(Circulation. 1997;96:1445-1453.)
© 1997 American Heart Association, Inc.
Articles |
Effects of Platelet Glycoprotein IIb/IIIa Blockade With Tirofiban on Adverse Cardiac Events in Patients With Unstable Angina or Acute Myocardial Infarction Undergoing Coronary Angioplasty
Correspondence to Spencer B. King III, MD, Emory University Hospital–F606, 1364 Clifton Rd, Atlanta, GA 30322-1104.
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Abstract |
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Background Adverse cardiovascular events associated with thrombotic occlusion occur in 4% to 12.8% of patients after coronary angioplasty. Recently, potent antiplatelet agents have been used to reduce those thrombotic complications. Tirofiban is a highly selective, short-acting inhibitor of fibrinogen binding to platelet glycoprotein (GP) IIb/IIIa that inhibits ex vivo platelet aggregation in response to a variety of agonists.
Methods and Results The RESTORE trial (Randomized Efficacy
Study of Tirofiban for Outcomes and REstenosis) was a
randomized, double-blind, placebo-controlled trial of tirofiban in
patients undergoing coronary interventions (balloon angioplasty
or directional atherectomy) within 72 hours of presentation
with an acute coronary syndrome (unstable angina pectoris or
acute myocardial infarction). The end points of the study were death
from any cause, myocardial infarction, coronary bypass surgery
due to angioplasty failure or recurrent ischemia, repeat
target-vessel angioplasty for recurrent ischemia, and insertion
of a stent due to actual or threatened abrupt closure of the dilated
artery, and the primary end point was a composite
representing the occurrence of any of these events. The
prespecified primary hypothesis of the study was that tirofiban,
administered as a bolus of 10 µg/kg over a 3-minute period and
followed by a 36-hour infusion of 0.15 µg ·
kg-1 · min-1,
would result in a reduction in the 30-day composite end point compared
with placebo. Patients (n=2139) who were already receiving treatment
with aspirin and heparin were randomized to receive tirofiban or
placebo. The primary composite end point at 30 days was reduced from
12.2% in the placebo group to 10.3% in the tirofiban group, a 16%
relative reduction (P=.160). However, 2 days after
angioplasty, the tirofiban group had a 38% relative reduction in the
composite end point (P
.005), and at 7 days there was a
27% relative reduction (P=.022), largely because of a reduction in
nonfatal myocardial infarction and the need for repeat angioplasty.
When repeat angioplasty or coronary artery bypass surgery
procedures were included in the composite only if performed on an
urgent or emergency basis, the composite 30-day event rates were 10.5%
for the placebo group and 8.0% for the tirofiban group, a relative
reduction of 24% (P=.052). Major bleeding, including
transfusion, was not significantly different between the two groups
(3.7% in the placebo group and 5.3% in the tirofiban group;
P=.096). When the Thrombolysis In Myocardial
Infarction (TIMI) criteria for major bleeding were used, the incidence
was 2.1% in the placebo group compared with 2.4% in the tirofiban
group (P=.662). Thrombocytopenia was similar in the placebo
and tirofiban groups (0.9% for the placebo group versus 1.1% for the
tirofiban group; P=.709).
Conclusions In patients undergoing coronary angioplasty for acute coronary syndromes, tirofiban protects against early adverse cardiac events related to thrombotic closure. At 30 days, however, the reduction in adverse cardiac events was no longer statistically significant. The bleeding observed with tirofiban was not statistically different from that observed with placebo.
Key Words: angioplasty • platelets • glycoproteins • receptors
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Introduction |
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Interventional cardiology procedures directed against coronary artery obstructions inevitably produce damage to the endothelium and, to varying degrees, the underlying arterial wall. The exposed surfaces are highly thrombogenic and contribute to acute complications in the form of death, MI, or recurrent ischemia requiring repeat PTCA, stent placement, or CABG surgery. These events have multiple causes but commonly are mediated by a thrombotic event. Intra-arterial thrombosis in this setting is initiated by platelet adhesion, activation, and aggregation. The drug therapy commonly used to prevent thrombosis is a combination of heparin and aspirin.1 2 These agents, however, have not been completely effective, and several studies have shown that events associated with thrombotic closure during PTCA occur in 4% to 12.8% of patients.3 4 5
Recently, more potent antiplatelet agents have been used to reduce platelet-mediated thrombotic complications.5 6 7 8 9 10 11 12 13 14 Abciximab, the c7E3 monoclonal antibody directed against the platelet GP integrin receptor IIb/IIIa, has significantly reduced thrombotic complications occurring after PTCA in a high-risk population.5 15 16 17 Abciximab reduced the composite incidence of death, MI, emergency repeat angioplasty, emergency CABG, or stent implantation by 35% at both 2 and 30 days.5 15 However, bleeding complications were increased. The purpose of the present study was to investigate the effectiveness of tirofiban, a synthetic, small-molecule nonpeptide GP IIb/IIIa receptor blocker, in patients undergoing high-risk coronary interventions.
Tirofiban, a tyrosine derivative with a molecular weight of 495 kD, is a novel, highly selective inhibitor of fibrinogen binding to platelet GP IIb/IIIa.18 19 20 21 22 23 24 Preclinical and clinical studies have confirmed that tirofiban inhibits ex vivo platelet aggregation in response to a variety of agonists, including ADP, collagen, epinephrine, and thrombin. Potential advantages of such a drug include immediate onset of action, rapid reversal of antiplatelet activity after drug discontinuation, suitability for multiple repeat administrations, and high specificity for the IIb/IIIa receptor.
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Methods |
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Study Population
The RESTORE trial was a randomized, double-blind, placebo-controlled trial of tirofiban in patients who were undergoing coronary interventions (balloon angioplasty or DCA) within 72 hours of presentation with an acute coronary syndrome (unstable angina pectoris or acute MI). Unstable angina was defined as angina at rest or with minimal effort and either ECG changes, hemodynamic changes suggestive of ischemia, or angiographic evidence of coronary artery thrombus. Patients were also included if acute MI had occurred within the previous 72 hours. Infarction was defined as ischemic pain lasting >20 minutes with ST-T changes or pathological Q waves (ie, non–Q-wave or Q-wave infarction) and CK elevation more than twice the upper limit of normal or an elevated CK-MB value.
Patients were excluded from the study if they had received thrombolytic therapy within 24 hours, had a contraindication to anticoagulation, had a history of a platelet disorder or thrombocytopenia, had a history of stroke or other intracranial pathology likely to predispose to bleeding, or were scheduled for elective stent placement or if angioplasty using a rotablator or transluminal extraction catheter device was planned.
Procedures
The intervention was performed at the discretion of the operator
by standard methods. Informed consent was obtained before the
intervention, but randomization was to be delayed until a guidewire was
successfully passed across the lesion intended for dilation or
atherectomy.
