh is on an Advisory Board of Abbott Vascular; and is a consultant for Gilead Sciences and Merck. Dr. Massaro received funding from Harvard Clinical Research Institute for statistical services for the manuscript. Dr. Cutlip received research funding (paid to his institution) from Medtronic, Boston Scientific, and Celonov. Dr. Steg has received research funding from Sanofi and Servier; is a consultant for Amarin, AstraZeneca, Bayer, Boehringer Ingelheim, Bristol-Myers Squibb, CSL-Behring, Daiichi-Sankyo-Lilly, GlaxoSmithKline, Janssen, Medtronic, Merck-Sharpe Dohme, Novartis, Pfizer, Regeneron, Sanofi, Servier, and The Medicines Company; and is a stockholder in Aterovax. Dr. Gershlick has received lecture fees and travel bursaries from Medtronic, The Medicines Company, AstraZeneca, and Abbott Vascular. Dr. Meredith is an international proctor for the Lotus Valve for Boston Scientific; and is on the Scientific Advisory Boards of Boston Scientific and Medtronic. Dr. Ormiston is on the advisory board of and receives minor honoraria from Boston Scientific. Dr. Tanguay has received consultant’s fees/honoraria and research funding from Abbott Vascular, AstraZeneca, and Eli Lily and Company. Dr. Windecker has received research funding (to his institution) from Abbott, Biotronik, Boston Scientific, Edwards Lifesciences, Medtronic, The Medicines Company, and St. Jude Medical; and has received speaker’s fees from AstraZeneca, Eli Lilly and Company, Abbott, Biotronik, Boston Scientific, Medtronic, and Bayer. Dr. Garratt is a consultant for Boston Scientific, Daiichi-Sankyo/Lilly, The Medicines Company, AstraZeneca, Abbott Vascular; and receives research support from Abbott Vascular, CeloNova; and has equity in Infarct Reduction Technologies, Guided Delivery Systems, and Arstasis. Dr. Kandzari has received research/grant support from Medtronic, Boston Scientific, and Biotronik; and has received consulting honoraria from Medtronic and Boston Scientific. Dr. Lee is a consultant to and receives research funding from Boston Scientific. Dr. Simon is on the Advisory Board of Medtronic. Dr. Mauri has received grants (to her institution) from Abbott, Boston Scientific, Cordis, Medtronic, Eli Lilly and Company, Daiichi Sankyo, Sanofi, Bristol-Myers Squibb, and Biotronik; and is a consultant for Medtronic, Eli Lilly and Company, Boehringer Ingelheim, AstraZeneca, and Biotronik. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Abbreviations and Acronyms
- acute coronary syndromes
- bare-metal stent(s)
- dual antiplatelet therapy
- drug-eluting stent(s)
- major adverse cardiovascular and cerebrovascular events
- percutaneous coronary intervention
- paclitaxel-eluting stent(s)
- risk difference
- ST-segment elevation myocardial infarction
- Received March 6, 2015.
- Revision received May 7, 2015.
- Accepted May 8, 2015.
- 2015 American College of Cardiology Foundation
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