Original Article
Complementary Clinical Benefits of Coronary-Artery Stenting and Blockade of Platelet Glycoprotein IIb/IIIa Receptors
N Engl J Med 1999; 341:319-327July 29, 1999
- Abstract
Background
Inhibition of the platelet glycoprotein IIb/IIIa receptor with the monoclonal-antibody fragment abciximab reduces the acute ischemic complications associated with percutaneous coronary revascularization, whereas coronary-stent implantation reduces restenosis. We conducted a trial to determine the efficacy of abciximab and stent implantation in improving long-term outcome.
Methods
A total of 2399 patients were randomly assigned to stent implantation and placebo, stent implantation and abciximab, or balloon angioplasty and abciximab. The patients were followed for six months.
Results
At six months, the incidence of the composite end point of death or myocardial infarction was 11.4 percent in the group that received a stent and placebo, as compared with 5.6 percent in the group that received a stent and abciximab (hazard ratio, 0.47; 95 percent confidence interval, 0.33 to 0.68; P<0.001) and 7.8 percent in the group assigned to balloon angioplasty and abciximab (hazard ratio, 0.67; 95 percent confidence interval, 0.49 to 0.92; P=0.01). The hazard ratio for stenting plus abciximab as compared with angioplasty plus abciximab was 0.70 (95 percent confidence interval, 0.48 to 1.04; P=0.07). The rate of repeated revascularization of the target vessel was 10.6 percent in the stent-plus-placebo group, as compared with 8.7 percent in the stent-plus-abciximab group (hazard ratio, 0.82; 95 percent confidence interval, 0.59 to 1.13; P=0.22) and 15.4 percent in the angioplasty-plus-abciximab group (hazard ratio, 1.49; 95 percent confidence interval, 1.13 to 1.97; P=0.005). The hazard ratio for stenting plus abciximab as compared with angioplasty plus abciximab was 0.55 (95 percent confidence interval, 0.41 to 0.74; P<0.001). Among patients with diabetes, the combination of abciximab and stenting was associated with a lower rate of repeated target-vessel revascularization (8.1 percent) than was stenting and placebo (16.6 percent, P=0.02) or angioplasty and abciximab (18.4 percent, P=0.008).
Conclusions
For coronary revascularization, abciximab and stent implantation confer complementary long-term clinical benefits.
Media in This Article
Figure 1
Kaplan–Meier Estimates of the Incidence of the Efficacy End Points.Figure 2
Kaplan–Meier Estimates of the Incidence of Repeated Target-Vessel Revascularization within Six Months after Randomization, According to Treatment Assignment, among Patients with Diabetes (Panel A) and Patients without Diabetes (Panel B).Article Activity
- Article
Since the introduction of balloon angioplasty more than 20 years ago, two therapies have been demonstrated to improve outcomes after the procedure and have been widely adopted into clinical practice. Inhibition of platelet aggregation by blockade of the platelet surface glycoprotein IIb/IIIa receptor with abciximab, a monoclonal-antibody Fab fragment, was shown to reduce the incidence of periprocedural ischemic complications among patients undergoing balloon angioplasty or atherectomy.1-3 The development of techniques for blocking the glycoprotein IIb/IIIa receptor was paralleled by the widespread acceptance of coronary-artery stent implantation as the predominant means of percutaneous coronary intervention, on the basis of the efficacy of the device in reducing rates of repeated revascularization.4-7
In the Evaluation of Platelet IIb/IIIa Inhibition in Stenting (EPISTENT) trial, a randomized, placebo-controlled study, the effect of abciximab therapy among patients undergoing stent implantation or balloon angioplasty was evaluated and compared with the effect of stent implantation alone. As compared with stenting plus placebo, administration of abciximab in addition to either stenting or angioplasty significantly reduced the risk of ischemic complications within 30 days of the procedure.8 The known efficacy of stenting, however, is largely due to reductions in the rates of long-term restenosis and repeated target-vessel revascularization, benefits that would not be manifest within the first 30 days. In this report, we present the results of clinical and angiographic follow-up of the patients in the EPISTENT study at six months, which provide evidence that stent implantation and platelet glycoprotein IIb/IIIa receptor blockade have complementary clinical effects on the long-term efficacy and safety of percutaneous coronary revascularization.
Methods
Patients
The details of the trial design have been reported previously.8 In brief, 2399 patients undergoing elective or urgent percutaneous coronary revascularization were enrolled between July 22, 1996, and September 25, 1997, at 63 centers throughout the United States and Canada. Patients were eligible for enrollment if they had at least one target lesion suitable for treatment either by stenting or by balloon angioplasty and were not undergoing primary intervention for acute myocardial infarction. The protocol was approved by the institutional review board at each clinical site, and all the patients gave written informed consent.
Study Protocol
All the patients were treated with aspirin. Ticlopidine was to be given after stent implantation, and according to the protocol, one or more doses could be given before study-drug administration. Patients were randomly assigned (by means of telephone calls to the randomization center at the Duke Clinical Research Institute) to one of three groups: stenting and placebo, stenting and abciximab, or balloon angioplasty and abciximab. The stent manufactured by Johnson and Johnson (New Brunswick, N.J.) was to be used unless it could not be deployed. Criteria were specified for unplanned stent implantation to maintain patency after manifest or threatened abrupt closure in patients assigned to angioplasty, and crossover to stenting occurred in 19 percent of these patients. Investigators were blinded to the drug assignment (abciximab or placebo) of the two groups that also underwent stenting, but they could not be blinded to the drug assignment of the angioplasty group, since only abciximab was given. Abciximab (ReoPro, Centocor, Malvern, Pa.) was administered as a bolus of 0.25 mg per kilogram of body weight 10 to 60 minutes before balloon inflation, followed by an infusion of 0.125 μg per kilogram per minute (maximal dosage, 10 μg per minute) for 12 hours. Patients assigned to abciximab received low-dose, weight-adjusted heparin, and those assigned to placebo received heparin at a standard, weight-adjusted dose.2
Angiographic Substudy
The first 899 consecutive patients in the trial gave their consent to be included in an angiographic substudy and underwent repeated angiography 184 to 275 days after randomization. Angiographic follow-up was to be carried out if the index revascularization procedure (performed at the time of randomization) was successful (residual stenosis, ≤50 percent) in at least one target lesion, unless the patient subsequently died or underwent repeated revascularization of all target lesions within seven days of the index procedure. Angiograms that were obtained before repeated revascularization or three to six months after randomization or that demonstrated occlusion of all the target lesions were included in the angiographic analysis. Computerized quantitative analysis of procedural and follow-up cineangiograms was performed at a core laboratory with an AngioComm Review Station (Quinton Instruments, Bothell, Wash.). Quantitative coronary analysis was carried out with first- and second-derivative automated edge-detection software (CathView, version 2.6, Quinton Instruments).9
Study End Points
Two principal end points were defined for assessment 6 months (≥183 days) after randomization: death or myocardial infarction as a composite measure and repeated revascularization of a target vessel. Classifications with respect to the end points were made by a clinical-events committee, which was blinded to the patients' study-group assignments. An in-hospital myocardial infarction was defined as the presence of new “significant” Q waves (according to the Minnesota code10) in two or more contiguous electrocardiographic leads or an elevation of creatine kinase or its MB isoenzyme to at least three times the upper limit of normal at each hospital's laboratory in two samples collected at different times. Myocardial infarction after hospital discharge was defined as the development of new Q waves or an elevation of creatine kinase or its MB isoenzyme to more than two times the upper limit of normal.
