Background Blockade of the platelet glycoprotein IIb/IIIa receptorwith abciximab (a monoclonal-antibody Fab fragment directedagainst the receptor) has been shown to diminish ischemic complicationsamong patients undergoing high-risk coronary angioplasty oratherectomy but increases bleeding complications. The widespreadapplicability of this treatment is unknown, particularly inview of the observed risk of hemorrhage.
Methods In a prospective, double-blind trial, we randomly assignedpatients undergoing urgent or elective percutaneous coronaryrevascularization at 69 centers to receive abciximab with standard-dose,weight-adjusted heparin (initial bolus of 100 U per kilogramof body weight); abciximab with low-dose, weight-adjusted heparin(initial bolus of 70 U per kilogram); or placebo with standard-dose,weight-adjusted heparin. The primary efficacy end point wasdeath from any cause, myocardial infarction, or urgent revascularizationwithin 30 days of randomization.
Results The trial was terminated at the first interim analysis,with 2792 of the planned 4800 patients enrolled. At 30 days,the composite event rate was 11.7 percent in the group assignedto placebo with standard-dose heparin; 5.2 percent in the groupassigned to abciximab with low-dose heparin (hazard ratio, 0.43;95 percent confidence interval, 0.30 to 0.60; P<0.001); and5.4 percent in the group assigned to abciximab with standard-doseheparin (hazard ratio, 0.45; 95 percent confidence interval,0.32 to 0.63; P<0.001). There were no significant differencesamong the groups in the risk of major bleeding, although minorbleeding was more frequent among patients receiving abciximabwith standard-dose heparin.
Conclusions Inhibition of the platelet glycoprotein IIb/IIIareceptor with abciximab, together with low-dose, weight-adjustedheparin, markedly reduces the risk of acute ischemic complicationsin patients undergoing percutaneous coronary revascularization,without increasing the risk of hemorrhage.
New strategies for preventing ischemic complications duringpercutaneous coronary revascularization have focused on theplatelet surface-membrane glycoprotein IIb/IIIa receptor.1 Ina previous large-scale trial (Evaluation of 7E3 for the Preventionof Ischemic Complications, or EPIC), blockade of this receptorby abciximab (c7E3 Fab, ReoPro, Centocor, Malvern, Pa.), a human–murinechimeric antibody Fab fragment, was shown to reduce the incidenceof acute ischemic events by 35 percent among patients undergoing"high-risk" percutaneous coronary revascularization2 but wasaccompanied by a doubling of the incidence of major bleedingcomplications. Important questions were thus raised regardingthe balance between risk and benefit with glycoprotein IIb/IIIareceptor blockade during coronary intervention, particularlyamong patients not considered to be at high risk for ischemiccomplications. The concurrent administration of high doses ofheparin, however, may have potentiated the hemorrhagic toxicityof abciximab observed in the EPIC trial.2,3 A pilot study suggestedthat the blood loss associated with abciximab might be attenuatedby using lower doses of heparin, as well as by early removalof the vascular sheath to eliminate the need for the postproceduralinfusion of heparin.4
The objectives of the present trial were first, to determinewhether the clinical benefits of abciximab therapy could beextended to all patients undergoing coronary intervention, regardlessof their risk of ischemic complications, and second, to evaluatewhether the incidence of hemorrhagic complications associatedwith this agent could be reduced without loss of efficacy byadjusting the heparin dose for body weight or reducing it.
