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300 Part III / GPIIb/IIIa Blockade for Ischemic Syndromes
The standard TNK arm in ASSENT-2 and ASSENT-3 had a very similar outcome,
suggesting that the population enrolled in the two trials was comparable. The incidence
of non-ICH major bleeding was markedly lower in ASSENT-3 (2.2% vs 4.7%, p < 0.01),
probably reflecting the earlier adjustment of aPTT after fibrinolysis in the latter trial.
SUMMARY AND RECOMMENDATIONS
Reperfusion therapy for AMI has changed significantly in the last half decade. The new
paradigm has shifted the emphasis from epicardial reperfusion (which remains necessary)
to myocardial reperfusion, which has become the ultimate goal. To this end, pharmaco-
logic reperfusion regimens based on dual fibrin and platelet antagonists seemed to prom-
ise both enhanced epicardial reperfusion and substantial improvement in myocardial
perfusion. Six small trials with angiographic endpoints have confirmed that, in general,
the combination of half the dose of a fibrinolytic agent and a GPIIb/IIIa platelet antagonist
improves epicardial and myocardial reperfusion, compared with standard-dose fibrinoly-
sis, on the background of aspirin and UFH.
Larger trials designed to detect differences in critical ischemic complications have failed
to confirm the advantage of these regimens over fibrinolysis monotherapy with respect
to short-term mortality. Nevertheless, important secondary endpoints, such as reinfarc-
tion, refractory ischemia, and complications of the original infarction have been favorably
affected by these new regimens. A number of questions remain unanswered:
1. Will improved background antithrombin therapy, such as low-molecular-weight heparin
or direct thrombin inhibitors, interact positively with combination fibrin and platelet lysis
to reduce ischemic complications of AMI further?
2. Are certain combination and dosing regimens better than others, and is there a correlation
between the level of platelet inhibition and outcome? Particularly germane is the possibil-
ity that certain lytic agents, such as TNK, are better suited for lightweight patients and for
those presenting at considerable delay from symptom onset.
Fig. 10. Thirty-day primary efficacy and safety endpoint by diabetes mellitus (DM) status and age in
ASSENT-3.
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Chapter 13 / Adjunctive Therapy to Fibrinolysis 301
3. Will a reduction in ischemic complications and an improvement in functional status or
myocardial salvage justify the incremental cost of combination therapy?
4. Will combination therapy reduce the need for rescue PCI and facilitate definitive mechani-
cal revascularization, or will primary PCI remain the optimal, yet logistically difficult, ther-
apy for AMI? This important issue is addressed by two randomized clinical trials comparing
primary PCI with GPIIb/IIIa inhibition vs combination fibrin and platelet lysis followed
by PCI for high-risk AMI patients.
Until more data become available, it appears that combination therapy with a potent anti-
platelet agent and reduced-dose fibrinolysis is a viable alternative to fibrinolysis monother-
apy in patients younger than 75 yr. Longer term follow-up will clarify whether reductions
in immediate ischemic complications eventually improve survival.
REFERENCES
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Lancet 1986;1:397–401.
2. ISIS-3 (Third International Study of Infarct Survival) Collaborative Group. ISIS-3: a randomised com-
parison of streptokinase vs tissue plasminogen activator vs anistreplase and of aspirin plus heparin vs
aspirin alone among 41,299 cases of suspected acute myocardial infarction. Lancet 1992;339:753–770.
3. GUSTO-I Investigators. An international randomized trial comparing four thrombolytic strategies for
acute myocardial infarction. N Engl J Med 1993;329:673–682.
4. Lincoff AM, Topol EJ. Illusion of reperfusion. Does anyone achieve optimal reperfusion during acute
myocardial infarction? [corrected and republished article originally printed in Circulation 1993;87:
1792–1805]. Circulation 1993;88:1361–1374.
5. Ito H, Okamura A, Iwakura K, et al. Myocardial perfusion patterns related to thrombolysis in myocardial
infarction perfusion grades after coronary angioplasty in patients with acute anterior wall myocardial
infarction. Circulation 1996;93:1993–1999.
6. The GUSTO III Investigators. A comparison of reteplase and alteplase for acute myocardial infarction.
N Engl J Med 1997;337:1118–1123.
7. INTIME-II Investigators. Intravenous n-PA for the treatment of infarcting myocardium early. InTIME-
II, a double-blind comparison of single-bolus lanoteplase vs accelerated alteplase for the treatment of
patients with acute myocardial infarction. Eur Heart J 2000;21:2005–2013.