In the angiographic substudy, analysis was carried out on a per-lesion basis. Luminal dimensions were taken as the average of measured values in two orthogonal projections (or in one projection if only one was available). The principal end point for the angiographic substudy was the minimal luminal diameter at follow-up.
Data Collection and Statistical Analysis
For assessment of the outcome at 6 months, all patients were to be contacted by investigators at the individual study sites and electrocardiography was to be performed 183 days or more after randomization. Hospital records, death certificates, and autopsy reports were obtained when relevant. Investigators and study coordinators remained blinded to the study-group assignments of individual patients.
Differences among patients with regard to efficacy were examined in an intention-to-treat analysis. To be considered complete, the 6-month follow-up evaluation had to have been performed at least 165 days after randomization. Pairwise comparisons between each of the two abciximab groups (stenting and balloon angioplasty) and the stent-plus-placebo group were made with use of the log-rank test, and event rates were calculated by the Kaplan–Meier method. A secondary comparison was made between the two abciximab groups. Reported P values were two-sided. Analysis of outcomes among the subgroups of patients with and without diabetes mellitus was prospectively planned; patients with diabetes were identified by a documented medical history of hyperglycemia with dietary or pharmacologic therapy.
30-Day Outcome and Completeness of Follow-up
The results of the analysis of the primary efficacy end point at 30 days have been reported previously.8 This primary efficacy end point consisted of the composite of death, myocardial infarction, or urgent repeated revascularization and occurred in 10.8 percent of the patients in the stent-plus-placebo group, 5.3 percent of those in the stent-plus-abciximab group, and 6.9 percent of those in the angioplasty-plus-abciximab group (P<0.001 and P=0.007, respectively, for the comparison with stent plus placebo).
No additional entries were permitted in the six-month follow-up data base after July 27, 1998. Survival status at 165 days was unknown for 14 of the 2399 patients enrolled (0.6 percent); for these 14 patients, the median follow-up time was 34 days. For the assessment of events other than death, a total of 42 patients (1.8 percent) had fewer than 165 days of follow-up with no report of an end-point event. Rates of completeness of follow-up were similar among the three treatment groups.
Results
Base-Line Characteristics
Base-line clinical characteristics of the study patients have been described previously.8 Of the 2399 patients, 491 (20 percent) had diabetes. At the time of randomization, 379 of these patients (77 percent) were receiving oral hypoglycemic agents, insulin, or both; of the others, 21 had previously been treated with oral hypoglycemic agents.
Angiographic characteristics were well matched among the three treatment groups. In 25 percent of patients multiple coronary lesions were treated. Coronary vessels that required treatment were the left anterior descending, circumflex, and right coronary arteries in 39 percent, 25 percent, and 42 percent of patients, respectively; a coronary-artery bypass graft was treated in 4 percent. Characteristics of complex lesions included a length of more than 10 mm in 50 percent of patients, eccentricity in 56 percent, moderate or extreme tortuosity in 24 percent, moderate or extreme angulation in 15 percent, calcification in 11 percent, thrombus in 13 percent, and total occlusion in 7 percent, with some patients having lesions with several of these features.
Before administration of the study drug, 53 percent of the patients received at least one dose of ticlopidine.
Clinical Efficacy at Six Months
Six months after treatment, the incidence of the composite end point of death or myocardial infarction was 11.4 percent in the group randomly assigned to stent implantation and placebo, as compared with 5.6 percent in the group assigned to stent implantation and abciximab (hazard ratio, 0.47; 95 percent confidence interval, 0.33 to 0.68; P<0.001) and 7.8 percent in the group assigned to balloon angioplasty and abciximab (hazard ratio, 0.67; 95 percent confidence interval, 0.49 to 0.92; P=0.01); the hazard ratio for stent implantation and abciximab as compared with angioplasty and abciximab was 0.70 (95 percent confidence interval, 0.48 to 1.04; P=0.07) (Figure 1AFigure 1
Kaplan–Meier Estimates of the Incidence of the Efficacy End Points.). The effect of abciximab treatment was achieved early and was maintained throughout the 6-month follow-up period; the absolute reduction in the number of events that met the definition of the composite end point (number of events prevented per 100 patients treated) as compared with the number in the group that underwent stent implantation with placebo was 5.5 at 30 days and 5.8 at 6 months in the stent-plus-abciximab group and 4.4 at 30 days and 3.6 at 6 months in the angioplasty-plus-abciximab group.Results with respect to individual components of the composite end point (death or myocardial infarction), as well as revascularization procedures performed on an urgent basis, are shown in Table 1Table 1
Incidence of the Efficacy End-Point Events at Six Months.. As compared with stenting accompanied by placebo, stenting and abciximab resulted in reductions of a similar magnitude with respect to each of these end-point events. As compared with stenting accompanied by placebo, balloon angioplasty accompanied by abciximab was associated with a lower risk of myocardial infarction but similar rates of death or urgent revascularization procedures. Among patients who received abciximab, mortality was significantly lower among those who underwent stent implantation than among those who underwent balloon angioplasty (0.5 percent vs. 1.8 percent, P=0.02).At six months, the incidence of repeated revascularization of the target vessel was 10.6 percent in the stent-plus-placebo group, as compared with 8.7 percent in the stent-plus-abciximab group (hazard ratio, 0.82; 95 percent confidence interval, 0.59 to 1.13; P=0.22) and 15.4 percent in the angioplasty-plus-abciximab group (hazard ratio, 1.49; 95 percent confidence interval, 1.13 to 1.97; P=0.005) (Table 2Table 2
Repeated Revascularization Procedures within Six Months after Randomization. and Figure 1B). Rates of target-vessel revascularization and overall revascularization were significantly lower among patients who underwent stenting with or without abciximab than among those who underwent balloon angioplasty with abciximab; this beneficial effect was confined to eliminating the need for nonurgent percutaneous revascularization (Table 2). Event curves for repeated target-vessel revascularization procedures began to diverge after approximately 60 days (Figure 1B). Among the patients in the two abciximab groups, random assignment to stent implantation rather than angioplasty resulted in a 44 percent lower incidence of target-vessel revascularization (hazard ratio, 0.55; 95 percent confidence interval, 0.41 to 0.74; P<0.001).Among patients with diabetes mellitus, rates of repeated revascularization of the target vessel after stent implantation were significantly lower among patients given abciximab than among those given placebo (Figure 2AFigure 2
Kaplan–Meier Estimates of the Incidence of Repeated Target-Vessel Revascularization within Six Months after Randomization, According to Treatment Assignment, among Patients with Diabetes (Panel A) and Patients without Diabetes (Panel B).). Among these patients, stenting accompanied only by placebo was not associated with a significantly lower rate of subsequent target-vessel revascularization than was balloon angioplasty accompanied by abciximab, whereas the rate of this end point was roughly half as high among patients assigned to stenting and abciximab. Abciximab had no effect on the need for repeated revascularization among patients without diabetes (Figure 2B). The effect of abciximab on the end point of death or myocardial infarction at six months was similar among patients with diabetes and those without diabetes.Angiographic Substudy
Of the 899 patients enrolled in the angiographic substudy, 816 were eligible for analysis; the others were excluded because of an unsuccessful index revascularization procedure, revascularization performed within seven days of the index procedure or without a previous angiogram, or death. Of the 816 eligible patients, follow-up angiography was not performed in 105, and angiograms were technically inadequate or unavailable or were obtained more than 275 days after the index procedure in an additional 65 patients. Thus, follow-up angiograms from a total of 646 of the 816 eligible patients (79 percent) were analyzed in the angiographic substudy.