Methods
Study Population
The Evaluation in PTCA to Improve Long-Term Outcome with AbciximabGP IIb/IIIa Blockade (EPILOG) study was a randomized, double-blind,placebo-controlled trial conducted at 69 clinical sites in theUnited States and Canada. Patients undergoing elective or urgentpercutaneous coronary revascularization with a device approvedby the Food and Drug Administration were eligible for inclusionif they were over 21 years old and had a target lesion in whichthere was stenosis of at least 60 percent of the diameter ofthe vessel. Because the previous trial had suggested that abciximabprovided substantial clinical benefit among patients with acuteischemic syndromes,2 patients who had either acute myocardialinfarction or unstable angina with associated electrocardiographicchanges during the previous 24 hours were excluded. Other exclusioncriteria were planned stent implantation or rotational atherectomy;percutaneous coronary intervention performed within the previousthree months; a left-main-coronary-artery stenosis of more than50 percent not protected by collateral vessels; concurrent warfarintherapy or a base-line prothrombin time more than 1.2 timesthe control value; cerebrovascular accident within the previoustwo years or a residual neurologic deficit; intracranial neoplasm,aneurysm, or arteriovenous malformation; history of vasculitis,known hemorrhagic diathesis, or active internal bleeding; hypertension,with a systolic blood pressure of more than 180 mm Hg or a diastolicblood pressure of more than 100 mm Hg; and major surgery, gastrointestinalbleeding, or genitourinary bleeding within the previous sixweeks. The protocol was approved by the institutional reviewboard at each clinical site, and all patients gave informedconsent.
Study Protocol
Patients were given 325 mg of aspirin orally two hours beforethe percutaneous revascularization procedure and daily thereafter.Patients were randomly assigned in a double-blind fashion bymeans of a central telephone hot line to one of three treatmentgroups: placebo with standard-dose, weight-adjusted heparin;abciximab with standard-dose, weight-adjusted heparin; or abciximabwith low-dose, weight-adjusted heparin. For those receivingabciximab, a bolus of 0.25 mg per kilogram of body weight wasadministered 10 to 60 minutes before inflation of the balloonor activation of the device, followed by an infusion of 0.125µg per kilogram per minute (maximum, 10 µg per minute)for 12 hours. The standard-dose, weight-adjusted heparin regimenconsisted of an initial bolus of 100 U of heparin per kilogram(maximum, 10,000 U) before the interventional procedure, withadditional weight-adjusted boluses calculated according to analgorithm intended to achieve and maintain an activated clottingtime of at least 300 seconds. The group assigned to low-dose,weight-adjusted heparin received an initial bolus of 70 U ofheparin per kilogram (maximum, 7000 U), with additional bolusesas necessary to achieve and maintain an activated clotting timeof at least 200 seconds. To preserve the blinding of all investigatorsand personnel involved in patient care, a heparin coordinatorat each clinical site performed all measurements of activatedclotting time and directed the administration of heparin. Theprotocol recommended that heparin be discontinued immediatelyafter the interventional procedure and that vascular sheathsbe removed when the activated clotting time was 175 secondsor less (usually 2 to 6 hours later).
Implantation of stents was discouraged and was reserved as ameans of maintaining patency after manifest or threatened abruptclosure. Specific guidelines for sites of vascular access stressedthe early removal of sheaths, avoidance of routine placementof venous sheaths, selective anterior-arterial-wall puncture,compression of the femoral access site for 30 minutes to achievehemostasis after removal of the vascular sheath, and strictbed rest and immobilization of limbs for 6 to 8 hours afterthe cessation of abciximab treatment and removal of sheaths.Algorithms were provided for the management of uncontrolledbleeding, urgent coronary-artery bypass surgery, and thrombocytopenia,and it was recommended that red-cell transfusions be administeredaccording to the clinical guidelines of the American Collegeof Physicians.5
Study End Points
The primary efficacy end point was a composite of death fromany cause, myocardial infarction or reinfarction, or severemyocardial ischemia requiring urgent coronary bypass surgeryor repeated percutaneous coronary revascularization within 30days after randomization. A second efficacy end point was acomposite of death, myocardial infarction, or coronary bypasssurgery or repeated percutaneous revascularization (urgent ornonurgent) within six months after randomization. End-pointclassifications of a clinical-events committee, blinded to study-groupassignment, were used for the final analyses.