8. Assessment of the Safety and Efficacy of a New Thrombolytic (ASSENT-2) Investigators. Single-bolus
tenecteplase compared with front-loaded alteplase in acute myocardial infarction: the ASSENT-2 dou-
ble-blind randomised trial. Lancet 1999;354:716–722.
9. Lesaffre E, Bluhmki E, Wang-Clow F, et al. The general concepts of an equivalence trial, applied to
ASSENT-2, a large-scale mortality study comparing two fibrinolytic agents in acute myocardial infarc-
tion. Eur Heart J 2001;22:898–902.
10. Weinberger I, Fuchs J, Davidson E, Rotenberg Z. Circulating aggregated platelets, number of platelets
per aggregate, and platelet size during acute myocardial infarction. Am J Cardiol 1992;70:981–983.
11. Topol EJ. Toward a new frontier in myocardial reperfusion therapy: emerging platelet preeminence. Circu-
lation 1998;97:211–218.
12. Coller B, Folts J, Smith S, Scudder L, Jordan R. Abolition of in vivo platelet thrombus formation in pri-
mates with monoclonal antibodies to the platelet GPIIb/IIIa receptor (correlation with bleeding time, plate-
let aggregation, and blockade of GPIIb/IIIa receptors). Circulation 1989;80:1766–1774.
13. Gold HK, Garabedian HD, Dinsmore RE, et al. Restoration of coronary flow in myocardial infarction
by intravenous chimeric 7E3 antibody without exogenous plasminogen activators. Observations in ani-
mals and humans. Circulation 1997;95:1755–1759.
14. Kleiman NS, Ohman ME, Califf RM, et al. Profound inhibition of platelet aggregation with monoclonal
antibody 7E3 fab after thrombolytic therapy. Results of the thrombolysis and angioplasty in myocardial
infarction (TAMI) 8 pilot study. J Am Coll Cardiol 1993;22:381–389.
15. Ohman EM, Kleiman NS, Gacioch G, et al., for the IMPACT-AMI Investigators. Combined accelerated
tissue-plasminogen activator and platelet glycoprotein IIb/IIIa integrin receptor blockade with Integrilin
in acute myocardial infarction. Results of a randomized, placebo-controlled, dose-ranging trial. Circula-
tion 1997;95:846–854.
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302 Part III / GPIIb/IIIa Blockade for Ischemic Syndromes
16. Ronner E, van Kesteren HA, Zijnen P, et al. Safety and efficacy of eptifibatide vs placebo in patients
receiving thrombolytic therapy with streptokinase for acute myocardial infarction. A phase II dose esca-
lation, randomized, double-blind study. Eur Heart J 2000;21:1530–1536.
17. The PURSUIT Trial Investigators. Inhibition of platelet glycoprotein IIb/IIIa with eptifibatide in patients
with acute coronary syndromes. Platelet Glycoprotein IIb/IIIa in Unstable Angina: Receptor Suppression
Using Integrilin Therapy. N Engl J Med 1998;339:436–443.
18. PARADIGM Investigators. Combining thrombolysis with the platelet glycoprotein IIb/IIIa inhibitor lami-
fiban: results of the Platelet Aggregation Receptor Antagonist Dose Investigation and Reperfusion Gain
in Myocardial Infarction (PARADIGM) trial. J Am Coll Cardiol 1998;32:2003–2010.
19. Antman EM, Giugliano RP, Gibson CM, et al. Abciximab facilitates the rate and extent of thrombolysis:
results of the thrombolysis in myocardial infarction (TIMI) 14 trial. The TIMI 14 Investigators. Circula-
tion 1999;99:2720–2732.
20. The SPEED Investigators. Trial of abciximab with and without low-dose reteplase for acute myocardial
infarction. Strategies for Patency Enhancement in the Emergency Department (SPEED) Group. Circula-
tion 2000;101:2788–2794.
21. Brener SJ, Zeymer U, Adgey AAJ, et al. Eptifibatide and low-dose tissue plasminogen activator in acute
myocardial infarction: the INtegrilin and low-dose ThRombolysis in Acute Myocardial Infarction—INTRO
AMI Trial. J Am Coll Cardiol 2002;39:377–386.
22. Giugliano RP, Roe MT, Zeymer U, et al. Restoration of epicardial and myocardial perfusion in acute ST-
elevation myocardial infarction with combination eptifibatide+reduced-dose tenecteplase: dose-finding
results from the INTEGRITI trial. Circulation 2001;104:II–538 (abstract).
