Author + information
- Received October 14, 2013
- Revision received October 22, 2013
- Accepted October 22, 2013
- Published online February 25, 2014.
- Philippe Généreux, MD∗,†,‡,
- Gregg W. Stone, MD∗,†,
- Robert A. Harrington, MD§,
- C. Michael Gibson, MD‖,
- Ph. Gabriel Steg, MD¶,
- Sorin J. Brener, MD†,#,
- Dominick J. Angiolillo, MD, PhD∗∗,
- Matthew J. Price, MD††,
- Jayne Prats, PhD‡‡,
- Laura LaSalle, MPH†,
- Tiepu Liu, MD, PhD††,
- Meredith Todd, BSc††,
- Simona Skerjanec, PharmD††,
- Christian W. Hamm, MD§§,
- Kenneth W. Mahaffey, MD§,
- Harvey D. White, DSc‖‖,
- Deepak L. Bhatt, MD, MPH¶¶∗ (, )
- CHAMPION PHOENIX Investigators
- ∗Columbia University Medical Center, New York, New York
- †Cardiovascular Research Foundation, New York, New York
- ‡Hôpital du Sacré-Coeur de Montréal, Université de Montréal, Montréal, Quebec, Canada
- §Stanford University, Stanford, California
- ‖Cardiovascular Division, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts
- ¶Institut National de la Santé et de la Recherche Médicale–Unité 698, Assistance Publique–Hôpitaux de Paris, Hôpital Bichat, and Université Paris-Diderot, Sorbonne-Paris Cité, Paris, France, and Royal Brompton Hospital, London, United Kingdom
- #New York Methodist Hospital, Brooklyn, New York
- ∗∗University of Florida College of Medicine-Jacksonville, Jacksonville, Florida
- ††Scripps Clinic and Scripps Translational Science Institute, La Jolla, California
- ‡‡The Medicines Company, Parsippany, New Jersey
- §§University of Giessen and Kerckhoff Heart Center, Bad Nauheim, Germany
- ‖‖Auckland City Hospital, Auckland, New Zealand
- ¶¶Brigham and Women's Hospital, and Harvard Medical School, Boston, Massachusetts
- ↵∗Reprint requests and correspondence:
Dr. Deepak L. Bhatt, Brigham and Women's Hospital, 75 Francis Street, Boston, Massachusetts 02115.
Objectives This study sought to evaluate the clinical impact of intraprocedural stent thrombosis (IPST), a relatively new endpoint.
Background In the prospective, double-blind, active-controlled CHAMPION PHOENIX (Clinical Trial Comparing Cangrelor to Clopidogrel Standard of Care Therapy in Subjects Who Require Percutaneous Coronary Intervention) trial, cangrelor significantly reduced periprocedural and 30-day ischemic events in patients undergoing percutaneous coronary intervention (PCI), including IPST.
Methods An independent core laboratory blinded to treatment assignment performed a frame-by-frame angiographic analysis in 10,939 patients for the development of IPST, defined as new or worsening thrombus related to stent deployment at any time during the procedure. Adverse events were adjudicated by an independent, blinded clinical events committee.
Results IPST developed in 89 patients (0.8%), including 35 of 5,470 (0.6%) and 54 of 5,469 (1.0%) patients in the cangrelor and clopidogrel arms, respectively (odds ratio: 0.65; 95% confidence interval: 0.42 to 0.99; p = 0.04). Compared to patients without IPST, IPST was associated with a marked increase in composite ischemia (death, myocardial infarction [MI], ischemia-driven revascularization, or new-onset out-of-laboratory stent thrombosis [Academic Research Consortium]) at 48 h and at 30 days (29.2% vs. 4.5% and 31.5% vs. 5.7%, respectively; p < 0.0001 for both). After controlling for potential confounders, IPST remained a strong predictor of all adverse ischemic events at both time points.