Qualified patients received aspirin (325 mg) within 12 hours before the PTCA procedure and preprocedure heparin according to individual cardiac catheterization laboratory procedures. Investigators were provided with guidelines for heparin administration during PTCA that recommended a maximum heparin bolus of 10 000 U before the procedure (weight-adjusted to 150 µ/kg for patients weighing <70 kg) and heparin as required during the procedure to maintain an ACT of 300 to 400 seconds.
After randomization, a bolus of tirofiban (10 µg/kg) or placebo was administered intravenously over a 3-minute period once the angioplasty guidewire was across the lesion. After the bolus was administered, an intravenous infusion of tirofiban (0.15 µg · kg-1 · min-1) or placebo was started and maintained for 36 hours. This dosing regimen for tirofiban has been shown to achieve rapid and sustained inhibition of platelet aggregation.23 It resulted in a mean inhibition of platelet aggregation (5 µmol/L ADP) of 96% at 5 minutes, 100% at 2 hours, and 95% at the end of the infusion. The angioplasty balloon catheter or atherectomy catheter was advanced across the lesion and inflated or activated after the tirofiban bolus. Investigators were instructed to limit intracoronary stent implantation to urgent "bailout" situations such as actual or threatened abrupt closure. The protocol guidelines advised investigators to discontinue heparin after the procedure and to remove arterial and venous sheaths when the ACT was <180 seconds. Investigators could modify these guidelines at their discretion to meet the medical needs of individual patients. Patients could be discharged after completion of the 36-hour study drug infusion.
Periprocedural clinical event monitoring was supplemented by periodic laboratory evaluations. Hematocrit and hemoglobin and platelet counts were checked 6, 24, and 48 hours after initiation of the study drug and more frequently as necessary if bleeding occurred.
A 12-lead ECG and a CK measurement with CK-MB isoenzyme levels were obtained at the end of the tirofiban/placebo infusion and as needed clinically to evaluate myocardial ischemia. A routine serum chemistry panel and urinalysis were also performed at the end of study drug infusion (36 hours after angioplasty).
End Points
The end points of the study were death from any cause, MI, CABG
surgery owing to angioplasty failure or recurrent ischemia,
repeat target-vessel angioplasty for recurrent ischemia,
insertion of a stent owing to actual or threatened abrupt closure of
the target artery, and a composite end point that
represented the occurrence of any of these events. End
points were evaluated on a per-patient basis so that each patient was
counted only once in the composite end point. End points were evaluated
at 2 days, 7 days, 30 days, and 6 months. In addition, a subset of
patients underwent repeat angiography at 6 months to evaluate the
angiographic incidence of restenosis. The present study
reports the results 30 days after the initial procedure. The
prespecified primary hypothesis of the study was that tirofiban would
result in a reduction in the 30-day composite end point compared with
placebo.
All end points were adjudicated by an independent, blinded end-point adjudication committee according to the following definitions:
1. Death (due to any cause).
2. MI.
a. In patients entering the study with unstable angina and normal
CK/CK-MB values at screening, without a history of MI within 72 hours
before randomization, the development of a new MI after PTCA/DCA and
before hospital discharge was defined as follows: (1) typical chest
pain with new ST-T changes or new pathological Q waves (
0.04 seconds
in duration or with a depth >25% of the corresponding R-wave
amplitude in two or more contiguous leads) and an elevated CK-MB level
(or a serum CK level more than twice the upper limit of normal if CK-MB
level was not available) or (2) CK-MB level 3 times the upper limit
of normal or CK level 3 times the upper limit of normal with an
elevated CK-MB level, unaccompanied by chest pain and/or ECG changes.
b. In patients entering the study within 72 hours after an acute MI
(including patients undergoing primary PTCA/DCA), the development of a
new MI after PTCA/DCA and before hospital discharge was defined as
follows: (1) a CK-MB level (or CK level if CK-MB level was not
available) 3 times the upper limit of normal and
representing an increase of 33% from the previous valley
(defined as a decrease of 25% from a previous peak value but
remaining at least twice the upper limit of normal) or (2) a CK-MB
level (or CK level if CK-MB level was not available) 3 times the
upper limit of normal and representing an increase of
100% from the previous value that was <50% of peak value and less
than twice the upper limit of normal.
c. In all patients, the development of a new MI after PTCA/DCA and
after hospital discharge was defined as follows: (1) typical chest pain
with new ST-T changes or new pathological Q waves (0.04 seconds in
duration or with a depth >25% of the corresponding R-wave amplitude
in two or more contiguous leads) and an elevated CK-MB level (or a
serum CK level more than twice the upper limit of normal if CK-MB level
was not available); or (2) a CK-MB level 2 times the upper limit of
normal or CK level 2 times the upper limit of normal with an elevated
CK-MB level, unaccompanied by chest pain and/or ECG changes.
In the case of an MI that occurred in association with a CABG procedure, the development of a new Q wave was required for evidence of infarction.
3. CABG. CABG was considered an end point when performed owing to a complication (eg, large dissection or perforation) or failure of the initial PTCA/DCA attempt or owing to recurrent ischemia after completion of the initial PTCA/DCA. CABG end points were also categorized as to whether or not they were performed on an emergency basis. An emergency procedure was defined as one that could not be delayed for 24 hours but required a rush to the procedure (operating) room.
4. Repeat coronary angioplasty. Repeat percutaneous intervention was considered an end point when performed for recurrent ischemia (ie, after completion of the initial PTCA/DCA) on the same vessel that was dilated at the initial procedure. Revascularization end points were also categorized as to whether or not they were performed on an emergency basis. An emergency procedure was defined as above but also included non–target-vessel emergency PTCA procedures for consistency with the definition used in other trials.5 16
5. Stent placement. Insertion of an intracoronary stent was considered an end point when performed because of procedure failure. Placement of a stent immediately after an unsuccessful initial PTCA/DCA attempt was considered an end point if there was imminent or complete abrupt closure before stent placement, as demonstrated by TIMI grade 0 or 1 flow in the target vessel or TIMI grade 2 flow in the target vessel associated with a large dissection or residual stenosis >50%. Angiographic assessment of stent placement for procedure failure was performed by an independent core laboratory in a blinded manner. Stent placement for suboptimal result, as opposed to true procedural failure, was not considered an end point.
Bleeding complications were defined as major if they were associated with a decrease in hemoglobin level >5 g/dL, a requirement for transfusion of >2 U, or corrective surgery or if the bleeding site was intracranial or retroperitoneal. Bleeding was also categorized by use of the TIMI criteria for major bleeding (decrease in hemoglobin level >5 g/dL or intracranial bleed).25 Thrombocytopenia was defined as a confirmed platelet count <90 000/mm3.