23. Antman EM, Louwerenburg HW, Baars HF, et al., for the ENTIRE-TIMI 23 Investigators. Enoxaparin
as adjunctive antithrombin therapy for ST-elevation myocardial infarction: results of the ENTIRE-Throm-
bolysis in Myocardial Infarction (TIMI) 23 Trial. Circulation 2002;105:1642–1649.
24. Gibson CM, Cannon CP, Murphy SA, et al. Relationship of TIMI myocardial perfusion grade to mor-
tality after administration of thrombolytic drugs. Circulation 2000;101:125–130.
25. Chesebro J, Knatterud G, Roberts R, et al. Thrombolysis in Myocardial Infarction (TIMI) Trial, phase
I: a comparison between intravenous tissue plasminogen activator and intravenous streptokinase. Clini-
cal findings through hospital discharge. Circulation 1987;76:142–154.
26. Herrmann HC, Moliterno DJ, Ohman EM, et al. Facilitation of early percutaneous coronary intervention
after reteplase with or without abciximab in acute myocardial infarction: results from the SPEED (GUSTO-
4 pilot) trial. J Am Coll Cardiol 2000;36:1489–1496.
27. Schweiger MJ, Cannon CP, Murphy SA, et al. Early coronary intervention following pharmacologic
therapy for acute myocardial infarction (the combined TIMI 10B-TIMI 14 experience). Am J Cardiol
2001;88:831–836.
28. Ellis S, Van de Werf F, Ribeiro-daSilva E, Topol E. Present status of rescue coronary angioplasty: cur-
rent polarization of opinion and randomized trials. J Am Coll Cardiol 1992;19:681–686.
29. Abbottsmith CW, Topol EJ, George BS, et al. Fate of patients with acute myocardial infarction with
patency of the infarct-related vessel achieved with successful thrombolysis versus rescue angioplasty.
J Am Coll Cardiol 1990;16:770–778.
30. Ellis SG, Da Silva ER, Spaulding CM, Nobuyoshi M, Weiner B, Talley JD. Review of immediate angio-
plasty after fibrinolytic therapy for acute myocardial infarction: insights from the RESCUE I, RESCUE
II, and other contemporary clinical experiences. Am Heart J 2000;139:1046–1053.
31. GUSTO V Investigators. Reperfusion therapy for acute myocardial infarction with fibrinolytic therapy
or combination reduced fibrinolytic therapy and platelet glycoprotein IIb/IIIa inhibition: the GUSTO V
randomised trial. Lancet 2001;357:1905–1914.
32. Barbash GI, Birnbaum Y, Bogaerts K, et al. Treatment of reinfarction after thrombolytic therapy for acute
myocardial infarction : an analysis of outcome and treatment choices in the Global Utilization of Strepto-
kinase and Tissue Plasminogen Activator for Occluded Coronary Arteries (GUSTO I) and Assessment
of the Safety of a New Thrombolytic (ASSENT 2) Studies. Circulation 2001;103:954–960.
32a.Lincoff AM, Califf RM, Van De Werf F, et al. Mortality at 1 year with combination platelet glycoprotein
IIb/IIIa inhibition and reduced-dose fibrinolytic therapy vs conventional fibrinolytic therapy for acute
myocardial infarction: GUSTO V randomized trial. JAMA 2002;288:2130–2135.
33. ASSENT-3 Investigators. Efficacy and safety of tenecteplase in combination with enoxaparin, abcixi-
mab, or unfractionated heparin: the ASSENT-3 randomized trial in acute myocardial infarction. Lancet
2001;358:605–613.
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Chapter 14 / GPIIb/IIIa Economics 303
IV
PRACTICAL ISSUES
AND FUTURE APPLICATIONS
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304 Part IV / Practical Issues and Future Applications
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Chapter 14 / GPIIb/IIIa Economics 305
305
From: Contemporary Cardiology: Platelet Glycoprotein IIb/IIIa
Inhibitors in Cardiovascular Disease, 2nd Edition
Edited by: A. M. Lincoff © Humana Press Inc., Totowa, NJ
14 Economics
of Glycoprotein IIb/IIIa Inhibition
Daniel B. Mark, MD, MPH
CONTENTS
INTRODUCTION
ECONOMIC ANALYSIS OF GLYCOPROTEIN IIb/IIIa RECEPTOR
ANTAGONISTS
SUMMARY
REFERENCES
INTRODUCTION
Basic Concepts of Economic Analysis
Medical cost analysis is a hybrid field that incorporates concepts from both accounting
and economics (1). Economics provides much of the theoretical and conceptual frame-
work for cost analysis while accounting provides us with practical measurement tools
and concepts. One consequence of this admixture is that there are several distinct but
overlapping sets of terminology used in cost analysis. We will start our review of this area
by considering some of the basic concepts and terms that the clinician is likely to encoun-
ter in reading the medical cost literature.