An end-point in-hospital myocardial infarction was defined byone of two criteria: new, clinically significant Q waves intwo or more contiguous electrocardiographic leads; or elevationin creatine kinase or its MB isoenzyme to at least three timesthe upper limit of normal, representing an increase of at least50 percent over the previous trough level, in two samples collectedat different times (enzyme analysis was conducted on blood obtainedbefore and 2 hours after the initiation of treatment with thestudy agent, every 6 hours up to 24 hours, and then every 8hours up to 48 hours or discharge). After discharge from thehospital, myocardial infarction was defined by the occurrenceof Q waves or the elevation of creatine kinase or its MB isoenzymeto more than twice the upper limit of normal. The MB isoenzymevalue was used if it was available; if not, the total creatinekinase value was used.
Bleeding events were classified as major or minor accordingto the criteria used by the Thrombolysis in Myocardial InfarctionStudy Group.6 Hemoglobin was measured before and 12 and 36 hoursafter initiation of the study agent (or at discharge). To accountfor the influence of red-cell transfusions on measured hemoglobinvalues, the estimated decreases in hemoglobin were adjustedaccording to the technique suggested by Landefeld et al.7 Plateletcounts were obtained before and 1/2, 2, 12, 24, 48, and 72 hoursafter administration of the study agent (or at discharge). Allsuspected occurrences of stroke or intracranial hemorrhage wereadjudicated by an independent neurologist.
Data Management and Statistical Analysis
Data were collected on case-report forms by study coordinatorsat the clinical sites and verified with medical records by studymonitors. The investigators, study coordinators, and trial sponsor(Centocor) remained blinded to the treatment assignments untilafter the data were entered and reviewed by the clinical-eventscommittee and the analysis plan was made final.
The differences among patients with regard to efficacy and bleedingvariables were examined according to an intention-to-treat analysis.Hazard ratios were based on time-to-event analyses using theCox proportional-hazards model. The P values for efficacy endpoints were derived from the log-rank statistic, and the P valuesfor dichotomous safety end points were calculated with the Pearsonchi-square statistic or Fisher's exact test.
An interim analysis was performed to review efficacy and safetydata for the first 1500 patients, in order to ensure that thelow-dose heparin regimen did not result in a higher rate ofischemic complications than placebo. The primary end point ofthis interim analysis was the occurrence of death or myocardialinfarction within 30 days after randomization. An unbalancedstopping rule was applied that favored termination of the trialfor reasons of safety rather than efficacy, requiring a one-sidedP value of <0.025 if an abciximab group had a higher eventrate than the placebo group, but a one-sided P value of <0.0005if an abciximab group had a lower event rate than the placebogroup.
The goal of the prespecified final analyses was to test whethereither abciximab group had a lower rate of the 30-day or 6-monthcomposite end point than the placebo group. Simulations wereperformed for the computation of the type I error. We controlledfor type I error for each end point by requiring consistenteffects for the combined abciximab groups as compared with theplacebo group; a screening test was required to show significanceat a level of P = 0.0287 for a given end point before pairwisetesting could be performed. Both screening and pairwise testswere one-sided. With this strategy, the total probability ofconcluding that either abciximab group fared better than theplacebo group with respect to any one or more of the 30-day,6-month, or interim-analysis end points was less than 5 percentif, in fact, no difference existed. A sample of 4800 patientswas chosen to provide an 80 percent power to detect a 35 percentreduction in the rate of the 30-day primary end point, assuminga base-line (placebo-group) event rate of 7 percent.
Results
Enrollment began on February 27, 1995. End-point and safetydata for the first 1500 patients were reviewed by the Data andSafety Monitoring Committee on December 11, 1995. This interimanalysis revealed that the incidence of death or myocardialinfarction at 30 days was 8.2 percent for patients in the placebogroup, as compared with 2.6 percent for patients treated withabciximab and low-dose heparin, and 3.6 percent for patientstreated with abciximab and standard-dose heparin (P<0.001).Since the prespecified stopping rule was met, the trial wasterminated on December 14, 1995, with a total of 2792 of theplanned 4800 patients enrolled.