Conclusions In the large-scale CHAMPION PHOENIX trial, the occurrence of IPST was strongly predictive of subsequent adverse cardiovascular events. The potent intravenous adenosine diphosphate antagonist cangrelor substantially reduced IPST, contributing to its beneficial effects at 48 h and 30 days. (Clinical Trial Comparing Cangrelor to Clopidogrel Standard of Care Therapy in Subjects Who Require Percutaneous Coronary Intervention [PCI] [CHAMPION PHOENIX]; NCT01156571)
The prospective, double-blind, active-controlled CHAMPION PHOENIX (Clinical Trial Comparing Cangrelor to Clopidogrel Standard of Care Therapy in Subjects Who Require Percutaneous Coronary Intervention) has demonstrated the superiority of cangrelor, a novel, intravenous, rapidly acting, and potent P2Y12 platelet receptor inhibitor, compared with clopidogrel in patients undergoing percutaneous coronary intervention (PCI) for various clinical indications (1). Cangrelor was shown at 48 h after PCI to significantly reduce the rate of ischemic events, a composite endpoint that included stent thrombosis (ST). ST was defined in CHAMPION PHOENIX as the occurrence of events occurring after the PCI procedure, as classified by the Academic Research Consortium (ARC) definition (2), as well as intraprocedural ST (IPST), the development of new or increasing thrombus in or adjacent to an implanted stent during the PCI procedure. Although previous reports have linked IPST to future ischemic events (3–5), its recognition and inclusion as a stand-alone angiographic endpoint in randomized trials is not yet universally accepted, and not all prior studies employed an independent blinded angiographic core laboratory to assess IPST events. We therefore sought to determine the incidence, predictors, and clinical impact of IPST from the CHAMPION PHOENIX trial, which incorporated the largest independent angiographic core laboratory analysis to date.
The CHAMPION PHOENIX trial rationale and results have been described in detail (1,6). In brief, 11,145 patients presenting with either stable angina, non–ST-segment elevation acute coronary syndromes (NSTE-ACS), or ST-segment elevation myocardial infarction (STEMI) were randomized 1:1 in a double dummy, double-blind design, after angiography, to intravenous cangrelor or oral clopidogrel administered at the time of PCI. Cangrelor (or matching placebo) was administered as a bolus of 30 μg/kg followed by an infusion of 4 μg/kg/min for at least 2 h or the duration of the procedure, whichever was longer. A clopidogrel loading dose (300 to 600 mg, at the discretion of the operator) or matching placebo and aspirin (75 to 325 mg) were administered to all patients. The protocol required clopidogrel (75 mg) to be administered during the first 48 hours; thereafter, clopidogrel or another P2Y12 inhibitor could be administered at the discretion of the investigator. The choice of access site, procedural anticoagulant (bivalirudin, unfractionated heparin, low-molecular-weight heparin, or fondaparinux) and sheath management were per-site routine. Glycoprotein IIb/IIIa inhibitors were allowed only as rescue therapy during PCI to treat thrombotic complications.
The primary efficacy endpoint was the composite rate of all-cause mortality, MI, ischemia-driven revascularization (IDR), or ST in the 48 h after randomization. The key secondary endpoint was the incidence of ST at 48 hours. ST was defined as the occurrence of IPST or ARC ST (further classified as definite, probable, or possible ST) (2). IPST was defined as any angiographically new or worsening thrombus related to stent implantation occurring during the PCI procedure, as assessed in frame-by-frame analysis by a blinded independent core laboratory (Cardiovascular Research Foundation, New York, New York) (5). Thrombus was defined as any discrete, mobile, intraluminal filling defect, with defined borders, with or without associated contrast staining or a total occlusion with convex edges and staining. Thrombus was described as: 1) occlusive (TIMI [Thrombolysis In Myocardial Infarction] flow grade 0, occupying the entire lumen); 2) globular (definite border on 3 edges); 3) filling defect (definite borders on 2 edges); or 4) hazy (irregular contour, smooth convex meniscus or haziness at the site of the lesion). Thrombus area was traced to better characterize the thrombotic burden. In cases of complete occlusion, the thrombus area was measured after wire introduction (when possible) and before any device therapy (thromboaspiration, balloon, or stent). Interobserver level of agreement for thrombus detection at baseline and during PCI was 0.95 and 0.8 (kappa statistic), respectively, indicative of an almost perfect level of agreement (7). The primary safety endpoint was severe bleeding not related to coronary artery bypass grafting according to the GUSTO (Global Use of Strategies to Open Occluded Coronary Arteries) criteria at 48 h. Detailed definitions of the primary and major secondary endpoints have been previously reported (1). The primary efficacy endpoints occurring during the first 30 days after randomization were adjudicated by an independent clinical events committee (Duke Clinical Research Institute, Durham, North Carolina).