Statistical Methods
The study sample size was chosen to detect a 35% reduction in a
composite event rate of 12.8% in the placebo group5 with
90% power. This sample size of 1050 per group resulted in 
80%
power to detect a 30% reduction in the composite event rate.
Statistical significance of the difference between treatment groups for
the primary end point, the composite of events at 30 days, was assessed
by use of a 
2 test. To investigate the time
course of end points during a 30 day-period, these results were
corroborated with a log-rank test that truncated the analysis
at days 2, 7, and 30. A similar analysis was performed for the
composite end point that included only urgent or emergency procedures
instead of all repeat revascularizations. This
latter post hoc analysis was done to permit comparison with
other published trials of GP IIb/IIIa inhibitors in
patients undergoing PTCA.5 16 26 Individual end points
were compared by use of a 2 test. Cumulative
event rates over time were plotted with the use of Kaplan-Meier curves.
Treatment groups were also compared with respect to the frequency of
patients experiencing protocol-defined major bleeding complications. A
similar analysis that used the more restrictive TIMI definition
for major bleeding was also performed. Statistical significance of the
difference between groups with respect to the incidence of major
bleeding was performed by use of Fisher's exact test. All tests were
two-sided, and statistical significance was declared if
P.05.
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Results |
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Patient Population
A total of 2212 patients were randomized in the trial. Recruitment began on January 9, 1995, and ended on December 1, 1995. The goals of recruitment were met within the time frame specified in the protocol. Seventy-one patients were randomized but never received the study drug (tirofiban or placebo) for an administrative or technical reason (most often because the angioplasty procedure was not done or the indication for angioplasty changed). In the majority of these cases, randomization preceded guidewire placement across the lesion. Therefore, the 2141 patients for whom the study drug infusion was actually initiated were included in the efficacy and safety analyses according to the intention-to-treat principle specified in the protocol.
Baseline Characteristics
Table 1
identifies the baseline
characteristics of the patients in the trial. The mean age was 60
years, and >70% of the patients were male. Baseline characteristics
were similar in the placebo and tirofiban groups. Twenty percent of
patients in both groups had a history of diabetes, and in the placebo
and tirofiban groups, respectively, 56% and 54% of patients had
hypertension, 49% and 50% had elevated serum cholesterol
levels, 67% and 64% had a history of smoking, and 34% and 35% had a
history of prior MI. Unstable angina pectoris was the most common
diagnosis for inclusion in the placebo (68%) and tirofiban (67%)
groups. The mean time from the qualifying episode of chest pain to the
time of angioplasty was 30 hours. Intervention after the acute phase of
MI was the reason for inclusion in 26% of patients. Thirty-two percent
of these patients had received prior thrombolytic
therapy. Angioplasty was performed during the acute phase of MI as a
primary recanalization procedure (primary PTCA) in
6% and 7% of patients in the placebo and tirofiban groups,
respectively. The initial procedure was most often balloon angioplasty
(93% in the placebo group and 92% in the tirofiban group), with
atherectomy used in the remaining patients. Single-lesion angioplasty
was performed in 79% and 77% of patients in the placebo and tirofiban
groups, respectively.
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End Points
The primary analysis for the composite end point from
randomization through 30 days is shown in Fig 1 (cumulative event rate), and individual
event rates for components of the composite end point are tabulated in
Table 2. At 30 days, the primary
composite end point as defined in the protocol showed a reduction from
12.2% in the placebo group to 10.3% in the tirofiban group, a 16%
relative reduction (P=.160). However, 2 days after the
intervention, the tirofiban group had a 38% reduction in the composite
end point (P=.005), with a reduction in nonfatal MI and
repeat angioplasty. The incidence of the composite end point at 2 days
was reduced from 8.7% to 5.4%, and at 7 days the tirofiban group had
a 27% relative reduction in the composite end point
(P=.022).
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The end-point adjudication criteria in this trial included repeat
angioplasty or surgery for any target-vessel ischemia. To
interpret the present study with respect to other
studies,5 16 an analysis was also performed that
included CABG or repeat revascularization only for
urgent or emergency indications. Accordingly, in a post hoc
analysis, the RESTORE end-point adjudication committee
evaluated all CABG and repeat PTCA end points (including
non–target-vessel PTCA) for emergency indication, blinded to the
treatment assignment. These results are shown in Fig 2 and Table 3. Sixty-six percent of the repeat PTCA
procedures and 63% of the CABG procedures during the first 30 days
after randomization were adjudicated as emergency procedures. Most of
the nonemergency procedures occurred later than the emergency
procedures, as evidenced by a change in the mean number of days from
the initial procedure to occurrence of repeat angioplasty from 6.5 (all
target-vessel revascularization owing to
ischemia) to 3.6 days (emergency target- or
non–target-vessel revascularization only) and
of CABG from 6.4 to 1.6 days when only emergency procedures were
included. Including only urgent or emergency angioplasty or bypass
surgery as components of the end point, the composite 30-day event
rates were 10.5% for the placebo group and 8.0% for the tirofiban
group, a relative risk reduction of 24% (P=.052). Fig 3 shows the cumulative event rate during
a 30-day period for acute MI. The tirofiban and placebo group
incidences of MI were parallel after the 36-hour drug infusion and did
not demonstrate a rebound phenomenon in the tirofiban group
after drug discontinuation.
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The 30-day end-point events were examined on the basis of inclusion criteria (unstable angina, post MI, or primary PTCA) and procedure performed (balloon angioplasty or atherectomy). The event rate trended lower in the tirofiban-treated patients in all groups when groups were based on inclusion diagnosis. There was a trend for atherectomy patients to have a greater benefit from tirofiban therapy than balloon angioplasty patients, although the number of patients was relatively small and the difference was not statistically significant.
Bleeding complications were not significantly different between the two
treatment groups (see Table 4). Major
bleeding, defined as a decrease in hemoglobin level >5 g/dL,
transfusion of >2 U of blood, or corrective surgery or as a
retroperitoneal or intracranial bleed, was not significantly higher in
the tirofiban group (5.3%) than in the placebo group (3.7%)
(P=.096). When the TIMI criteria for major bleeding were
used (decrease in hemoglobin level >5 g/dL or intracranial
bleed), the incidence was 2.4% in the tirofiban group compared with
2.1% in the placebo group (P=.662). Thrombocytopenia, a
concern in this class of drug, was not significantly increased in the
tirofiban group (1.17% versus 0.9% in the placebo group;
P=.831). Severe thrombocytopenia (<50 000/mm3)
was a rare occurrence in both groups (0.2% in the tirofiban group
versus 0.1% in the placebo group; P=1.000).