There were no significant differences in base-line characteristicsamong patients in the three treatment groups (Table 1). Notably,despite the exclusion of patients with unstable angina accompaniedby reversible electrocardiographic changes within the previous24 hours, 48 percent of the patients enrolled met other clinicalcriteria for unstable angina.
Table 1. Base-Line Demographic, Clinical, and Procedural Characteristics of the Study Patients.
The incidence of the composite end point of death, myocardialinfarction, or urgent revascularization for severe myocardialischemia at 30 days (Figure 1) was 11.7 percent in the placebogroup, 5.2 percent in the group assigned to abciximab with low-doseheparin (hazard ratio, 0.43; 95 percent confidence interval,0.30 to 0.60; P<0.001), and 5.4 percent in the group assignedto abciximab with standard-dose heparin (hazard ratio, 0.45;95 percent confidence interval, 0.32 to 0.63; P<0.001). Eachof the components of the composite end point was similarly reduced(Table 2). The treatment effect of abciximab with either heparinregimen was homogeneous among all patient groups (Figure 2).Proportional-hazards regression using the base-line variablesin Table 1 identified no significant interactions between thecharacteristics of the patients and the effect of abciximabtreatment.
Figure 1. Kaplan–Meier Estimate of the Probability of the Primary Efficacy End-Point Events (Death, Myocardial Infarction, or Urgent Repeated Revascularization) within 30 Days after Randomization, According to Treatment Assignment.
Figure 2. Hazard Ratios and 95 Percent Confidence Intervals for the 30-Day Primary Efficacy End Point in Prespecified Subgroups Defined According to Risk Stratum, Indication for Revascularization, Weight, Age, and Sex.
LD denotes low-dose, weight-adjusted heparin; SD standard-dose, weight-adjusted heparin; and MI myocardial infarction. The high-risk stratum was defined at the time of randomization as the patients with myocardial infarction within the previous seven days or adverse lesion morphology on angiography2; all other patients were considered to be at low risk. Hazard ratios are for the abciximab groups as compared with the placebo group.
The rates of hemorrhagic complications during hospitalizationare summarized in Table 3. There were no significant differencesamong the treatment groups in the risk of major bleeding. Patientsreceiving abciximab with standard-dose heparin, but not thosereceiving abciximab with low-dose heparin, had significantlymore minor bleeding events than patients receiving placebo.The rate of red-cell transfusions was significantly lower amongpatients receiving abciximab with low-dose heparin than amongthose receiving placebo. One patient in each abciximab group,but none in the placebo group, had a hemorrhagic stroke; twopatients receiving abciximab with standard-dose heparin hadother intracranial bleeding or a nonhemorrhagic stroke. Severethrombocytopenia (platelet count, <50,000 per cubic millimeter)occurred in four patients in the placebo group (0.4 percent),four patients assigned to abciximab and low-dose heparin (0.4percent), and eight patients in the group assigned to abciximaband standard-dose heparin (0.9 percent, P = 0.260).
At six months, the cumulative incidence of death, myocardialinfarction, or repeated revascularization was 25.8 percent inthe placebo group, 22.8 percent in the group assigned to abciximabwith low-dose heparin (11.7 percent risk reduction, P = 0.07),and 22.3 percent in the group assigned to abciximab with standard-doseheparin (13.7 percent risk reduction, P = 0.04). The treatmenteffect observed at 30 days for the reduction in acute ischemiccomplications (death, myocardial infarction, or urgent revascularization)was maintained throughout the 6-month follow-up period; thus,the attenuation of risk reduction observed for the 6-month compositeend point was due to the lack of effect of abciximab on theincidence of nonurgent repeated revascularization procedures(Table 4). There were no significant differences in the incidenceof target-vessel revascularization among the three treatmentgroups.
Table 4. Components of the Six-Month Composite Efficacy End Point.