All of the analyses were performed with data from the modified intention-to-treated (mITT) population, as previously described (1). Continuous variables are summarized as medians and quartiles or as mean ± SD, as appropriate, and were compared using the Student t test or Mann-Whitney rank sum test accordingly. Categorical variables are presented as rate (%) and were compared by the chi-square or Fisher exact test. Time-to-event curves were constructed using Kaplan-Meier methodology and compared with the log-rank test. Logistic regression was performed to identify independent predictors of IPST. The multivariable model was built by selecting variables of clinical interest and/or satisfying the entry criterion of α < 0.05 in the univariate analysis. The number of variables included in the model was chosen to avoid overfitting. The final model was derived with a stepwise regression procedure with entry/stay α criteria of 0.10. To assess the association between the occurrence of IPST and subsequent all-cause death, MI, ARC ST, ARC definite ST, and IDR, logistic regression was used to derive a propensity score for IPST, which was then included in a logistic regression model (along with IPST) for 48-h and 30-day outcomes. Interaction between the occurrence of IPST and different subgroups on major adverse events was tested using the Breslow-Day method. No adjustment was made for multiple comparisons. All statistical analyses were performed with SAS version 9.2 (SAS Institute Inc., Cary, North Carolina).
Patients and baseline characteristics
Detailed angiographic core laboratory analysis was completed in 10,939 of 10,942 randomized patients (99.9%) in the mITT cohort. Among those, IPST occurred in 89 patients (0.8%), including 35 of 5,470 (0.6%) and 54 of 5,469 (1.0%) patients in the cangrelor and clopidogrel arms, respectively (odds ratio [OR]: 0.65; 95% confidence interval [CI: 0.42 to 0.99; p = 0.04). IPST occurred in 32 of 6,138 patients (0.5%) presenting with stable angina, 33 of 2,810 patients (1.2%) presenting with NSTE-ACS, and 24 of 1,991 patients (1.2%) presenting with STEMI (p = 0.0006). Among IPST patients, 48 of 89 (53.9%) had new evidence of thrombus, and 41 of 89 (46.1%) had worsening or growing thrombus.
Baseline clinical, angiographic, and procedural characteristics of patients with and without IPST are shown in Tables 1 and 2. Patients with versus without IPST were more frequently current smokers, treated outside of the United States, presented with NSTE-ACS or STEMI rather than stable angina, had elevated baseline cardiac biomarkers (troponin and/or creatine kinase-MB), and received a loading dose of 300 mg rather 600 mg of clopidogrel. Patients with IPST more frequently had baseline and final TIMI flow grade <3, had thrombotic lesions, underwent multivessel PCI, were treated with bare-metal stents rather than drug-eluting stents and longer stents, and had a lengthier PCI procedure. Of note, 78.4% of IPST patients had TIMI flow grade 3 after the procedure, suggesting resolution of the thrombotic event in most patients. IPST was also associated with a doubling of the duration of hospitalization (Table 1).
As shown in Table 3, by multivariate analysis, NSTE-ACS and STEMI at presentation, angiographic thrombus prior to PCI, and total stent length were independent predictors of IPST. The use of cangrelor at randomization (compared to clopidogrel) was independently associated with freedom from IPST during PCI.
IPST was associated with a marked increase in mortality, MI, IDR, and ARC ST at 48 h and at 30 days (Table 4, Fig. 1). After controlling for potential confounders, IPST remained a strong predictor of all adverse ischemic events, including mortality and ARC ST (definite and definite or probable) outside the catheterization laboratory, at both time periods. The independent association between IPST and these adverse ischemic events remained independent, even among patients in whom IPST treatment restored final angiographic TIMI flow grade 3 (Table 5). The impact of IPST on 30-day mortality was consistent among specified subgroups (Fig. 2). The association between the occurrence of IPST and ARC definite ST (at 48 h and 30 days) and subsequent mortality is shown in Figure 3. Among patients experiencing definite ST by 48 h and 30 days, 3 of 34 (8.8%) and 4 of 65 (6.2%) patients, respectively, had an earlier IPST. Similarly, 84 of 89 patients with IPST did not experience ARC ST at 30 days, and 86 of 91 ARC ST did not have IPST, indicating little overlap between both outcomes. IPST was also associated with an increase in bleeding events (moderate and mild GUSTO bleeding, minor TIMI bleeding, Bleeding Academic Research Consortium [BARC] 3a, and ACUITY [Acute Catheterization and Urgent Intervention Triage Strategy] major bleeding [excluding hematoma ≥5 cm]) at 48 h (Table 6).
Use of cangrelor resulted in a significant reduction in the rate of IPST compared with clopidogrel in the entire study population and separately in the patient cohorts presenting with stable angina, NSTE-ACS, and STEMI (Fig. 4).