Patients included in the substudy were representative of the overall population in the trial, and there were no significant differences in base-line characteristics or clinical outcomes between those who were included in the substudy and those who were not. Angiographic outcomes among the patients in the substudy are summarized in Table 3Table 3
Outcomes in the Angiographic Substudy.. Minimal luminal diameters after the intervention and early gains in diameter were significantly greater among patients who underwent stent implantation than among those who underwent angioplasty. Among patients who received a stent, the net gain in diameter was significantly greater among those who received abciximab than among those assigned to placebo, with a trend toward greater minimal luminal diameters at six months and a lower loss index (late loss divided by early gain) (Table 3). Key angiographic variables among patients with diabetes and those without it are illustrated in Figure 3AFigure 3
Angiographic Measurements of Restenosis in 127 Patients with Diabetes and 519 Patients without Diabetes at the Six-Month Follow-up. and Figure 3B. At follow-up, minimal luminal diameters and net gain were substantially lower among patients with diabetes than among those without this condition in the angioplasty-plus-abciximab and stent-plus-placebo groups. In contrast, among those who underwent stenting and received abciximab, there were virtually no differences between patients with diabetes and those without it with regard to these angiographic variables.Discussion
The design of our trial allowed the roles of platelet glycoprotein IIb/IIIa receptor blockade and coronary-artery stenting to be defined in patients requiring coronary revascularization. We were able to compare stenting with balloon angioplasty among patients receiving abciximab and to compare the effectiveness of abciximab with that of placebo among patients who received a stent. The results at six months indicate that stent implantation and potent inhibition of platelet aggregation with abciximab provide important and complementary long-term clinical benefits after coronary intervention. Specifically, the results validated the effectiveness of stenting in reducing restenosis in a diverse group of patients, showed that late mortality is lower with stenting than with angioplasty when treatment is accompanied by abciximab therapy, demonstrated that abciximab has a long-lasting effect in reducing acute ischemic complications, and provided evidence that abciximab is associated with a reduction in the risk of restenosis among patients with diabetes mellitus who have received a stent.
In this trial, the entry criteria were broad and were intended to reflect the practice of percutaneous coronary revascularization in the real world, rather than revascularization in a narrow or idealized subgroup of patients with stenoses, as has been evaluated in previous trials that have compared stenting with balloon angioplasty. The six-month results confirm the efficacy of stenting in reducing angiographic restenosis and its clinical manifestation, the need for repeated revascularization of the target vessel, in this diverse group of patients with a variety of coronary lesions. As compared with angioplasty accompanied by abciximab, stent implantation, both by itself and with abciximab therapy, reduced the need for repeated target-vessel revascularization (by 31 percent and 44 percent, respectively). In the angiographic substudy, stent implantation was associated with a significantly greater average minimal luminal diameter of the target vessel after six months. Moreover, with abciximab therapy, stenting conferred a benefit as compared with angioplasty with respect to mortality: mortality was more than 70 percent lower with stenting than with angioplasty. This finding confirms that the combination of stenting and abciximab sets a new standard of safety and efficacy during coronary intervention.
The early reduction in the risk of ischemic complications produced by abciximab among patients who underwent stenting was maintained without attenuation over the long term. This durability of treatment effect is concordant with the long-term follow-up results of previous randomized trials of this agent among patients undergoing balloon angioplasty and atherectomy.2,11-13 Ischemic events tended to take place early after the interventional procedure, at a time when the abciximab infusion exerts its protective effect through potent inhibition of platelet thrombus formation in the coronary vessels. The durability of this early clinical benefit suggests that the stimulus for new thrombus formation is largely attenuated within a few days after treatment of the coronary plaque.
In a previous trial of platelet glycoprotein IIb/IIIa receptor blockade during coronary intervention, therapy with abciximab was associated, by six months, with a 26 percent reduction in the rate of repeated target-vessel revascularization procedures, a finding that suggested that this agent might inhibit the restenotic process after balloon angioplasty or atherectomy.11 In subsequent trials of angioplasty, however, significant differences in the rates of late revascularization of the target vessel were not observed between the placebo and abciximab groups.2,3 The six-month results of the current trial, however, again suggest that abciximab may inhibit one or more of the mechanisms of restenosis, at least in some subgroups of patients. Among patients randomly assigned to undergo stenting, therapy with abciximab, as compared with placebo, was associated with a nonsignificant trend toward a reduction in the incidence of target-vessel revascularization, a benefit that was confined to patients with diabetes mellitus. The time-to-event curves for this end point in the stent-plus-abciximab group and the stent-plus-placebo group began to diverge approximately 90 days after stent implantation, during the period when restenosis at the site of the stent can become clinically manifest. This finding indicates that any salutary effect of abciximab was not due simply to a reduction in the need for early urgent revascularization procedures.
An influence of abciximab on in-stent restenosis among patients with diabetes is not inconsistent with the absence of a reproducible effect of abciximab on the rates of restenosis after balloon angioplasty. Stent implantation essentially eliminates the processes of elastic recoil and adverse remodeling, thereby isolating neointimal hyperplasia as the predominant mechanism of in-stent restenosis.14 Increased rates of restenosis due to neointimal hyperplasia after stenting have been consistently observed among patients with diabetes.15-18 In the current study, patients with diabetes who were randomly assigned to stenting and placebo had a substantially higher incidence of late target-vessel revascularization than did their nondiabetic counterparts (16.6 percent vs. 9.0 percent, respectively), and in contrast to the outcome among nondiabetic patients, stent implantation without abciximab did not significantly reduce the rate of late revascularization as compared with the rate with angioplasty. Treatment with abciximab in addition to stenting, however, diminished the incidence of target-vessel revascularization among patients with diabetes by 51 percent, neutralizing the excess risk of this end point among patients with diabetes (as compared with those without it). Angiographic results among patients with diabetes were concordant with clinical outcomes: minimal luminal diameters and net gains in diameter at follow-up were markedly improved by stenting accompanied by abciximab, but not by stenting alone, as compared with angioplasty. By reducing thrombus formation as well as by providing nonspecific blockade of the αvβ3 receptor on endothelial and smooth-muscle cells, treatment with abciximab may inhibit the neointimal hyperplastic response to arterial injury in these patients.19
Percutaneous coronary revascularization is performed in more than 1 million patients worldwide each year. Protection against the ischemic complications of death and myocardial infarction and the need for repeated revascularization remains the principal objective in the development of new devices and adjunct therapies for this procedure. In the combination of an improved mechanical technique for revascularization with potent pharmacologic therapy to suppress platelet thrombosis, substantial progress has been made in achieving this goal. Stent implantation and blockade of the platelet glycoprotein IIb/IIIa receptor with abciximab provide potent complementary benefits, such that percutaneous revascularization can be performed at a new standard of safety and efficacy.