Discussion
The EPIC study demonstrated the efficacy of abciximab in reducingcomplications among patients at high risk during coronary interventionbecause of unstable ischemic syndromes or unfavorable lesionmorphology on angiography.2 However, important questions wereraised regarding whether such a strategy should be used forall patients undergoing percutaneous coronary revascularization,particularly in view of the increased risk of hemorrhage associatedwith the use of abciximab. In the current trial, abciximab administeredwith a reduced-dose, weight-adjusted heparin regimen decreasedthe rate of the composite 30-day end point by 56 percent acrossa broad spectrum of patients without an attendant increase inthe risk of major bleeding complications.
A noteworthy consistency of treatment effect was observed foreach of the components of the composite end point, as well asfor the magnitude of benefit among the various subgroups ofpatients. The reduction in acute ischemic complications afterabciximab treatment was durable over six months of follow-up,although incremental efficacy in reducing the need for nonurgentrevascularization procedures was not observed. This study notonly establishes the central role of platelet aggregation inthe pathogenesis of acute ischemic complications associatedwith routine percutaneous revascularization, regardless of thepatient's risk profile, but also provides proof that the clinicalbenefit derived from the inhibition of platelet thrombus formationby blockade of glycoprotein IIb/IIIa receptor may be uncoupledfrom the risk of hemorrhage.
Although it is correlated with the risk of hemorrhage duringcatheterization or interventional procedures,8,9,10,11 adjunctiveheparin therapy is universally employed in patients undergoingpercutaneous revascularization. On the basis of observationaldata indicating that the probability of abrupt vessel closureor ischemic complications may be related to lower levels ofanticoagulation,12,13,14 the standard of care in many catheterizationlaboratories has been the routine administration of a bolusof 10,000 to 15,000 U of heparin to achieve an activated clottingtime of at least 300 to 350 seconds before coronary angioplastyis begun.15,16
Previous studies demonstrating benefit from aggressive anticoagulanttherapy with heparin during percutaneous coronary revascularizationmay not, however, be relevant when more potent platelet inhibitionis achieved. Moreover, heparin appears to potentiate the bleedingrisk of glycoprotein IIb/IIIa receptor blockade. In the EPICstudy,2 the rate of major bleeding was increased from 6.6 percentamong patients receiving placebo to 14 percent among those receivingabciximab, with the greatest risk of bleeding in the patientsof lowest body weight, for whom the fixed heparin doses werehighest on a weight-adjusted basis.2,3
Because the heparin doses in the current trial were adjustedfor body weight (Table 1), even the patients on the standard-doseheparin regimen received less heparin than the boluses of 10,000to 15,000 U that are frequently used empirically in clinicalpractice. Moreover, other interventions included early removalof the sheath (with elimination of postprocedural heparin infusion),meticulous care of the vascular access site, and transfusionguidelines. With this integrated strategy, major hemorrhageand the need for transfusions occurred infrequently in all threetreatment groups, although the lowest rates of hemorrhagic complications,particularly minor bleeding, were observed when abciximab wasadministered with low-dose heparin.
Despite the reduction in the dosage of heparin, the treatmenteffect of abciximab in limiting ischemic complications of coronaryrevascularization was marked: for every 1000 patients treated,65 fewer had acute adverse events. No other therapy has beenreported to produce this degree of reduction in important myocardialischemic events in a broad population of patients undergoingcoronary intervention. The rates of myocardial infarction, mostfrequently non–Q-wave infarction, and of urgent revascularizationwere reduced by a similar magnitude (relative risk reductionsof 58 and 68 percent, respectively). Although the clinical significanceof periprocedural non–Q-wave myocardial infarction afterpercutaneous coronary revascularization remains somewhat controversial,several recent reports have clearly demonstrated that patientswho have elevated levels of creatine kinase after coronary interventionare at significantly greater risk for late death from cardiaccauses than those who do not.17,18,19,20,21 An increased riskof late events has been observed in these studies even amongpatients with small elevations of creatine kinase MB (from morethan 1 to 1.5 times the control value),19,21 but the risk ofdeath appears to be proportional to the degree of enzyme elevation.The reduction in the rate of periprocedural myocardial infarctionby abciximab in this trial occurred mainly for large, non–Q-waveinfarctions (creatine kinase MB, >5 times the control value).This observation confirms that the ischemic events that wereprevented would have been clinically relevant and not merelylaboratory abnormalities.