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Discussion |
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Drugs that block platelet GP IIb/IIIa receptors appear to have important beneficial effects on ischemic complications occurring after coronary angioplasty. This study showed a reduction in acute ischemic complications during the 36-hour infusion period of tirofiban, and this benefit persisted for several days thereafter. At 2 days, there was a 3.3% absolute or 38% relative reduction in the composite event rate of death, MI, CABG, repeat PTCA, or stent placement for abrupt closure (P<.005), and at 7 days there was a 2.8% absolute or 27% relative reduction (P=.022). By 30 days, the absolute difference had narrowed to 1.9%, with a relative reduction of 16% (P=.16), largely owing to nonemergency CABG and repeat PTCA procedures. Abciximab, the GP IIb/IIIa antibody, demonstrated a similar early efficacy but a greater late (30-day) reduction in adverse cardiovascular events in the EPIC trial.5 It may be that although both tirofiban and abciximab are equally effective in preventing early ischemic complications after angioplasty, the antibody might be more effective at 30 days. Differences between abciximab and tirofiban, including the longer duration of effect of the antibody27 and possibly other non–GP IIb/IIIa receptor–blocking activities of the antibody, could account for what appears to be a more sustained clinical benefit with abciximab. Before ascribing differences in the 30-day results of EPIC and RESTORE to biological differences between abciximab and tirofiban, it is important to note that the end-point definitions differ between the trials. As indicated in Table 2
of the original
report of the EPIC trial5 and as confirmed in a recent
report on health economic aspects of EPIC,28 the composite
end point in that trial included only emergency CABG and emergency
repeat PTCA procedures. In contrast, the present trial considered
all target-vessel revascularizations owing to
ischemia within 30 days as contributing to the composite end
point. Accordingly, an attempt was made to analyze the
RESTORE trial results using end-point definitions similar to
those in the EPIC and IMPACT II studies.5 16 26 When a
common definition of repeat intervention is used (ie, CABG or PTCA for
urgent or emergency indications only), the difference in outcome
between the studies narrows. Another potentially important difference between RESTORE and previous trials concerns the use of stents. The use of stents for abrupt closure became more prevalent during the most recent trial (RESTORE) and increased from 0.6% in the EPIC trial to 1.4% in IMPACT II and 2.5% in RESTORE. Conversely, the use of CABG surgery decreased from 3.6% in EPIC to 2.8% in IMPACT II and 1.3% in RESTORE (using the similar definition of urgent or emergency surgery). These changes in practice patterns in the more recent study further compound the difficulty in understanding differences between drug effects on the basis of these separate clinical trials.
Serum CK sampling frequency was also different between the trials. In the EPIC trial, the serum CK value was measured at multiple time points after PTCA. In the RESTORE trial, serum CK was measured according to protocol only at the completion of infusion of the drug. Additional CK measurements were done at the discretion of the investigator and were most often prompted by clinical evidence of ischemia. Thus, the lower nonfatal MI rate in patients receiving placebo in RESTORE (5.7%) versus EPIC (8.6%) may reflect differences in the frequency of serum CK measurement rather than a true difference in event rates. However, another potential factor accounting for this difference could be the randomization of patients before PTCA in EPIC as opposed to after guidewire placement across the lesion in RESTORE. Because of these variations in study design and protocol, it is difficult to determine if these agents provide different levels of protection from adverse ischemic events after angioplasty or atherectomy in high-risk patients.
Thrombocytopenia and bleeding are potential side effects of GP IIb/IIIa receptor antagonists.5 11 12 In the present study, there was no statistically significant increase in thrombocytopenia or major bleeding associated with tirofiban, despite the concomitant use of aspirin and heparin. This result contrasts with the 1.6- to 2.0-fold increase in major bleeding due to abciximab in the EPIC trial.5 However, the bleeding incidence due to abciximab can be decreased by the use of lower doses of heparin, as shown in the EPILOG trial.16 The recommendation to discontinue heparin after the PTCA procedure and to remove the arterial sheath early (either once the ACT is <180 seconds or 4 hours after heparin cessation) probably contributed to the safety profile of tirofiban and has now become common practice in angioplasty trials.16
In summary, in patients undergoing coronary angioplasty for acute coronary syndromes, tirofiban was protective against adverse cardiac events during administration of the drug (38% reduction; P=.005) and 7 days thereafter (27% reduction; P=.027). This relative reduction was not statistically demonstrable in the primary end point at 30 days largely because of ongoing nonemergency revascularization that occurred over time. If only urgent revascularization was considered as contributing to the composite end point, there was a 24% reduction in the composite end point attributable to tirofiban (P=.052). The difference between the rates of nonurgent and urgent procedures may in part reflect a stabilization by the GP IIb/IIIa receptor blocker of suboptimally treated lesions that subsequently required elective reintervention for unresolved ischemia. The demonstrated reduction in early adverse cardiovascular events after angioplasty was achieved at a dose of tirofiban and heparin that did not result in any excess major bleeding. It is possible that longer GP IIb/IIIa inhibition, such as might be afforded by an oral agent, could prolong the early benefit achieved by intravenous tirofiban; alternatively, the early reduction in thrombotic events may salvage some patients who will still require future elective intervention. A study of extended GPIIb/IIIa inhibition could help resolve this issue.