Supported by Centocor (Malvern, Pa.) and Eli Lilly (Indianapolis).
Source Information
From the Departments of Cardiology (A.M.L., D.J.M., S.G.E., J.E.B., E.J.T.) and Biostatistics and Epidemiology (S.K.S.), Cleveland Clinic Foundation, Cleveland; the Department of Medicine, Duke Clinical Research Institute, Duke University, Durham, N.C. (R.M.C.); the University of Manitoba, Winnipeg, Man., Canada (J.D.); Our Lady of Lourdes Medical Center, Cherry Hill, N.J. (J.H.K.); Baylor College of Medicine, Houston (N.S.K.); Sunnybrook Health Science Centre, Toronto (E.A.C.); and Centocor, Malvern, Pa. (C.F.C.).
Address reprint requests to Dr. Lincoff at the Department of Cardiology, Desk F25, Cleveland Clinic Foundation, Cleveland, OH 44195.
The principal investigators and study coordinators of the Evaluation of Platelet IIb/IIIa Inhibition in Stenting (EPISTENT) Study Group are listed in the Appendix.
Other authors were James E. Tcheng, M.D. (Duke Clinical Research Institute), J. David Talley, M.D. (University of Arkansas, Little Rock), Paul O. Caramori, M.D. (Toronto Hospital, Toronto), Jeffrey R. Burton, M.D. (University of Alberta Hospital, Edmonton, Alta., Canada), Thomas A. Kelly, M.D. (Moses Cone Memorial Hospital, Greensboro, N.C.), and Tom B. Ivanc, M.S. (Cleveland Clinic Foundation).
Appendix
The principal investigators and study coordinators of the EPISTENT Study Group were as follows: Operations Committee — E.J. Topol (study chairman), R.M. Califf, A.M. Lincoff, J.E. Tcheng. Principal investigators and study coordinators (numbers of patients enrolled are given in parentheses) — University of Manitoba, Winnipeg, Man., Canada (153): J. Ducas, P.K. Cheung, U. Schick; Our Lady of Lourdes Medical Center, Cherry Hill, N.J. (147): J.H. Kramer, P. Koren, R. Wilson; University of Arkansas, Little Rock (142): J.D. Talley, J. McClellan, M. Dearen; Toronto Hospital, Toronto (138): A.G. Adelman, P. Caramori, S. Webber; Baylor College of Medicine, Houston (135): N.S. Kleiman, J. Taylor, T. Ferrando; Sunnybrook Health Science Centre, Toronto (132): E. Cohen, L. Balleza; Cleveland Clinic Foundation, Cleveland (118): A.M. Lincoff, C. Rouse; University of Alberta Hospital, Edmonton, Alta., Canada (108): J. Burton, E. Anderson, N. Hogg; Moses Cone Memorial Hospital, Greensboro, N.C. (97): T. Kelly, S. Alston; St. Paul's Hospital, Vancouver, B.C., Canada (81): J. Webb, S. VanWeinen; Vancouver Hospital and Health Sciences Centre, Vancouver, B.C., Canada (76): D.R. Ricci, S. Mockman; Institut de Cardiologie de Montréal, Montreal (68): J.F. Tanguay, A.M. Poitras; William Beaumont Hospital, Royal Oak, Mich. (65): G. Timis, D. Davey; Northern Californian Medical Association, Santa Rosa, Calif. (57): P. Coleman, P. Herrold-Runge; Victoria General Hospital, Halifax, N.S., Canada (57): B.J. O'Neill, K. Foshey, N. Fitzgerald; London Health Sciences Centre, London, Ont., Canada (52): D. Almond, W. Kostuk, J. White; Graduate Hospital, Philadelphia (52): R. Gottlieb, H. Snyder, P. Koren, J. Lavoie; University of Connecticut Health Center, Farmington (48): M. Azrin, D. Murphy; Geisinger Medical Center, Danville, Pa. (47): J. Blankenship, L. Demko; Henry Ford Heart and Vascular Institute, Detroit (47): P. Kraft, L. Dvorak; Royal Columbian Hospital, New Westminster, B.C., Canada (45): R. Brown, M. Colclough, K. Stevens; University of Virginia, Charlottesville (45): I. Sarembock, L. Snyder, S. Sayre; Watson Clinic, Lakeland, Fla. (44): K. Browne, M. Roy; Presbyterian Hospital, Charlotte, N.C. (43): B. Reen, R. Short; Rochester General Hospital, Rochester, N.Y. (37): M. Thompson, V. Chiodo, D. Hoffman; University Medical Center, Jacksonville, Fla. (35): T.A. Bass, M. Zenni, G. Rohman; Ottawa Civic Hospital, Ottawa, Ont., Canada (35): J.F. Marquis, F. Reid, J. Jelley; Harbor–University of California at Los Angeles Medical Center, Torrance (30): W. French, S. Goldberg, S. Wang; Western Pennsylvania Hospital, Pittsburgh (27): A. Gradman, L. Botley, J. Collins; Lancaster Heart Foundation, Lancaster, Pa. (20): S. Worley, L. Hollywood; Midwest Cardiology Research Foundation, Columbus, Ohio (20): S. Yakibov, C. Gilliland; Florida Hospital, Orlando (19): R. Ivanhoe, K. Potter; Deborah Heart and Lung Center, Brown Mills, N.J. (19): M. Taylor, E. Cleary; Iowa Heart Center, Des Moines (18): M. Tannenbaum, A. Hartz; St. Luke's–Roosevelt Hospital, New York (13): J. Hochman, J. Slater; University of Michigan Medical Center, Ann Arbor (12): E. Bates, P. Fox-Bruenger; Orlando Regional Medical Center–Columbia, Orlando, Fla. (12): M. Gonzalez, L. Jopperri; University of Cincinnati Medical Center, Cincinnati (12): J.P. Runyon, N. Higby; Durham Veterans Affairs Medical Center, Durham, N.C. (11): J. Tcheng, M. Rund; St. Louis University Hospital, St. Louis (8): R. Bach, C. Mechem; Hartford Hospital, Farmington, Conn. (8): M. Azrin, D. Murphy; Milwaukee Heart and Vascular Clinic, Milwaukee (5): F.E. Cummins, J. Nonweiler; Christ Hospital, Cincinnati (4): J.P. Runyon, N. Higby; Western Montana Clinic, Missoula (4): M. Sanz, C. Cole; Tampa General Hospital, Tampa, Fla. (4): M.W. Weston; University of Texas Medical School, Houston (3): H.V. Anderson, L. Weigelt; Evanston Hospital, Evanston, Ill. (3): T. Larkin, B.J. Jackson; Lutheran General Hospital, Park Ridge, Ill. (3): M.J. Rosenberg, S. Tully; Sentra Norfolk General Hospital, Norfolk, Va. (2): C. Hartman, S. Lunow; Prairie Cardiovascular Consult, Springfield, Ill. (2): C. Lucore, G. Miskel, K. McShane; LDS Hospital, Salt Lake City (2): B. Muhlestein, J. Jerman; Louisiana State University Medical Center, New Orleans (2): G. Sander, A. Stevens; St. Michael's Hospital, Toronto (2): R. Chisholm, S. Webber; Creighton Cardiac Center, Omaha, Nebr. (1): M. Del Core, L. Stengel; Coordinating Center — J. Booth (study coordinator), R. Cannata, V. Castle, H. Cohen, S. DeLuca, M. Kutner, T. Knuth, A. Lincoff, T. McCollough, J. McPhearson, J. Melton, D. Miller, M. Pulliam, S. Sapp, K.N. Sigmon; Clinical Events Committee — M. Templin, E. Montague, J. Carlson, L. Heil, V. Zovkic, K. Malone, S. Rodkey, G. Haas, R. Harrington, S. Kapadia, L. Campbell, D. Mukherjee, M. Deedy, R. Augostini, J. Alexander, D. Whellan, C. Bajzer, R. Rabbani; Electrocardiographic Core Laboratory — P. Clemons, R. Baishnab, R. Randall, D. Underwood, M.A. Lauer, M.S. Lauer, M. Roe, R. Farhy, R. Schweikert, T. Grady; Angiographic Core Laboratory — S.G. Ellis, D.J. Moliterno (medical directors), D. Debowey (director), T. Ivanc, L. Ols, R. Poliszcuk, E. Balazs, B. Witherspoon; Centocor — K.M. Anderson, E. Barnatham, C.F. Cabot, G.L. Stoner, H.F. Weisman.