When most people hear the term “cost,” they think of money. An economist, on the other
hand, thinks of cost in a much more theoretical way (2,3). A major precept of economics
is that any societal decision to employ the resources of society in the production of goods
and services is necessarily accompanied by lost opportunities to do something else with
those resources (4,5). Health care services and programs engender a “cost” through their
consumption of resources, which are then lost to other uses. The technical term for this
concept is “opportunity cost” (1,6). Economists are far more concerned with this notion
of opportunity cost than they are with measuring dollars spent.
Another important related concept from economics holds that society’s collective
resources are finite. Consequently, there will not be sufficient resources to fulfill all of
society’s goals, forcing the need for choices to be made among competing priorities.
Economics therefore strives to provide a set of tools to help policy and other decision
makers decide how to allocate societal resources efficiently. In the most general terms,
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306 Part IV / Practical Issues and Future Applications
resources are divided into large categories such as land, labor, and capital (e.g., stores of
raw material, factories, machines). Technology allows society to convert these raw resources
into desired goods and services, including medical care. In order to understand societal
alternatives for the use of such resources, it is necessary to assess the opportunity cost
of various types of health care as well as that of investments in defense, public education,
transportation, and other societal priorities. To compare the resource requirements of these
needs, a common metric must be found. Some societies still use barter to match goods
and services, but most industrialized societies employ markets (collections of sellers and
buyers), with money used as the standard exchange intermediary. The market price in
these societies represents the monetary equivalent in value of the total resource inputs used
in the production of the particular good or service. Money then is a convenient shorthand
for valuing all these resources, but the underlying resources themselves are the primary
concern for the economist.
Unfortunately, the economic concept of opportunity cost, while representing the purest
definition of “true cost,” is actually a theoretical construct that does not have a practical
measurement analog (1). Accountants, being more concerned with measurement than
economists, have made some important simplifications to allow approximation of oppor-
tunity cost. In each costing exercise, because the cost information itself has a cost, the
analyst must decide how much detail is necessary to satisfy the particular study require-
ment. In addition, cost needs to be assessed from an explicitly defined perspective. In health
care, a variety of valid perspectives are possible. If a patient receives a $10,000 cardiac
procedure but only pays her deductible and copayment amounting to $1000 (with the
remainder paid by insurance), then for that patient the cost of the procedure is $1000. The
cost to the insurance company may be only $6000 if they have negotiated discounted pay-
ments with the hospital. The cost to the hospital of delivering the care in question is dif-
ferent from both these figures. The societal perspective is the one most often used by cost
analysts in medicine. This is the broadest possible perspective since it incorporates all
costs and health benefits created by the contemplated change in medical care (5).
Costs can be classified according to their behavior as production is increased or decreased
(variable vs fixed costs) and in terms of their traceability to the production of health care
services (direct vs indirect costs). V ariable costs increase in direct proportion to production
of extra health care. Disposable supplies in a catheterization laboratory are an example
of variable costs. Fixed costs, as the name implies, do not change with the volume of care
provided (e.g., the depreciation of the catheterization facility itself) (1). Direct costs can
be readily linked to the production of a particular health care product or service (e.g., dis-
posable supplies, labor), whereas indirect costs (or overhead) cannot (e.g., heating, elec-
tricity, laundry, medical records, hospital administrators).
Two terms are used to describe the effect on costs resulting from shifts in the use of health
services. Marginal cost refers to the extra cost involved in generating one extra unit of
a good or service within the context of a given health care intervention [e.g., performing
one extra coronary angioplasty (PTCA)] and is equivalent to variable cost. Incremental
cost is the cost involved in shifting from one health care intervention to an alternative
(e.g., from thrombolysis to direct angioplasty); this is a fundamental notion that underlies
cost-effectiveness analysis.