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Selected Abbreviations and Acronyms |
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Appendix 1 |
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The following are the principal investigators of the RESTORE Study Group, listed in alphabetical order by city:
Klinikum der Rhine–Westphalian Technical University Aachen, Aachen, Germany—P. Hanrath, J. vom Dahl; O.L.V. Ziekenhuis, Aalst, Belgium—W. Paulus, G. Heyndrickx; St. Peter's Hospital, Albany, NY—J.A. Sosa; University of Michigan Medical Center, Ann Arbor, Mich—D. Muller; Emory University Hospital, Atlanta, Ga—S.B. King III; The Johns Hopkins Hospital, Baltimore, Md—J.R. Resar; University of Maryland Hospital, Baltimore, Md—W. Herzog; Eastern Maine Medical Center, Bangor, Me—M.T. Silver; Swedish Hospital Medical Center, Bellevue, Wash—B. Green; Providence Medical Center, Bellevue, Wash—H.S. Lewis; Universitaets Klinikum Benjamin Franklin, Berlin, Germany—H.P. Schultheiss; Medizinische Universitaetsklinik Inselspital, Bern, Switzerland—B. Meier; Beth Israel Hospital, Boston, Mass—D. Cohen; Massachusetts General Hospital, Boston—I.-K. Jang; St. Elizabeth's Medical Center, Boston, Mass—D.W. Losordo; New England Medical Center, Boston, Mass—T. Palabrica; Brigham & Women's Hospital, Boston, Mass—R. Piana; Albert Einstein College of Medicine, Bronx, NY—E.S. Monrad; Maimonides Medical Center, Brooklyn, NY—J. Shani; Cliniques Universitaires Saint-Luc, Brussels, Belgium—M.F. Rousseau, J. Col; Millard Fillmore Hospital, Buffalo, NY—J.Corbelli; Medical Center Hospital of Vermont, Burlington, Vt—P.T. Vaitkus; Medical University of South Carolina, Charleston—M.J. Miller; University of Virginia Health Sciences Center, Charlottesville—E. Powers; University of Chicago Medical Center, Chicago, Ill—J.D. Carroll; Northwestern University Medical School, Chicago, Ill—C. Davidson; The Christ Hospital, Cincinnati, Ohio—D. Kereiakes; University of Cincinnati Medical Center, Cincinnati, Ohio—J.P. Runyon; The Cleveland Clinic Foundation, Cleveland, Ohio—C. Simpfendorfer; Ohio State University Medical Center, Columbus—R. Magorien; Riverside Methodist Hospitals, Columbus, Ohio—S. Yakubov; University of Texas Southwest Medical Center, Dallas—C. Landau; Baylor University Medical Center, Dallas, Tex—B. Leonard; Delray Community Hospital, Delray Beach, Fla—L.D. Snyder; Iowa Heart Center, Des Moines—M. Ghali; Broward General Medical Center, Fort Lauderdale, Fla—A. Niederman; Southwest Florida Regional Medical Center, Fort Myers—E. Toggart; University of Florida at Gainesville Medical College—C. Pepine; Lady Davis Carmel Hospital, Haifa, Israel—B. Lewis; Hartford Hospital, Hartford, Connecticut—M. Azrin; The Milton S. Hershey Medical Center, Hershey, Pa—M. Kozak; University of Texas Medical School, Houston—H.V. Anderson; The Methodist Hospital, Houston, Tex—N.S. Kleiman; Huntsville Hospital, Huntsville, Ala—D. Drenning; St. Vincent Hospital and Health Care Center, Indianapolis, Ind—E. Fry; University of Iowa Hospitals and Clinics, Iowa City—J. Rossen; Shaare Zedek Medical Centre, Jerusalem, Israel—D. Tzivioni; Green Hospital of Scripps Clinic, La Jolla, Calif—P. Teirstein; Lancaster General Hospital, Lancaster, Pa—P. Casale; Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland—L. Kappenberger; Saint Joseph Hospital, Lexington, Ky—B. Harris; Hôpital Cardiologique, Lille, France—M. Bertrand; Baptist Medical Center, Little Rock, Ark—R.F. Hundley; The Royal Brompton Hospital, London, UK—S. Davies; St. Mary's Hospital, London, UK—R.A. Foale; Kaiser Permanente Hospitals, Los Angeles, Calif—P. Mahrer; Good Samaritan Hospital, Los Angeles, Calif—T. Shook; Audubon Regional Medical Center, Louisville, Ky—W. Schmidt; Clinica Cardiovascular Santa Maria, Medellin, Colombia—J.E. Mesa; Jackson Memorial Hospital, Miami, Fla—R.F. Sequeira; Winthrop University Hospital, Mineola, NY—L. Heller; The University of Minnesota Hospital and Clinic, Minneapolis—C.W. White; Technical University of Munich, Munich, Germany—F.J. Neumann; Klinikum Grosshadern, Munich, Germany—G. Steinbeck, W. von Scheidt; Vanderbilt University Medical Center, Nashville, Tenn—D. Vaughan; Yale University School of Medicine, New Haven, Conn—M. Cleman; Ochsner Clinic, New Orleans, La—T. Collins; Medical Center of Delaware, Newark—M.E. Stillabower; Munroe Regional Medical Center, Ocala, Fla—R. Feldman; University of Oklahoma Health Sciences Center, Oklahoma City—A. Kugelmass; Oklahoma Foundation for Cardiovascular Research, Oklahoma City—D. Schmidt; Florida Hospital, Orlando—H.B. Whitworth, R. Ivanhoe; Allegheny University, Philadelphia, Pa—M. Cohen; Temple University Hospital, Philadelphia, Pa—E. Deutsch; Thomas Jefferson University Hospital, Philadelphia, Pa—S. Goldberg; Graduate Hospital, Philadelphia, Pa—R. Gottlieb; University of Pennsylvania Medical Center, Philadelphia—H. Herrmann; Pennsylvania Hospital, Philadelphia—G.J. Reis; University of Pittsburgh Medical Center, Pittsburgh, Pa—M. Feldman; The Western Pennsylvania Hospital, Pittsburgh—A. Gradman; Allegheny General Hospital, Pittsburgh, Pa—N. Reichek; Maine Medical Center, Portland—M.A. Kellett; Oregon Health Sciences University, Portland—M. Morton; Rhode Island Hospital, Providence—D.O. Williams; Wake Medical Center, Raleigh, NC—J.T. Mann III; Medical College of Virginia, Richmond—G.W. Vetrovec; Mayo Clinic, Rochester, Minn—M. Bell; Strong Memorial Hospital, Rochester, NY—M. Cunningham; William Beaumont Hospital, Royal Oak, Mich—R.D. Safian; University of California–Davis Medical Center, Sacramento—G. Gregoratos; Sharp Memorial Hospital, San Diego, Calif—J. Gordon; University of California–San Diego/San Diego VA Medical Center—W.F. Penny; Goleta Valley Community Hospital, Santa Barbara, Calif—J. Vogel; Santa Rosa Memorial Hospital, Santa Rosa, Calif—R. Miller; Sarasota Memorial Hospital, Sarasota, Fla—M. Frey; University of Washington Medical Center, Seattle—W.D. Weaver, J. Chambers; Jewish Hospital, St. Louis, Mo—P.L. Cole; Washington University School of Medicine, St. Louis, Mo—P.A. Ludbrook; Stanford University Medical Center, Stanford, Calif—A. Yeung; James A. Haley VA Hospital, Tampa, Fla—R.G. Zoble; University of Arizona Health Sciences Center, Tucson—S. Butman; Universitaetskilinik fuer Innere Medizin, Vienna, Austria—P. Probst; Georgetown University Medical Center, Washington, DC—D.J. Diver; Washington Hospital Center, Washington, DC—J.J. Popma; George Washington University Medical Center, Washington, DC—A.M. Ross; John F. Kennedy Medical Center, West Palm Beach, Fla—J. Midwall; West Roxbury VA Medical Center, West Roxbury, Mass—C.M. Gibson; Bowman Gray/Baptist Hospital, Winston-Salem, NC—M. Kutcher; St. Vincent Hospital, Worcester, Mass—J.R. Benotti; University of Massachusetts Medical Center, Worcester—B.H. Weiner.
Committee Members
Steering Committee: S.B. King III (chair), M. Bertrand, P.I.
Chang (nonvoting), L.I. Deckelbaum (nonvoting), S. Goldberg, W.