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Karin Mauer, Jorge F. Saucedo. 2011. Cardiology-In-Depth Look: Advances in Antiplatelet Therapy. .
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R. Scott Wright, Jeffrey L. Anderson, Cynthia D. Adams, Charles R. Bridges, Donald E. Casey, Steven M. Ettinger, Francis M. Fesmire, Theodore G. Ganiats, Hani Jneid, A. Michael Lincoff, Eric D. Peterson, George J. Philippides, Pierre Theroux, Nanette K. Wenger, James Patrick Zidar. (2011) 2011 ACCF/AHA Focused Update of the Guidelines for the Management of Patients With Unstable Angina/Non–ST-Elevation Myocardial Infarction (Updating the 2007 Guideline). Journal of the American College of Cardiology 57:19, 1920-1959
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Eric Heller, George D. Dangas. 2011. Heparin, LMWH, GIIb/IIIa, and Direct Thrombin Inhibitors. , 110-143.
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Michael Koutouzis, Bo Lagerqvist, Jonas Oldgren, Axel Åkerblom, Magnus Wahlin, Thomas Karlsson, Per Albertsson, Göran Matejka, Lars Grip. (2010) Long-Term Results Following Switch From Abciximab to Eptifibatide During Percutaneous Coronary Intervention. Clinical Cardiology 33:11, 686-692
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Xavier Bosch, Jaume Marrugat, Juan Sanchis, Xavier Bosch. 2010. Platelet glycoprotein IIb/IIIa blockers during percutaneous coronary intervention and as the initial medical treatment of non-ST segment elevation acute coronary syndromes. .
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Douglass A. Morrison. (2010) Limitations of stints: A good, albeit imperfect, therapy; For a less than perfect world. Catheterization and Cardiovascular Interventions 75:3, 343-344
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G. G. Camici, J. Steffel, I. Amanovic, A. Breitenstein, J. Baldinger, S. Keller, T. F. Luscher, F. C. Tanner. (2010) Rapamycin promotes arterial thrombosis in vivo: implications for everolimus and zotarolimus eluting stents. European Heart Journal 31:2, 236-242
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Serdar Farhan, Thomas Höchtl, Alexandra Kautzky-Willer, Johann Wojta, Kurt Huber. (2010) Antithrombotic therapy in patients with coronary artery disease and with type 2 diabetes mellitus. Wiener Medizinische Wochenschrift 160:1-2, 30-38
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Ana Blagojevic, Joseph A.C. Delaney, Linda E. Lévesque, Nandini Dendukuri, Jean-Francois Boivin, James M. Brophy. (2009) Investigation of an interaction between statins and clopidogrel after percutaneous coronary intervention: a cohort study. Pharmacoepidemiology and Drug Safety 18:5, 362-369
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A. Siddique, M. Butt, E. Shantsila, G. Y. H. Lip. (2009) New antiplatelet drugs: beyond aspirin and clopidogrel. International Journal of Clinical Practice 63:5, 776-789
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R. A. G. Patel, C. J. White. (2008) Survival Benefit With Concomitant Oral Platelet Therapy After Coronary Angiography and Before Ad Hoc Percutaneous Coronary Intervention. Mayo Clinic Proceedings 83:9, 978-979
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Raisuke Iijima, Gjin Ndrepepa, Julinda Mehilli, Josef Dirschinger, Jürgen Pache, Melchior Seyfarth, Albert Schömig, Adnan Kastrati. (2008) Effect of Abciximab on Clinical and Angiographic Restenosis in Patients With Non–ST-Segment Elevation Acute Coronary Syndromes. The American Journal of Cardiology 101:9, 1226-1231
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Kirsten H. Long, Henry H. Ting, Erin K. McMurtry, Ryan J. Lennon, Douglas L. Wood, David R. Holmes, Ganesh Raveendran, Charanjit S. Rihal. (2008) A Longitudinal Analysis of Outcomes Associated with Abciximab and Eptifibatide in a Consecutive Series of 3074 Percutaneous Coronary Interventions. Value in Health 11:3, 462-469
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Stephen D Wiviott, Eugene Braunwald, Carolyn H McCabe, Ivan Horvath, Matyas Keltai, Jean-Paul R Herrman, Frans Van de Werf, William E Downey, Benjamin M Scirica, Sabina A Murphy, Elliott M Antman. (2008) Intensive oral antiplatelet therapy for reduction of ischaemic events including stent thrombosis in patients with acute coronary syndromes treated with percutaneous coronary intervention and stenting in the TRITON-TIMI 38 trial: a subanalysis of a randomised trial. The Lancet 371:9621, 1353-1363
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David M. Kent, Thomas A. Trikalinos. (2008) Are “treatment” bare metal stents superior to “control” bare metal stents? A meta-analytic approach. American Heart Journal 155:4, 624-629.e2
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William E. Boden, Prediman K. Shah, Vipul Gupta, E. Magnus Ohman. (2008) Contemporary Approach to the Diagnosis and Management of Non–ST-Segment Elevation Acute Coronary Syndromes. Progress in Cardiovascular Diseases 50:5, 311-351
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M. Cattaneo. (2008) Haemorrhagic stroke during anti-platelet therapy. European Journal of Anaesthesiology 25:Supplement 42, 12-15
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ROD STABLES. 2008. Patient selection for percutaneous coronary intervention. , 19-27.