The current analysis from 10,939 patients enrolled in the multinational, prospective, double-blind randomized CHAMPION PHOENIX trial is the largest study to specifically evaluate the incidence, predictors, and impact of IPST on the early prognosis of patients undergoing elective, urgent, and emergent PCI. The main results of the present study are as follows: 1) IPST occurred in approximately 1% of patients undergoing PCI; 2) NSTE-ACS or STEMI at presentation, the presence of angiographic thrombus, and the total stent length implanted were independently associated with the occurrence of IPST, and cangrelor use independently associated with freedom of IPST; 3) IPST was associated with a significant increase in mortality, MI, IDR, and ARC definite or probable ST at 48 h and at 30 days; and 4) treatment with cangrelor compared to clopidogrel at the time of the PCI procedure significantly decreased the occurrence of IPST and adverse events through 30 days.
IPST was an infrequent event during PCI, occurring in 0.8% of PCI patients in the CHAMPION PHOENIX trial. Similar results have been reported by previous groups, with an incidence varying from 0.5% to 0.7% (3–5). From a pooled analysis of the ACUITY (8) and HORIZONS-AMI (Harmonizing Outcomes with Revascularization and Stents in Acute Myocardial Infarction) trials (9), IPST occurred in 47 (0.7%) of the 6,591 analyzed patients, with a higher incidence in STEMI compared to NSTE-ACS (1.2% vs. 0.3%, respectively) (5). The rate of IPST in CHAMPION PHOENIX was similar to that in HORIZONS-AMI (1.2%), although IPST occurred more frequently in NSTE-ACS patients in the present study than in ACUITY (1.2% vs. 0.3%, respectively) (5). As the angiographic core laboratory and methodology to assess IPST were the same in both studies, this difference is likely explained by underlying differences in the patient populations and adjunct pharmacology between the 2 studies. In the present study, IPST was notably less common in patients with stable coronary artery disease (incidence 0.5%), consistent with the lower rate of out-of-laboratory ST in these patients compared to NSTE-ACS and STEMI.
The current study demonstrates a strong independent relationship between IPST and short-term mortality. After propensity-score–adjusted multivariable analysis, IPST was associated with increases of >20- and >12-fold in 48-h and 30-day mortality, respectively. Brener et al. (5) reported similar results in ACS patients, with IPST associated with a 10-fold increase in 30-day mortality. IPST was also a strong independent predictor of MI and IDR. Of note, while 5.6% of patients with IPST died within 48 h, an additional ∼5% died between 48 h and 30 days. This finding underscores the importance of preventing IPST, as well as close monitoring and optimal treatments should IPST occur. Additionally, in approximately one-third of the cases, IPST was associated with use of bailout glycoprotein IIb/IIIa inhibitors, with attendant bleeding hazards and financial implications. Furthermore, prevention of IPST may reduce costs because IPST was associated with a doubling in the length of stay.
In addition, IPST was independently predictive of ARC-ST and ARC definite ST outside the catheterization laboratory. Indeed, IPST was associated with increases of approximately 12-fold and 8-fold in (angiographically confirmed) newly symptomatic ARC definite ST at 48 h and 30 days, respectively. Moreover, while IPST was a relatively rare intraprocedural event, in the CHAMPION PHOENIX trial, its incidence (0.8%) was higher than that of ARC definite ST at 48 h (0.3%) and 30 days (0.6%), and was associated with a similar detrimental impact on short-term prognosis (1). Bleeding rates were also higher in patients experiencing IPST, likely due to the more frequent use of aggressive bailout antithrombotic strategies (such as glycoprotein IIb/IIIa inhibitors) to treat IPST. Moreover, the deleterious impact of IPST persisted even in patients in whom TIMI flow grade 3 was present at the end of the PCI procedure. The present study thus clearly establishes the prognostic utility of IPST, justifying its assessment in future clinical trials in which intraprocedural antithrombotic efficacy is being evaluated. These findings also suggest that future iterations of ST classifications should incorporate IPST as a discrete category.
Independent predictors of IPST in the current report were NSTE-ACS and STEMI at presentation, angiographic thrombus at baseline, and total stent length used during the index PCI. Previous studies have similarly identified ACS and thrombus to be predictors of out-of-laboratory ST (10–14). The fact that stent length was predictive of IPST is also consistent with prior reports of post-PCI ST (12,14). The use of cangrelor was also identified as an independent predictor of freedom from IPST. Because none of the novel oral P2Y12 receptor blockers (prasugrel, ticagrelor) showed efficacy in reducing acute ST per se (15–17), this finding may have major implications when selecting the most potent antithrombotic treatment during PCI.