Grossman (nonvoting), D.R. Holmes, Jr, K.H. Lipschutz (Project
Statistician), J.T. Mann III, A.M. Ross, F.L. Sax (ex officio), W.D.
Weaver, and J.T. Willerson. Data and Safety Monitoring Committee: L.S.
Cohen (Chairman), M. Cheitlin, L. Fisher, R.L. Frye, and J.W. Kennedy.
End-point Committee: M. Cleman, H. Herrmann, G.W. Vetrovec, and D.O.
Williams.
Angiographic Core Laboratory
C.M. Gibson.
Merck Research Laboratories
P.I. Chang, L.I. Deckelbaum, W. Grossman, K.H. Lipschutz, F.L.
Sax, W.C. Shaw, and S.M. Snapinn. Medical Program Coordinators: R.L.
Colamesta, R. Draper, P.A. Holmes, L.K. Kelly, C.J. Lis, G.A. Snyder,
and V.L. Willison.
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Footnotes |
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1 The principal investigators of the RESTORE (Randomized Efficacy Study of Tirofiban for Outcomes and REstenosis) trial are listed in the "Appendix."
Received May 6, 1997; accepted May 22, 1997.
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References |
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TopAbstractIntroductionMethodsResultsDiscussionAppendix 1References |
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W. H. Matthai Jr Thrombocytopenia in Cardiovascular Patients: Diagnosis and Management Chest, February 1, 2005; 127(2_suppl): 46S - 52S. [Abstract] [Full Text] [PDF]
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R. H. Aster Immune Thrombocytopenia Caused by Glycoprotein IIb/IIIa Inhibitors Chest, February 1, 2005; 127(2_suppl): 53S - 59S. [Abstract] [Full Text] [PDF]
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C. Patrono, B. Coller, G. A. FitzGerald, J. Hirsh, and G. Roth Platelet-Active Drugs: The Relationships Among Dose, Effectiveness, and Side Effects: The Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy Chest, September 1, 2004; 126(3_suppl): 234S - 264S. [Abstract] [Full Text] [PDF]
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J. J. Popma, P. Berger, E. M. Ohman, R. A. Harrington, C. Grines, and J. I. Weitz Antithrombotic Therapy During Percutaneous Coronary Intervention: The Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy Chest, September 1, 2004; 126(3_suppl): 576S - 599S. [Abstract] [Full Text] [PDF]
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M. Valgimigli, G. Percoco, D. Barbieri, F. Ferrari, G. Guardigli, G. Parrinello, O. Soukhomovskaia, and R. Ferrari The additive value of tirofiban administered with the high-dose bolus in the prevention of ischemic complications during high-risk coronary angioplasty: The advance trial J. Am. Coll. Cardiol., July 7, 2004; 44(1): 14 - 19. [Abstract] [Full Text] [PDF]
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M. L. Stadius Diminishing returns ...and too many choices ...the saga of pharmacologic therapy to reduce the complications of percutaneous coronary intervention J. Am. Coll. Cardiol., July 7, 2004; 44(1): 25 - 27. [Full Text] [PDF]
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K. S. Pieper, A. A. Tsiatis, M. Davidian, V. Hasselblad, N. S. Kleiman, E. Boersma, W.-C. Chang, J. Griffin, P. W. Armstrong, R. M. Califf, et al. Differential Treatment Benefit of Platelet Glycoprotein IIb/IIIa Inhibition With Percutaneous Coronary Intervention Versus Medical Therapy for Acute Coronary Syndromes: Exploration of Methods Circulation, February 10, 2004; 109(5): 641 - 646. [Abstract] [Full Text] [PDF]
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C. S R Baker Learning on the Web. Case 3: acute chest pain. Heart, January 1, 2004; 90(1): 112 - 112. [Full Text] [PDF]
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J. H. Cole and W. S. Weintraub Are Stenting and Glycoprotein IIb/IIIa Blockade of Good Value in Primary Percutaneous Coronary Intervention? Circulation, December 9, 2003; 108(23): 2831 - 2833. [Full Text] [PDF]
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M. Cohen, G. F. Gensini, F. Maritz, E. P. Gurfinkel, K. Huber, A. Timerman, M. Krzeminska-Pakula, N. Danchin, H. D. White, J. Santopinto, et al. The safety and efficacy of subcutaneous enoxaparin versus intravenous unfractionated heparin and tirofiban versus placebo in the treatment of acute ST-segment elevation myocardial infarction patients ineligible for reperfusion (TETAMI): A randomized trial J. Am. Coll. Cardiol., October 15, 2003; 42(8): 1348 - 1356. [Abstract] [Full Text] [PDF]
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F.-J. Neumann, A. Kastrati, G. Pogatsa-Murray, J. Mehilli, H. Bollwein, H.-P. Bestehorn, C. Schmitt, M. Seyfarth, J. Dirschinger, and A. Schomig Evaluation of Prolonged Antithrombotic Pretreatment ("Cooling-Off" Strategy) Before Intervention in Patients With Unstable Coronary Syndromes: A Randomized Controlled Trial JAMA, September 24, 2003; 290(12): 1593 - 1599. [Abstract] [Full Text] [PDF]
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M. J. Ross, H. C. Herrmann, D. J. Moliterno, J. C. Blankenship, L. Demopoulos, P. M. DiBattiste, S. G. Ellis, Z. Ghazzal, J. L. Martin, J. White, et al. Angiographic variables predict increased riskfor adverse ischemic events after coronarystenting with glycoprotein IIb/IIIa inhibition: Results from the TARGET trial J. Am. Coll. Cardiol., September 17, 2003; 42(6): 981 - 988. [Abstract] [Full Text] [PDF]
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H. M. Sadeghi, C. L. Grines, H. R. Chandra, S. R. Dixon, J. A. Boura, S. Dukkipati, K. J. Harjai, and W. W. O'Neill Percutaneous coronary interventions in octogenarians: glycoprotein IIb/IIIa receptor inhibitors' safety profile J. Am. Coll. Cardiol., August 6, 2003; 42(3): 428 - 432. [Abstract] [Full Text] [PDF]
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O. Topaz, E. C. Perin, R. L. Jesse, P. K. Mohanty, M. Carr, and U. Rosenschein Power Thrombectomy in Acute Ischemic Coronary Syndromes Angiology, July 1, 2003; 54(4): 457 - 468. [Abstract] [PDF]
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A. H. M. Moons, R. J. G. Peters, N. R. Bijsterveld, J. J. Piek, M. H. Prins, G. P. Vlasuk, W. E. Rote, and H. R. Buller Recombinant nematode anticoagulant protein c2, an inhibitor of the tissue factor/factor VIIa complex, in patients undergoing elective coronary angioplastyAppendix J. Am. Coll. Cardiol., June 18, 2003; 41(12): 2147 - 2153. [Abstract] [Full Text] [PDF]