Notably, the six-month outcome in the EPILOG trial differedfrom that in the EPIC trial with regard to the incidence ofrepeated revascularization events. In the EPIC trial, abciximabtherapy was associated with a 26 percent reduction in the needfor revascularization of the target vessel (defined as furtherrevascularization in a vessel treated during the index procedure),22leading to the hypothesis that this agent may inhibit the processof restenosis. In the EPILOG trial, in contrast, no differencesin long-term revascularization rates were observed. Acute ischemicevents (death, myocardial infarction, and urgent revascularization),however, were suppressed by abciximab throughout the six-monthfollow-up period. The reasons for the disparate effects of abciximabon nonurgent-revascularization rates in these two large-scaletrials are unknown, but they may relate in part to changes incoronary interventional practice (including the unplanned useof stents in 12 percent of the patients in the EPILOG trial),or to differences in patient populations or the dosage of heparin.
The clinical applicability of glycoprotein IIb/IIIa receptorblockade during percutaneous coronary revascularization is potentiallybroad. However, the cost of abciximab ($1,407 per dose, on average)23is an obstacle to the widespread use of this therapy. A formaleconomic analysis of the EPILOG trial will explore the key issueof the cost effectiveness of this treatment. Other importantconsiderations include the associated risk of thrombocytopeniaand the currently unknown consequences of readministration ofthis chimeric antibody fragment (IgG antibody response developsin approximately 6 percent of patients on first administration).
In summary, this trial establishes that blockade of plateletglycoprotein IIb/IIIa receptor with abciximab has potentiallybroad clinical use in reducing ischemic complications associatedwith percutaneous coronary revascularization. Optimal use ofthis treatment in clinical practice will require minimizingbleeding complications by using low-dose heparin therapy inconjunction with abciximab.
Supported by Centocor, Malvern, Pa., and Eli Lilly and Company,Indianapolis.
* The principal investigators and study coordinators of the Evaluationin PTCA to Improve Long-Term Outcome with Abciximab GP IIb/IIIaBlockade (EPILOG) Study Group are listed in the Appendix.
Source Information
Dr. Lincoff, as principal investigator of the study, assumes overall responsibility for the content and integrity of the article.
Address reprint requests to Dr. A. Michael Lincoff at the Department of Cardiology, F-25, Cleveland Clinic Foundation, 9500 Euclid Ave., Cleveland, OH 44195.
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Appendix