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Ralf Zahn, Thomas Ischinger, Matthias Hochadel, Bernd Mark, Uwe Zeymer, Jens Jung, Alexander Schramm, Karl-Eugen Hauptmann, Hubert Seggewiß, Ilse Janicke, Harald Mudra, Jochen Senges, . (2007) Glycoprotein IIb/IIIa antagonists during carotid artery stenting:. Clinical Research in Cardiology 96:10, 730-737
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Marino Labinaz, Chuong Ho, Srabani Banerjee, Janet Martin, Stella Chen, Shaila Mensinkai. (2007) Meta-analysis of clinical efficacy and bleeding risk with intravenous glycoprotein IIb/IIIa antagonists for percutaneous coronary intervention. Canadian Journal of Cardiology 23:12, 963-970
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Walid Hassan, Hani Al-Sergani, Jehad Al Buraiki, Bruce Dunn, Fawaz Al Turki, Nathem Akhras, Fayez ElShaer, Mahboob Nawaz, Suliman Kharabsheh, Naser ElKum. (2007) Immediate and intermediate results of intracoronary stand-alone bolus administration of eptifibatide during coronary intervention (ICE) study. American Heart Journal 154:2, 345-351
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José R. López-Mínguez, Juan M. Nogales, Reyes González, Carlos Palanco, Javier Doncel, Alejandra Vaello, Fernando Giménez, Angel Morales, Rafael Alonso, Antonio Merchán. (2007) Abciximab offers greater benefits to insulin-dependent diabetic patients undergoing coronary stent implantation. Cardiovascular Revascularization Medicine 8:3, 175-182
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Taku Kokubo, Hisashi Uchida, Eric T. Choi. (2007) Integrin αvβ3 as a target in the prevention of neointimal hyperplasia. Journal of Vascular Surgery 45:6, A33-A38
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W. Lepper, M. Kelm. (2007) Perioperative Therapie mit Thrombozytenaggregationshemmern. Der Anaesthesist 56:6, 592-598
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Nadine Gauthier, Michel R Le May. (2007) Percutaneous coronary intervention for left main coronary artery disease. Expert Review of Cardiovascular Therapy 5:2, 213-220
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Joost Daemen, Peter Wenaweser, Keiichi Tsuchida, Linda Abrecht, Sophia Vaina, Cyrill Morger, Neville Kukreja, Peter Jüni, Georgios Sianos, Gerrit Hellige, Ron T van Domburg, Otto M Hess, Eric Boersma, Bernhard Meier, Stephan Windecker, Patrick W Serruys. (2007) Early and late coronary stent thrombosis of sirolimus-eluting and paclitaxel-eluting stents in routine clinical practice: data from a large two-institutional cohort study. The Lancet 369:9562, 667-678
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Cinzia Capuano, Marco Sesana, Ornella Leonzi, Claudio Cuccia. (2006) Safety and efficacy of low-dose unfractionated heparin during percutaneous coronary revascularisation and the relationship between activated clotting time and haemorrhagic or ischaemic complications: our results. Journal of Cardiovascular Medicine 7:12, 866-871
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Adnan K. Chhatriwalla, Deepak L. Bhatt. 2006. Anticoagulation and Antiplatelet Agents. , 501-524.
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Kirsten Hall Long, Erin K. McMurtry, Ryan J. Lennon, Anne C. Chapman, Mandeep Singh, Charanjit S. Rihal, Douglas L. Wood, David R. Holmes, Henry H. Ting. (2006) Elective Percutaneous Coronary Intervention Without On-Site Cardiac Surgery. Medical Care 44:5, 406-413
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Stephen J. Nicholls, E. Murat Tuzcu, Tim Crowe, Ilke Sipahi, Paul Schoenhagen, Samir Kapadia, Stanley L. Hazen, Chuan-Chuan Wun, Michele Norton, Fady Ntanios, Steven E. Nissen. (2006) Relationship Between Cardiovascular Risk Factors and Atherosclerotic Disease Burden Measured by Intravascular Ultrasound. Journal of the American College of Cardiology 47:10, 1967-1975
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G. Grassi, H. Köhn, B. Dapas, R. Farra, J. Platz, S. Engel, S. Cjsareck, R. Kandolf, C. Teutsch, R. Klima, G. Triolo, A. Kuhn. (2006) Comparison between recombinant baculo- and adenoviral-vectors as transfer system in cardiovascular cells. Archives of Virology 151:2, 255-271
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Sidney C. Smith, Ted E. Feldman, John W. Hirshfeld, Alice K. Jacobs, Morton J. Kern, Spencer B. King, Douglass A. Morrison, William W. O’Neill, Hartzell V. Schaff, Patrick L. Whitlow, David O. Williams, Elliott M. Antman, Sidney C. Smith, Cynthia D. Adams, Jeffrey L. Anderson, David P. Faxon, Valentin Fuster, Jonathan L. Halperin, Loren F. Hiratzka, Sharon Ann Hunt, Alice K. Jacobs, Rick Nishimura, Joseph P. Ornato, Richard L. Page, Barbara Riegel. (2006) ACC/AHA/SCAI 2005 Guideline Update for Percutaneous Coronary Intervention. Journal of the American College of Cardiology 47:1, e1-e121
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Alain J Nordmann, Heiner Bucher, P Hengstler, Thomas Harr, James Young, Alain J Nordmann. 2005. Primary stenting versus primary balloon angioplasty for treating acute myocardial infarction. .