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M. A Crouch, J. M Nappi, and K. I Cheang Glycoprotein IIb/IIIa Receptor Inhibitors in Percutaneous Coronary Intervention and Acute Coronary Syndrome Ann. Pharmacother., June 1, 2003; 37(6): 860 - 875. [Abstract] [Full Text] [PDF]
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D L Brown Deaths associated with platelet glycoprotein IIb/IIIa inhibitor treatment Heart, May 1, 2003; 89(5): 535 - 537. [Abstract] [Full Text] [PDF]
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D. P. Lee, N. A. Herity, B. L. Hiatt, W. F. Fearon, M. Rezaee, A. J. Carter, M. Huston, D. Schreiber, P. M. DiBattiste, and A. C. Yeung Adjunctive Platelet Glycoprotein IIb/IIIa Receptor Inhibition With Tirofiban Before Primary Angioplasty Improves Angiographic Outcomes: Results of the TIrofiban Given in the Emergency Room before Primary Angioplasty (TIGER-PA) Pilot Trial Circulation, March 25, 2003; 107(11): 1497 - 1501. [Abstract] [Full Text] [PDF]
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R. V. Freeman, R. H. Mehta, W. Al Badr, J. V. Cooper, E. Kline-Rogers, and K. A. Eagle Influence of concurrent renal dysfunction on outcomes of patients with acute coronary syndromes and implications of the use of glycoprotein IIb/IIIa inhibitors J. Am. Coll. Cardiol., March 5, 2003; 41(5): 718 - 724. [Abstract] [Full Text] [PDF]
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D. J. Moliterno and A. W. Chan Glycoprotein IIb/IIIa inhibition in early intent-to-stent treatment of acute coronary syndromes: EPISTENT, ADMIRAL, CADILLAC, and TARGET J. Am. Coll. Cardiol., February 19, 2003; 41(4_Suppl_S): 49S - 54S. [Abstract] [Full Text] [PDF]
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W. E. Boden "Routine invasive" versus "selective invasive" approaches to non-ST-segment elevation acute coronary syndromes management in the post-stent/platelet inhibition era J. Am. Coll. Cardiol., February 19, 2003; 41(4_Suppl_S): 113S - 122S. [Abstract] [Full Text] [PDF]
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T. R. Tolleson, J. C. O'Shea, J. A. Bittl, W. B. Hillegass, K. A. Williams, G. Levine, R. A. Harrington, and J. E. Tcheng Relationship between heparin anticoagulation and clinical outcomes in coronary stent intervention: observations from the ESPRIT trial J. Am. Coll. Cardiol., February 5, 2003; 41(3): 386 - 393. [Abstract] [Full Text] [PDF]
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J.P. Ottervanger, P. Armstrong, E.S. Barnathan, E. Boersma, J.S. Cooper, E.M. Ohman, S. James, E. Topol, L. Wallentin, M.L. Simoons, et al. Long-Term Results After the Glycoprotein IIb/IIIa Inhibitor Abciximab in Unstable Angina: One-Year Survival in the GUSTO IV-ACS (Global Use of Strategies To Open Occluded Coronary Arteries IV--Acute Coronary Syndrome) Trial Circulation, January 28, 2003; 107(3): 437 - 442. [Abstract] [Full Text] [PDF]
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E. Karvouni, D. G. Katritsis, and J. P. A. Ioannidis Intravenous glycoprotein IIb/IIIa receptor antagonists reduce mortality after percutaneous coronary interventions J. Am. Coll. Cardiol., January 1, 2003; 41(1): 26 - 32. [Abstract] [Full Text] [PDF]
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R. K. Yarlagadda and W. E. Boden Cardioprotective effects of an early invasive strategy for non-ST-segment elevationacute coronary syndromes: Are we all becoming "interventional" cardiologists? J. Am. Coll. Cardiol., December 4, 2002; 40(11): 1915 - 1918. [Full Text] [PDF]
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M. E. Bertrand, M. L. Simoons, K. A.A. Fox, L. C. Wallentin, C. W. Hamm, E. McFadden, P. J. De Feyter, G. Specchia, and W. Ruzyllo Management of acute coronary syndromes in patients presenting without persistent ST-segment elevation Eur. Heart J., December 1, 2002; 23(23): 1809 - 1840. [Full Text] [PDF]
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W. B. Batchelor, T. R. Tolleson, Y. Huang, R. L. Larsen, R. M. Mantell, P. Dillard, M. Davidian, D. Zhang, W. J. Cantor, M. H. Sketch Jr, et al. Randomized COMparison of Platelet Inhibition With Abciximab, TiRofiban and Eptifibatide During Percutaneous Coronary Intervention in Acute Coronary Syndromes: The COMPARE Trial Circulation, September 17, 2002; 106(12): 1470 - 1476. [Abstract] [Full Text] [PDF]
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E.M. Antman 'I can see clearly now': a new view on the use of IV GP IIb/IIIa inhibitors in acute coronary syndromes Eur. Heart J., September 2, 2002; 23(18): 1408 - 1411. [Full Text] [PDF]
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A. W. Bonz, B. Lengenfelder, J.o. Strotmann, S. Held, O. Turschner, K. Harre, C. Wacker, C. Waller, N. Kochsiek, M. Meesmann, et al. effect of additional temporary glycoprotein IIb/IIIa receptor inhibition on troponin release in elective percutaneous coronary interventions after pretreatment with aspirin and clopidogrel (TOPSTAR trial) J. Am. Coll. Cardiol., August 21, 2002; 40(4): 662 - 668. [Abstract] [Full Text] [PDF]
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M. J. Quinn, E. F. Plow, and E. J. Topol Platelet Glycoprotein IIb/IIIa Inhibitors: Recognition of a Two-Edged Sword? Circulation, July 16, 2002; 106(3): 379 - 385. [Full Text] [PDF]
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D.J. Moliterno and E.J. Topol The TARGET trial: hit or miss? Eur. Heart J., June 1, 2002; 23(11): 835 - 837. [Full Text] [PDF]
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G. W. Stone, D. J. Moliterno, M. Bertrand, F.-J. Neumann, H. C. Herrmann, E. R. Powers, C. L. Grines, J. W. Moses, D. J. Cohen, E. A. Cohen, et al. Impact of Clinical Syndrome Acuity on the Differential Response to 2 Glycoprotein IIb/IIIa Inhibitors in Patients Undergoing Coronary Stenting: The TARGET Trial* Circulation, May 21, 2002; 105(20): 2347 - 2354. [Abstract] [Full Text] [PDF]
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P.J. de Feyter, P.W. Serruys, F. Unger, R. Beyar, V. de Valk, S. Milo, R. Simon, D. Regensburger, P.A. Crean, E. McGovern, et al. Bypass Surgery Versus Stenting for the Treatment of Multivessel Disease in Patients With Unstable Angina Compared With Stable Angina Circulation, May 21, 2002; 105(20): 2367 - 2372. [Abstract] [Full Text] [PDF]