Another important economic concept for the clinician is that of induced cost or induced
saving. If one performs a cardiovascular procedure, it is clear that the cost of that proce-
dure includes the cost of the equipment consumed in the procedure (such as coronary
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Chapter 14 / GPIIb/IIIa Economics 307
stents or balloon catheters). It may be less clear that the cost of the procedure also includes
things that happen later in the patient’s follow-up as a consequence of the decision to do
that procedure. For example, the need to have a second procedure to treat restenosis is an
induced cost of the initial procedure. The reduced need for a repeat procedure when a cor-
onary stent is substituted for a standard balloon catheter procedure is an induced saving
of the coronary stent procedure. The key concept is that it is not sufficient in most cases of
medical care to look only at the immediate costs of care. Downstream costs and cost sav-
ings must also be assessed in order to provide an accurate picture of the total economic
effects of a particular technology or strategy.
One other term that is often used in economic analysis is indirect cost. This term actually
has two meanings, an accounting meaning in which it refers to overhead (as described
above) and an economic meaning in which it refers to costs associated with lost productiv-
ity. Because of this confusion of terminology, many modern investigators substitute the
term productivity costs when they are referring to the latter type of indirect costs (5). In
medical care, typical productivity costs include those associated with time lost from work.
Difficulties encountered in assessing productivity costs relate in part to the proper methods
of assessing such costs for individuals who are retired from the workforce or those who
are working at home (not for pay). In practice, productivity costs are infrequently examined
in medical economic studies.
In an ideal competitive economic market, prices for goods and services are established
by the dynamic interplay between sellers and buyers. Such markets are characterized by
competition on price among many sellers (none of whom is large enough to control prices),
easy entry into the market by new sellers, and knowledgeable buyers who themselves pay
for the goods and services they consume (2). The “medical marketplace” has none of these
features. Patients are usually insulated from most of the cost of the care they consume by
insurance, and they do not have the technical knowledge to discriminate among the care
options they face. In most local health care markets, there are only a few buyers (insurance
companies) and sellers (medical care systems) of health care. Although managed care has
introduced price competition to medicine, it is not the ideal competition of economic text-
books. During the peak of the managed care era, managed care companies often controlled
large blocks of business, and providers were forced to accept a heavily discounted price
in order to retain this portion of their patient population. Because of these and related
issues and because of the fragmentation of the medical marketplace, providers may have
one price for self-pay patients (full charges, usually their highest price), another price for
discounted fee-for-service business, and yet another price for managed care. Typically,
none of these reflect the opportunity cost of the care provided. Thus, there is no market price
for medical care in the way that automobiles and refrigerators have a market price. Con-
sequently, several different approaches have been developed to estimate medical costs
(or prices). These are reviewed briefly in the next section.
Cost Measurement
Two general approaches are available to measure the costs of medical care services:
bottom-up and top-down. The bottom-up methods are all based on counting individual
resources consumed in a particular episode of care and assigning appropriate cost weights.
The gold standard bottom-up method is known as microcosting and involves a very detailed
enumeration of all resources consumed, estimation of cost weights for each individual
resource, and calculation of total costs through multiplication of the individual resources
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308 Part IV / Practical Issues and Future Applications
by their cost weights. Although microcosting analysis is possible for simple types of
medical care, such as administration of an intravenous antibiotic, it can be very laborious
and expensive for complex forms of care. Even things such as an admission for coronary
angioplasty or acute myocardial infarction are relatively complex when considering doing
a microcosting analysis. Fortunately, increasing numbers of hospitals in the United States
have installed detailed computer-based cost accounting systems that provide an approxi-
mate version of the gold standard bottom-up cost analysis. These systems have not been
well studied from a research point of view, but they do appear to offer a better estimate of
true underlying costs than is available through alternatives. Like any costing methodology,
they should not be accepted without question, and component inputs should be carefully
scrutinized for reasonableness whenever possible.
The simplest version of the bottom-up approach is the so-called big ticket method. This
is based on an identification of a subset of resources consumed that are considered the
most important and/or costly (the big tickets). This approach is the most inexpensive
method of costing and allows the analyst to concentrate on generating cost estimates for
a small subset of the entire portfolio of resources consumed. There are several potential
disadvantages to this simple method, however. Most importantly, the analysis may oversim-
plify the true resource effects of the strategies under study and therefore may miss impor-
tant cost differences. There are rarely sufficient prior data available to assure the analyst
that he or she has captured all the important resources in the appropriate amount of detail.
This approach also assumes that all big ticket resources of a particular type have the same
cost, which of course is clearly not true. Cost weights for this type of analysis are often chosen
more for convenience than established suitability for the task.