Importantly, use of the potent, rapid-acting ADP receptor antagonist cangrelor compared with clopidogrel (begun at the time of PCI) resulted in a 35% reduction in the rate of IPST, with efficacy in this regard evident in patients with stable angina, NSTE-ACS, and STEMI. Cangrelor may be particularly advantageous to prevent IPST in patients in whom potent oral agents have not been started prior to PCI or in situations in which their absorption is delayed, such as in STEMI (18,19). Thus, the present and prior findings emphasize the interplay between the patient/lesion thrombotic environment, stent platform, and antithrombotic therapy on the occurrence of intraprocedural and early ST. Optimization of each of these components is crucial if PCI outcomes are to be improved.
Although rigorous angiographic assessment was performed by an experienced, independent, angiographic core laboratory, IPST could be diagnosed only if appropriate angiographic documentation was provided by each site investigator. Thus, brief occurrences of abrupt vessel closure or treatment of thrombus that were not recorded would have escaped detection in this analysis. Coronary angiography has been shown to have great specificity for thrombus detection but low sensitivity compared with angioscopy, resulting in potential underestimation of thrombus burden at the lesion level (20). Although its clinical role still remains to be established, the use of novel intracoronary imaging techniques, such as optical coherence tomography, could have been useful to better characterize and quantify new or worsening intraprocedural thrombus compared with the conventional angiographic evaluation. The absolute number of IPST events prevented was 0.4%, meaning that many patients would need to be treated to prevent 1 event. However, IPST was 3-fold more common than ARC definite ST and has similar prognostic implications, warranting efforts to prevent its occurrence. IPST had a low positive predictive value for ARC ST after PCI, suggesting that different mechanisms may be responsible for IPST and later ST. Finally, although IPST was strongly related to subsequent adverse ischemic events in a multivariable model after propensity adjustment for those factors related to IPST (and other variables), the presence of residual confounding elements cannot be excluded.
In the large-scale CHAMPION PHOENIX trial, IPST was a relatively infrequent event, occurring in <1% of patients undergoing PCI, but was strongly associated with subsequent ischemic events, including out-of-laboratory ST, MI, and death. The reduction in IPST with cangrelor in CHAMPION PHOENIX contributed to this agent's effectiveness in reducing the rates of ARC-defined stent thrombosis and MI. These data provide strong evidence for a significant association between IPST and adverse short-term clinical outcomes after PCI and support the inclusion of IPST as an important endpoint in future pharmacological and device trials.
The authors thank Lanyu Lei, MS, and Yuyin Liu, MS, from Harvard Clinical Research Institute, for verifying the statistical analyses (funded by The Medicines Company).
A full list of the investigators can be found in Bhatt DL, Stone GW, Mahaffey KW, et al. N Engl J Med 2013;368:1303–13. The CHAMPION-PHOENIX trial was funded by The Medicines Company and designed collaboratively by the Executive Committee and the sponsor. The present analysis was externally validated by the Harvard Clinical Research Institute, Dr. Généreux has received speaker fees from Abbott Vascular. Dr. Stone has served as a consultant to Boston Scientific, Eli Lilly, Daiichi Sankyo Company, Inc., and AstraZeneca. Dr. Harrington is a consultant for Baxter, Bristol-Myers Squibb Company, CSL Behring, Daiichi-Lilly, Gilead, Johnson & Johnson Corporation, Janssen Pharmaceuticals, Merck, MyoKardia, and WebMD; and has received research grants/contracts from AstraZeneca, Bristol-Myers Squibb, CSL, GlaxoSmithKline, Merck, Portola, Regado, sanofi-aventis, and The Medicines Company. Dr. Gibson has received research grants from Angel Medical Corporation, Atrium Medical Systems, Bayer Corporation, Bristol-Myers Squibb Company, Ikaria, Inc., Janssen Pharmaceuticals, Johnson & Johnson Corporation, Lantheus Medical Imaging, Medtronic Vascular, Inc., Portola Pharmaceuticals, Stealth Peptides, Inc., St. Jude Medical, Volcano Corp, and Walk