The following centers and investigators participated in theEPILOG Trial: Operations Committee: E.J. Topol (Study Chairman),R.M. Califf, A.M. Lincoff, J.E. Tcheng, C.F. Cabot, H.F. Weisman.Site Principal Investigators and Study Coordinators (patientenrollment in parentheses): Christ Hospital and University ofCincinnati Medical Center, Cincinnati, OH (238): D. Kereiakes,D. Lausten, J.P. Runyon, W. Howard. Moses Cone Memorial Hospital,Greensboro, NC (176): T. Kelly, D. Muncy. William Beaumont Hospital,Royal Oak, MI (148): G. Timmis, M. Safian, D. Davey. BaylorCollege of Medicine, Houston, TX (144): N.S. Kleiman, D. Rose,L. Basinger. Cleveland Clinic Foundation, Cleveland, OH (125):A.M. Lincoff, C. Rouse. Our Lady of Lourdes, Cherry Hill, NJ(124): J. Kramer, R. Wilson. University of Arkansas, LittleRock, AR (118): J.D. Talley, M. Boyles. Mother Frances Hospital,Tyler, TX (88): F.I. Navetta, R. LeBueuf. Henry Ford Heart andVascular Institute, Detroit, MI (85): P. Kraft, L. Dvorak. DukeUniversity Medical Center, Durham, NC (83): J. Tcheng, R.M.Smigla. Texas Heart Institute, Houston, TX (73): J. Ferguson,M. Harlan. Lakeland Regional Medical Center, Lakeland, FL (71):K. Browne, M. Telatnik. Geisinger Medical Center, Danville,PA (70): J. Blankenship, L. Demko. Florida Hospital, Orlando,FL (67): R.J. Ivanhoe, C. Jackson. Presbyterian Hospital, Albuquerque,NM (62): N. Shadoff, S. Goebel. Deborah Heart and Lung Center,Browns Mills, NJ (56): M. Taylor, E. Cleary. Rochester GeneralHospital, Rochester, NY (53): G. Gacioch, V. Chiodo. Universityof Michigan Medical Center, Ann Arbor, MI (53): E. Bates, L.Quain. Cooper Medical Center, Haddon Heights, NJ (49): H. Snyder,R. Wilson. University Medical Center, Jacksonville, FL (43):T.A. Bass, G. Rohman. Western Pennsylvania Hospital, Pittsburgh,PA (41): A. Gradman, L. Boltey. Iowa Heart Center, Des Moines,IA (38): M. Tannenbaum, D. Stengl. Miriam Hospital, Providence,RI (36): P. Gordon, N. Wright. Milwaukee Heart and VascularClinic, Milwaukee, WI (36): F. Cummins, J. Nonnweiler. JohnsHopkins Hospital, Baltimore, MD (34): T. Aversano, L. Peltzer.Methodist Hospital–Iowa Heart, Des Moines, IA (34): P.Bear, M.B. Craig. United Medical Center, Cheyenne, WY (30):L. Hattel, G. Tooke. Hermann Hospital, Houston, TX (30): H.V.Anderson, L. Weigelt. Dartmouth–Hitchcock Medical Center,Lebanon, NH (30): B. Hettleman, S. Kennedy. Scripps Clinic andResearch Foundation, La Jolla, CA (29): P.S. Teirstein, D. Claire.University of Virginia, Charlottesville, VA (28): I. Sarembock,S. Sayre. Northwestern Memorial Hospital, Chicago, IL (26):C.J. Davidson, A. Schaechter. St. Louis University Hospital,St. Louis, MO (25): F. Aguirre, T. Stonner. University of ConnecticutHealth Center, Farmington, CT (25): M. Azrin, J. Bodett, M.B.Barry. Lancaster General Hospital, Lancaster, PA (24): S. Worley,L.A. Frey. Ottawa Civic Hospital, Ottawa, ON (24): J.F. Marquis,F. Reid. Morton Plant Hospital, Clearwater, FL (23): D.J. Spriggs,S.A. Wahl. Hartford Hospital, Hartford, CT (23): M. Azrin, D.Hall. Tampa General Hospital, Tampa, FL (22): M.W. Weston, K.Yedinak. Riverside Hospital, Columbus, OH (21): B. George, D.Smith, C. Gilliland, D. Smith. Vancouver General Hospital, Vancouver,BC (21): D.R. Ricci, R. Fox. Sentara Norfolk General Hospital,Norfolk, VA (20): C. Hartman, S. Lunow. Allegheny General Hospital,Pittsburgh, PA (20): T. Farah, S. Petruolo. Louisiana StateUniversity Medical Center, New Orleans, LA (20): G. Sander,A. Stevens, K. Delise. Presbyterian Hospital, Charlotte, NC(18): B. Reen, D. Whisnant, L. Henderson. Arizona Heart Instituteand Foundation, Phoenix, AZ (18): R. Heuser, K. Swiderski, M.Kaluzniak. Evanston