The other major approach to cost estimation is the top-down approach. Two different
methods can be used here. The most common method used in medical cost research appli-
cations involving hospital-based care is the collection of hospital billing information and
the conversion of the charges on the hospital bills into costs using correction factors that
are published in each hospital’s annual cost report. The vast majority of hospitals in the
United States generate the type of bills (UB-92) and the Medicare Cost Reports that are
necessary to accomplish this conversion. (Notable exceptions are Veterans Administra-
tion Hospitals and some fully capitated HMOs.) Physician costs can also be collected as
billing information, although this is generally onerous because physician billing for a
particular medical center is often done from individual offices rather than from a central-
ized billing office. In addition, there are no standardized conversion factors to correct phys-
ician charges back to costs. For that reason, many current analysts use the Medicare Fee
Schedule as a national standard for physician costs.
The Medicare Fee Schedule also provides the best current source for costs of outpatient
visits and testing. A much simpler top-down approach that is used primarily when there
are limited details available in the database about resources consumed is to assign each
inpatient episode of patient care to a diagnosis-related group (DRG) category and assign
price weights to the entire episode of care based on this type of aggregating classification.
This approach has many of the same limitations described earlier for the big ticket bottom-
up approach. Clearly not all episodes of hospitalization for coronary angioplasty involve
the same amount of resources or should be given the same cost weight, just as different
hospitalizations for myocardial infarction or coronary bypass surgery should not be viewed
as economically uniform.
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Chapter 14 / GPIIb/IIIa Economics 309
Cost Measurement in Clinical Trials
Over the last decade, several groups have pioneered the use of empirical cost data
collection in large-scale randomized trials and in large, single-site observational studies
as the principal method for estimating medical costs (7–11). By generating an empirical
database of costs similar to the empirical clinical database that is typically generated in
clinical trials and outcome studies, we have a much richer source of investigation and can
perform analyses that do not appear as arbitrary and subject to analyst biases as earlier
literature and expert-based opinion analyses often did. We have shown that it is feasible
to collect hospital billing information on large numbers of patients enrolled in the United
States and that these data can reliably provide an estimate of medical costs. Ideally, we
would prefer to have access to a detailed hospital accounting system in every hospital in
which we enroll patients in a particular study, but this is rarely feasible. Consequently, we
anticipate that for at least the next 5 years we will continue to be measuring hospital costs
through the use of medical bills and correction factors as described above.
Cost-Effectiveness Analysis
Many clinicians tend to confuse cost-effectiveness analysis with economic analysis in
general, but these two concepts are not equivalent. Cost-effectiveness analysis is a speci-
fic type of economic analysis that attempts to assess the value of medical care by relating
in a structured fashion the added costs of a particular strategy to its added medical bene-
fits. Typically, cost-effectiveness analyses express their results in terms such as the extra
dollars required to add an additional life year with the new strategy relative to standard care.
The goal of cost-effectiveness analysis is not to assist the clinician at the bedside, but rather
to give policy analysts a tool to use in allocating societal resources. Although theoretically
attractive, this use of cost effectiveness is rarely attempted in actual practice and the chal-
lenge for modern analysts is to find ways of doing cost-effectiveness analysis that are more
relevant to the challenges and concerns of practitioners, administrators, health plans, and
patients in the modern era. Additional details on cost-effectiveness methodologies are
provided elsewhere (1,5).
ECONOMIC ANALYSIS
OF GLYCOPROTEIN IIb/IIIa RECEPTOR ANTAGONISTS
Studies of Percutaneous Coronary Revascularization
The three currently available intravenous glycoprotein (GP) IIb/IIIa platelet receptor
blockers have all been studied in large-scale clinical trials involving percutaneous revas-
cularization patients, as described in earlier chapters in this book. Six trials with prospec-
tive economic analysis of GPIIb/IIIa inhibitors in percutaneous intervention populations
have been completed: EPIC, EPILOG, and EPISTENT (involving abciximab); IMPACT
II and ESPRIT (eptifibatide); and RESTORE (tirofiban).
A
BCIXIMAB
The Evaluation of Monoclonal Antibody to Prevent Ischemic Complications (EPIC)
trial randomized 2099 high-risk PTCA patients to one of three arms: placebo, bolus abcix-
imab, and bolus plus infusion abciximab. All patients received aspirin and a fixed dose regi-
men of intravenous heparin. At 30 d, bolus plus 12-h infusion abciximab reduced ischemic
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