Vascular; and has received consultant's fees from Atrium Medical Systems, Baxter Healthcare, Boehringer Ingelheim, Bristol-Myers Squibb Company, Cardiovascular Research Foundation, CSL Behring, Cytori Therapeutics, Daiichi Sankyo Company, Inc., Eli Lilly & Company, Exeter Group, Google, Inc., Navigant, St. Jude Medical, The Medicines Company, and WebMD. Dr. Steg has received research grants (to INSERM U698) from the NYU School of Medicine, sanofi-aventis, and Servier; speaker's or consultant's honoraria from Amarin, AstraZeneca, Bayer Corporation, Boehringer-Ingelheim, Bristol-Myers Squibb, Daiichi-Sankyo, GlaxoSmithKline, Iroko Cardio, Lilly, Medtronic, Novartis, Otsuka, Pfizer, Roche, sanofi-aventis, Servier, The Medicines Company, and Vivus; and holds stock options in Aterovax. Dr. Angiolillo has received consultant's fees or honoraria from Bristol-Myers Squibb, sanofi-aventis, Eli Lilly, Daiichi Sankyo, The Medicines Company, AstraZeneca, Merck, Evolva, Abbott Vascular, and PLx Pharma; is involved in participation in review activities from Johnson & Johnson, St. Jude Medical, and Sunovion; has received institutional payments for grants from Bristol-Myers Squibb, sanofi-aventis, GlaxoSmithKline, Otsuka, Eli Lilly, Daiichi Sankyo, The Medicines Company, AstraZeneca, and Evolva; and has other financial relationships with Esther and King Biomedical Research Grant. Dr. Price has received consultant's honoraria from AstraZeneca, Daiichi Sankyo-Lilly, Medicure, The Medicines Company, Janssen Pharmaceuticals, Boston Scientific, Terumo Corporation, and St. Jude Medical; and speaker's honoraria from AstraZeneca and Daiichi Sankyo-Lilly. Dr. Hamm has been a member of the advisory boards of AstraZeneca, Boehringer Ingelheim, and Merck, Sharp, & Dohme; and has received speaker's honoraria from The Medicines Company, AstraZeneca, Daiichi Sankyo, Bayer, Boehringer Mannheim, sanofi-aventis, Bristol-Myers Squibb, and Pfizer. Dr. Mahaffey has received consultant's honoraria from Bayer, Boehringer Ingelheim, Bristol-Myers Squibb, Daiichi Sankyo, Eli Lilly, GlaxoSmithKline, Johnson & Johnson, Merck, Ortho/McNeill, Pfizer, and Polymedix; and has received institutional research grants from AstraZeneca, Boehringer Ingelheim, Daiichi Sankyo, Eli Lilly, GlaxoSmithKline, Johnson & Johnson, Merck, Portola, Regado Biotechnologies, sanofi-aventis, Schering-Plough (now Merck), and The Medicines Company. Dr. Bhatt has been a member of the advisory boards of Elsevier Practice Update Cardiology, Medscape Cardiology, and Regado Biosciences; is a member of the board of directors of Boston VA Research Institute and the Society of Cardiovascular Patient Care; is the chair of the American Heart Association Get With The Guidelines Steering Committee; has received honoraria from the American College of Cardiology (Editor, Clinical Trials, Cardiosource), Belvoir Publications (Editor-in-Chief, Harvard Heart Letter), Duke Clinical Research Institute (clinical trial steering committees), Population Health Research Institute (clinical trial steering committee), Slack Publications (Chief Medical Editor, Cardiology Today's Intervention), WebMD (CME steering committees); is the editor of the Journal of Invasive Cardiology; is a member of data monitoring committees for Duke Clinical Research Institute, Harvard Clinical Research Institute, Mayo Clinic, and the Population Health Research Institute, has received research grants from Amarin, AstraZeneca, Bristol-Myers Squibb, Eisai, Ethicon, Medtronic, Roche, sanofi-aventis, and The Medicines Company (for his role as the co-chair of the CHAMPION PCI, PLATFORM, and PHOENIX trials); and has been involved in unfunded research for FlowCo, PLx Pharma, and Takeda. All other authors have reported that they have no other relationships relevant to the contents of this paper to disclose.
- Abbreviations and Acronyms
- Academic Research Consortium
- bare metal stent(s)
- drug-eluting stent(s)
- ischemic-driven revascularization
- intra-procedural stent thrombosis
- myocardial infarction
- non–ST-segment elevation acute coronary syndrome
- percutaneous coronary intervention
- stent thrombosis
- ST-segment elevation myocardial infarction
- Received October 14, 2013.
- Revision received October 22, 2013.
- Accepted October 22, 2013.
- American College of Cardiology Foundation
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