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F.W.G. Leebeek, E. Boersma, C.P. Cannon, F.J.J. van de Werf, and M.L. Simoons Oral glycoprotein IIb/IIIa receptor inhibitors in patients with cardiovascular disease: why were the results so unfavourable Eur. Heart J., March 2, 2002; 23(6): 444 - 457. [Full Text] [PDF]
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J. C. O'Shea, C. E. Buller, W. J. Cantor, A. B. Chandler, E. A. Cohen, D. J. Cohen, I. C. Gilchrist, N. S. Kleiman, M. Labinaz, M. Madan, et al. Long-term Efficacy of Platelet Glycoprotein IIb/IIIa Integrin Blockade With Eptifibatide in Coronary Stent Intervention JAMA, February 6, 2002; 287(5): 618 - 621. [Abstract] [Full Text] [PDF]
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R.E. Brown, R.A. Henderson, D. Koster, J. Hutton, and M.L. Simoons Cost effectiveness of eptifibatide in acute coronary syndromes. An economic analysis of Western European patients enrolled in the PURSUIT trial Eur. Heart J., January 1, 2002; 23(1): 50 - 58. [Abstract] [Full Text] [PDF]
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F. Bizzarri, S. Scolletta, E. Tucci, M. Lucidi, G. Davoli, T. Toscano, E. Neri, L. Muzzi, and G. Frati Perioperative use of tirofiban hydrochloride (Aggrastat) does not increase surgical bleeding after emergency or urgent coronary artery bypass grafting J. Thorac. Cardiovasc. Surg., December 1, 2001; 122(6): 1181 - 1185. [Abstract] [Full Text] [PDF]
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W. R. P. Agema, J. W. Jukema, S. N. Pimstone, and J. J. P. Kastelein Genetic aspects of restenosis after percutaneous coronary interventions;towards more tailored therapy Eur. Heart J., November 2, 2001; 22(22): 2058 - 2074. [PDF]
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J.E. Tcheng, J. Strony, T.J. Lorenz, and J.C. O'Shea ESPRIT in context: pharmacology matters! Eur. Heart J., November 1, 2001; 22(21): 1965 - 1967. [PDF]
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J. Schweizer, A. Muller, L. Forkmann, G. Hellner, and W. Kirch Potential Use of a Low-Molecular-Weight Heparin to Prevent Restenosis in Patients with Extensive Wall Damage Following Peripheral Angioplasty Angiology, October 1, 2001; 52(10): 659 - 669. [Abstract] [PDF]
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G. GONZI, P. A. MERLINI, and D. ARDISSINO Invasive coronary revascularisation is better than conservative treatment in patients with acute coronary syndromes Heart, October 1, 2001; 86(4): 363 - 364. [Full Text] [PDF]
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M. Genoni, D. Zeller, O. Bertel, M. Maloigne, and M. Turina Tirofiban therapy does not increase the risk of hemorrhage after emergency coronary surgery J. Thorac. Cardiovasc. Surg., September 1, 2001; 122(3): 630 - 632. [Full Text] [PDF]
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E. Giannitsis, M. Muller-Bardorff, S. Lehrke, U. Wiegand, R. Tolg, B. Weidtmann, F. Hartmann, G. Richardt, and H. A. Katus Admission Troponin T Level Predicts Clinical Outcomes, TIMI Flow, and Myocardial Tissue Perfusion After Primary Percutaneous Intervention for Acute ST-Segment Elevation Myocardial Infarction Circulation, August 7, 2001; 104(6): 630 - 635. [Abstract] [Full Text] [PDF]
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W.S. Weintraub Economics of coronary stenting and GPIIb/IIIa blockade Eur. Heart J., August 2, 2001; 22(16): 1366 - 1368. [PDF]
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S. S. Kabbani, M. W. Watkins, T. Ashikaga, E. F. Terrien, P. A. Holoch, B. E. Sobel, and D. J. Schneider Platelet Reactivity Characterized Prospectively: A Determinant of Outcome 90 Days After Percutaneous Coronary Intervention Circulation, July 10, 2001; 104(2): 181 - 186. [Abstract] [Full Text] [PDF]
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K. M. Akkerhuis, J. W. Deckers, A. M. Lincoff, J. E. Tcheng, E. Boersma, K. Anderson, C. Balog, R. M. Califf, E. J. Topol, and M. L. Simoons Risk of Stroke Associated With Abciximab Among Patients Undergoing Percutaneous Coronary Intervention JAMA, July 4, 2001; 286(1): 78 - 82. [Abstract] [Full Text] [PDF]
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K. M. Anderson, R. M. Califf, G. W. Stone, F.-J. Neumann, G. Montalescot, D. P. Miller, J. J. Ferguson III, J. T. Willerson, H. F. Weisman, and E. J. Topol Long-term mortality benefit with abciximab in patients undergoing percutaneous coronary intervention J. Am. Coll. Cardiol., June 15, 2001; 37(8): 2059 - 2065. [Abstract] [Full Text] [PDF]
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S. C. Smith Jr, J. T. Dove, A. K. Jacobs, J. Ward Kennedy, D. Kereiakes, M. J. Kern, R. E. Kuntz, J. J. Popma, H. V. Schaff, D. O. Williams, et al. ACC/AHA guidelines for percutaneous coronary intervention (revision of the 1993 PTCA guidelines): A report of the American College of Cardiology/ American Heart Association Task Force on practice guidelines (Committee to revise the 1993 guidelines for percutaneous transluminal coronary angioplasty) endorsed by the Society for Cardiac Angiography and Interventions J. Am. Coll. Cardiol., June 15, 2001; 37(8): 2239 - 2239. [Full Text] [PDF]
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E. Braunwald Foreword Eur. Heart J. Suppl., May 1, 2001; 3(suppl_A): A1 - A2. [PDF]
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C.W. Hamm GP IIb/IIIa receptor antagonists in unstable angina: troponin level-based patient selection Eur. Heart J. Suppl., May 1, 2001; 3(suppl_A): A14 - A20. [Abstract] [PDF]
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K M Akkerhuis, M J B M van den Brand, C van der Zwaan, H O J Peels, H Suryapranata, L R van der Wieken, J Stibbe, J Hoffmann, T Baardman, J W Deckers, et al. Pharmacodynamics and safety of lefradafiban, an oral platelet glycoprotein IIb/IIIa receptor antagonist, in patients with stable coronary artery disease undergoing elective angioplasty Heart, April 1, 2001; 85(4): 444 - 450. [Abstract] [Full Text]
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