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MEHMET AGIRBASLI, NIYAZI GULER. (2005) Recovery of Left Ventricular Systolic Function after Left Anterior Descending Coronary Artery Stenting. Journal of Interventional Cardiology 18:2, 83-88
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Jeffrey W. Moses, Roxana Mehran, Eugenia Nikolsky, John M. Lasala, Woodrow Corey, Glenn Albin, Cary Hirsch, Martin B. Leon, Mary E. Russell, Stephen G. Ellis, Gregg W. Stone. (2005) Outcomes with the paclitaxel-eluting stent in patients with acute coronary syndromes. Journal of the American College of Cardiology 45:8, 1165-1171
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M. Kelm, B. E. Strauer. (2005) Das akute Koronarsyndrom. Der Internist 46:3, 265-274
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Serkan Cay, Mehmet Birhan Yilmaz, Sule Korkmaz. (2005) Intracranial Bleeding Associated with Clopidogrel. Cardiovascular Drugs and Therapy 19:2, 157-158
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Alberto Menozzi, Piera Angelica Merlini, Diego Ardissino. (2005) Tirofiban in acute coronary syndromes. Expert Review of Cardiovascular Therapy 3:2, 193-206
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J. Hausleiter, A. Kastrati, J. Mehilli, H. Schuhlen, J. Pache, F. Dotzer, C. Glatthor, S. Siebert, J. Dirschinger, A. Schomig, . (2004) A randomized trial comparing phosphorylcholine-coated stenting with balloon angioplasty as well as abciximab with placebo for restenosis reduction in small coronary arteries. Journal of Internal Medicine 256:5, 388-397
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Vassilis A. Voudris, John S. Skoularigis, Yvonne K. Dimitriou, Georgia N. Grapsa, John S. Malakos, Gregory S. Pavlides, Athanasios N. Manginas, Dennis V. Cokkinos. (2004) Diabetes mellitus and unstable coronary artery disease: improved clinical outcome of coronary artery stenting in an era of glycoprotein IIb/IIIa inhibitors and lipid-lowering therapy. Coronary Artery Disease 15:6, 353-359
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Richard W. Smalling, Gregory M. Giesler. (2004) Early and Aggressive Treatment of Patients With Acute ST Segment Elevation and Non-ST Segment Elevation Myocardial Infarction Leads to Improved Clinical Outcomes. Critical Pathways in Cardiology: A Journal of Evidence-Based Medicine 3:3, 121-127
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Ganesan Karthikeyan, Balram Bhargava. (2004) Prevention of restenosis after coronary angioplasty. Current Opinion in Cardiology 19:5, 500-509
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Michael S Lee, Eric M David, Raj R Makkar, James R Wilentz. (2004) Molecular and cellular basis of restenosis after percutaneous coronary intervention: the intertwining roles of platelets, leukocytes, and the coagulation–fibrinolysis system. The Journal of Pathology 203:4, 861-870
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Ron Waksman, Andrew E. Ajani, Luis Gruberg, Ellen Pinnow, Afework GebreEyesus, Regina Deible, Lowell F. Satler, Augusto D. Pichard, Rebecca Torguson, Kenneth M. Kent, William Suddath, Joseph Lindsay. (2004) Use of IIb/IIIa inhibitors in patients with in-stent restenosis treated with intracoronary ?-radiation: Integrilin WRIST. Catheterization and Cardiovascular Interventions 62:2, 162-166
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B. R. Curtis, A. Divgi, M. Garritty, R. H. Aster. (2004) Delayed thrombocytopenia after treatment with abciximab: a distinct clinical entity associated with the immune response to the drug. Journal of Thrombosis and Haemostasis 2:6, 985-992
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Kenneth Ouriel. (2004) Use of Concomitant Glycoprotein IIb/IIIa Inhibitors with Catheter-directed Peripheral Arterial Thrombolysis. Journal of Vascular and Interventional Radiology 15:6, 543-546
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Jeffrey W Moses, Roxana Mehran, George D Dangas, Yoshio Kobayashi, Alexandra J Lansky, Gary S Mintz, Eve D Aymong, Martin Fahy, Gregg W Stone, Martin B Leon. (2004) Short- and long-term results after multivessel stenting in diabetic patients. Journal of the American College of Cardiology 43:8, 1348-1354
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Michael H Rosove. (2004) Platelet glycoprotein IIb/IIIa inhibitors. Best Practice & Research Clinical Haematology 17:1, 65-76
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Ganeshkumar Anne, Luis Gruberg. (2004) Platelet glycoprotein IIb/IIIa inhibitors during percutaneous coronary interventions: a pharmacological and clinical review. Expert Opinion on Pharmacotherapy 5:2, 335-348
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Aman K. Kakkar, Ali Moustapha, Henry G. Hanley, Mitchell Weiss, Gloria Caldito, Praphul Misra, Pratap C. Reddy, Neeraj Tandon. (2004) Comparison of intracoronary vs. intravenous administration of abciximab in coronary stenting. Catheterization and Cardiovascular Interventions 61:1, 31-34
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Sherwin K B Sy, Aaron L Levenstadt. (2004) A Perspective on the Toxicological Mechanisms Possibly Contributing to the Failure of Oral Glycoprotein IIb/IIIa Antagonists in the Clinic. American Journal of Cardiovascular Drugs 4:1, 1-10
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Sandeep T. Laroia, Archana T. Laroia. (2004) Drug-Eluting Stents. Cardiology in Review 12:1, 37-43
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Eric J Topol, Franz-Josef Neumann, Gilles Montalescot. (2003) A preferred reperfusion strategy for acute myocardial infarction. Journal of the American College of Cardiology 42:11, 1886-1889
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Ian D. Conde, Neal S. Kleiman. (2003) Arterial thrombosis for the interventional cardiologist: From adhesion molecules and coagulation factors to clinical therapeutics. Catheterization and Cardiovascular Interventions 60:2, 236-246
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Albert W Chan, David J Moliterno, Peter B Berger, Gregg W Stone, Peter M DiBattiste, Steven L Yakubov, Shelly K Sapp, Kathy Wolski, Deepak L Bhatt, Eric J Topol. (2003) Triple antiplatelet therapy during percutaneous coronary intervention is associated withimproved outcomes including one-year survival. Journal of the American College of Cardiology 42:7, 1188-1195
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Mitchell J Ross, Howard C Herrmann, David J Moliterno, James C Blankenship, Laura Demopoulos, Peter M DiBattiste, Stephen G Ellis, Ziyad Ghazzal, Jack L Martin, Jennifer White, Eric J Topol. (2003) Angiographic variables predict increased riskfor adverse ischemic events after coronarystenting with glycoprotein IIb/IIIa inhibition. Journal of the American College of Cardiology 42:6, 981-988
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Jacqueline Saw, David Moliterno. (2003) Coronary Artery Disease 14:5, 373-380
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Jacqueline Saw, David J. Moliterno. (2003) Contemporary use of antiplatelet therapies in percutaneous coronary interventions. Coronary Artery Disease 14:5, 373-380
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Saila Vikman, Kari Niemelä, Tuomo Ilva, Kirsi Majamaa-Voltti, Matti Niemelä, Keijo Peuhkurinen, Ilkka Tierala, K.E.Juhani Airaksinen. (2003) Underuse of evidence-based treatment modalities in diabetic patients with non-ST elevation acute coronary syndrome. A prospective nation wide study on acute coronary syndrome (FINACS). Diabetes Research and Clinical Practice 61:1, 39-48
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Glenda Bilder, Dilip Amin, Lisa Morgan, Matthew McVey, Saul Needle, Helen Galczenski, Robert Leadley, Wei He, Michael Myers, Alfred Spada, Yongyi Luo, Chandra Natajaran, Mark Perrone. (2003) Stent-induced Restenosis in the Swine Coronary Artery Is Inhibited by a Platelet-Derived Growth Factor Receptor Tyrosine Kinase Inhibitor, TKI963. Journal of Cardiovascular Pharmacology 41:6, 817-829