Hospital, Evanston, IL (17): T. Larkin,B.J. Jackson. Washington Hospital Center, Washington, DC (17):J. Popma, N. Prunka. St. Patrick's Hospital, Missoula, MT (17):M. Sanz, D. Mayer, K. Mackey. University of Alberta Hospital,Edmonton, AB (17): J. Burton, N. Hogg. Royal Columbian Hospital,New Westminster, BC (14): R. Brown, K. Stevens. Harbor–UCLAMedical Center, Torrance, CA (13): W. French, S. Wang. MountSinai Hospital, Toronto, ON (13): A.G. Adelman, V. Foulger,S. Weber. Graduate Hospital, Philadelphia, PA (9): R. Gottlieb,J. Lavoie. Emory University Hospital, Atlanta, GA (9): S. King,F. Frerichs. St. Joseph's Hospital, Lancaster, PA (7): S. Worley,L. Hollywood. Health Sciences Center, Winnipeg, MB (7): J. Ducas,U. Schick. St. Luke's–Roosevelt Hospital, New York, NY(6): J.S. Hochman, J. Slater, D. Tormey. Victoria General Hospital,Halifax, NS (5): B.J. O'Neill, K. Foshay, N. Fitzgerald. St.Boniface General Hospital, Winnipeg, MB (5): P.K. Cheung, D.Bedard. Calgary Foothills Hospital, Calgary, AB (4): M.L. Knudtson,D. Galbraith, H. Watt. Baptist Memorial Hospital East, Memphis,TN (4): J. Samaha, B. Hamilton. Rush–Presbyterian–St.Luke's Medical Center, Chicago, IL (3): L.W. Klein, L. Hebson.Victoria Hospital Corp., London, ON (2): D. Almond, J. White.Lutheran General Hospital, Park Ridge, IL (1): M.J. Rosenberg,S. Teully. Keesler Medical Center, Keesler AFB, MS (1): M. Unks,K. Rodgers. Data and Safety Monitoring Committee: D. Faxon (Chairman),J. Gore, S. Kelsey, K. Lee, D. Sane, L. Walters. CoordinatingCenter: J. Booth (Study Coordinator), R. Cannata, V. Castle,H. Cohen, S. DeLuca, M. Kutner, T. Knuth, A. Lincoff, T. McCollough,J. McPherson, J. Melton, D. Miller, M. Pulliam, S. Sapp, K.N.Sigmon. Clinical Events Committee: E. Montague (Committee Coordinator),K. Alexander, R. Augostini, C. Bajzer, B. Bart, G. Belli, J.Carlson, R. Challapalli, B. Crenshaw, I. Dawson, S. DeLuca,A. Dickey, A. Echols, B. Erickson, M.B. Fontana, S. Ghaffari,C. Gordon, C. Granger, G. Grano, R. Grimm, T. Johnson, N. Juran,A. Kingsley, K. Kruse, M. Lauer, K. Mahaffey, K. Malone, D.Mark, T. Marwick, R. Migrino, J. Miller, K. Newby, C. Pace,E. Peterson, R. Rabbani, J. Ragan, C. Rimmerman, S. Rodkey,V. Savor, W.F. Shaw, C. Sila, M. Silver, W. Tan, D. Tobiasz,P. Vandervoort, C.W. Wang, C. Ward, J. Waters, D. Wiehle, M.Winchell. Electrocardiographic Core Laboratory: D. Underwood(Chairman), P. Clemons, S. Heupler, M. Lauer, J. Powers, D.Rubin, E. Sgarbossa, S. Steinhubl. Angiographic Core Laboratory:D. Moliterno (Medical Director), D. Debowey (Director), E. Balazs,T. Crowe, T. Ivanc, L. Ols, R. Poliszczuk, H. Vilsack, B. Witherspoon.Economics and Quality of Life: D. Mark, L. Davidson-Ray. Centocor,Inc.: K.M. Anderson, C.F. Cabot, K.M. Giel, M.H. Musco, G.L.Stoner, H.F. Weisman.
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Ndrepepa, G., Kastrati, A., Neumann, F.-J., Schmitt, C., Mehilli, J., Schomig, A.
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Hirsh, J., Raschke, R.
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Levine, M. N., Raskob, G., Beyth, R. J., Kearon, C., Schulman, S.
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