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JAMES E. TCHENG, MINA MADAN, J. CONOR O'SHEA, ERIC A. COHEN, CHRISTOPHER E. BULLER, A. MICHAEL LINCOFF, JEFFREY J. POPMA, PAUL S. TEIRSTEIN, MICHAEL M. KITT, TODD J. LORENZ, SALLY GREENBERG, NORMAN FOST, ROBERT M. CALIFF. (2003) Ethics and Equipoise: Rationale for a Placebo-Controlled Study Design of Platelet Glycoprotein IIb/IIIa Inhibition in Coronary Intervention. Journal of Interventional Cardiology 16:2, 97-105
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William E Boden, Carl J Pepine. (2003) Introduction to “optimizing management of non–ST-segment elevation acute coronary syndromes”. Journal of the American College of Cardiology 41:4, S1-S6
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Steven E Nissen. (2003) Pathobiology, not angiography, should guide managementin acute coronary syndrome/non–ST-segment elevation myocardial infarction. Journal of the American College of Cardiology 41:4, S103-S112
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Raymond G. McKay. (2003) “Ischemia-guided” versus “early invasive” strategies in the management of acute coronary syndrome/non–ST-segment elevation myocardial infarction. Journal of the American College of Cardiology 41:4, S96-S102
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David J. Moliterno, Albert W. Chan. (2003) Glycoprotein IIb/IIIa inhibition in early intent-to-stent treatment of acute coronary syndromes: EPISTENT, ADMIRAL, CADILLAC, and TARGET. Journal of the American College of Cardiology 41:4, S49-S54
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Evangelia Karvouni, Demosthenes G Katritsis, John P.A Ioannidis. (2003) Intravenous glycoprotein IIb/IIIa receptor antagonists reduce mortality after percutaneous coronary interventions. Journal of the American College of Cardiology 41:1, 26-32
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Tim Ibbotson, Jane K McGavin, Karen L Goa. (2003) Abciximab. Drugs 63:11, 1121-1163
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Venanzio Vella. (2003) Potential Costs and Effects of the National Service Framework for Coronary Heart Disease in the UK. PharmacoEconomics 21:1, 49-60
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Upendra Kaul, Ripen K. Gupta, Kottaram K. Haridas, Saligrama S. Ramesh, Kamal K. Sethi, Balbir Singh, Rajiv Agarwal, Ram D. Yadave, Tapan Ghose, Rakesh R. Sapra, Rajiv Bajaj, Madhukar Shahi, Ajit Bhagwat, Pramod Kumar, Omen P. Mathews, Pratik K. Soni, . (2002) Platelet glycoprotein IIb/IIIa inhibition using eptifibatide with primary coronary stenting for acute myocardial infarction: A 30-day follow-up study. Catheterization and Cardiovascular Interventions 57:4, 497-503
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R. K. Choi, N. H. Lee, D. S. Lim, S. K. Hong, H. K. Hwang. (2002) Pulmonary Hemorrhage After Percutaneous Coronary Intervention With Abciximab Therapy. Mayo Clinic Proceedings 77:12, 1340-1343
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Guido Schnyder, Yvonne Flammer, Marco Roffi, Riccardo Pin, Otto Martin Hess. (2002) Plasma homocysteine levels and late outcome after coronary angioplasty. Journal of the American College of Cardiology 40:10, 1769-1776
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Amar M Salam, Jassim Al Suwaidi. (2002) Platelet glycoprotein IIb/IIIa antagonists in clinical trials for the treatment of coronary artery disease. Expert Opinion on Investigational Drugs 11:11, 1645-1658
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Eric Van Belle, Marc Périé, David Braune, Akram Chmaït, Thibaud Meurice, Kaveh Abolmaali, Eugène P. McFadden, Christophe Bauters, Jean-Marc Lablanche, Michel E. Bertrand. (2002) effects of coronary stenting on vessel patency and long-term clinical outcome after percutaneous coronary revascularization in diabetic patients. Journal of the American College of Cardiology 40:3, 410-417
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David J Moliterno, Steven J Yakubov, Peter M DiBattiste, Howard C Herrmann, Gregg W Stone, Carlos Macaya, Franz-Josef Neumann, Diego Ardissino, Jean-Pierre Bassand, Lynn Borzi, Alan C Yeung, Katherine A Harris, Laura A Demopoulos, Eric J Topol. (2002) Outcomes at 6 months for the direct comparison of tirofiban and abciximab during percutaneous coronary revascularisation with stent placement: the TARGET follow-up study. The Lancet 360:9330, 355-360
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Heidar Arjomand, Satish K. Surabhi, Marc Cohen. (2002) Unfractionated versus fractionated heparin for percutaneous coronary intervention. Current Cardiology Reports 4:4, 327-333
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D. P. Chew, D. L. Bhatt. (2002) Optimizing glycoprotein IIb/IIIa inhibition: lessons from recent randomized controlled trials. Internal Medicine Journal 32:7, 338-345
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Hsien-Li Kao, Lung-Chun Lin, Chau-Chung Wu, Chiau-Suong Liau, Yuan-Teh Lee. (2002) Suppression of Cyclic Coronary Flow Variation and Reduction of Restenosis with Abciximab for Morphologically High-Risk Lesions Undergoing Percutaneous Coronary Intervention. Journal of Cardiovascular Pharmacology 39:6, 901-908
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Dale T. Ashby, George Dangas, Roxana Mehran, Martin B. Leon. (2002) Coronary artery stenting. Catheterization and Cardiovascular Interventions 56:1, 83-102
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Jacques R. Leclerc. (2002) Platelet glycoprotein IIb/IIIa antagonists: Lessons learned from clinical trials and future directions. Critical Care Medicine 30:Supplement, S332-S340
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Hazar Shadid, Salim Aziz, Sarfraz Ahmad, Jawed Fareed, Debra Hoppensteadt, Harry Messmore, William Wehrmacher, Mahmut Tobu, Omer Iqbal. (2002) Antithrombotic agents in the treatment of severe sepsis. Expert Opinion on Emerging Drugs 7:1, 111-139
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Adnan Kastrati, Julinda Mehilli, Josef Dirschinger, Ullrich Schricke, Jodi Neverve, Jürgen Pache, Stefan Martinoff, Franz-Josef Neumann, Stephan Nekolla, Rudolf Blasini, Melchior Seyfarth, Markus Schwaiger, Albert Schömig. (2002) Myocardial salvage after coronary stenting plus abciximab versus fibrinolysis plus abciximab in patients with acute myocardial infarction: a randomised trial. The Lancet 359:9310, 920-925
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Fenwei Wang, George A. Stouffer, Sergio Waxman, Barry F. Uretsky. (2002) Late coronary stent thrombosis: Early vs. late stent thrombosis in the stent era. Catheterization and Cardiovascular Interventions 55:2, 142-147
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JONATHAN D. MARMUR, ERDAL CAVUSOGLU. (2002) The Use of the Glycoprotein IIb/IIIa Receptor Antagonists During Percutaneous Coronary Intervention. Journal of Interventional Cardiology 15:1, 71-84
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Lars Grip. (2002) A Stent is a Stent, is a Stent, or?. Scandinavian Cardiovascular Journal 36:2, 70-72
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Albert W. Chan, David J. Moliterno. (2001) Defining the role of abciximab for acute coronary syndromes: Lessons from CADILLAC, ADMIRAL, GUSTO IV, GUSTO V, and TARGET. Current Opinion in Cardiology 16:6, 375-383
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Stéphane Rinfret, Cindy L Grines, Roberta S Cosgrove, Kalon K.L Ho, David A Cox, Bruce R Brodie, Marie-Claude Morice, Gregg W Stone, David J Cohen. (2001) Quality of life after balloon angioplasty or stenting for acute myocardial infarction. Journal of the American College of Cardiology 38:6, 1614-1621
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Yasuhiro Ishii, Anton W.M. van Weert, Ellen Hekking, Karen de Marie, Jeroen ter Horst, Pranobe V. Oemrawsingh, Johan H.C. Reiber. (2001) A novel quantitative method for evaluating diffuse in-stent narrowing at follow-up angiography. Catheterization and Cardiovascular Interventions 54:3, 309-317
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Xavier Bosch, Pablo Loma-Osorio, Jaume Marrugat, Xavier Bosch. 2001. Platelet glycoprotein IIb/IIIa blockers for percutaneous coronary intervention and the initial treatment of non-ST segment elevation acute coronary syndromes. .
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