Benefit of Coronary Reperfusion Before
Intervention on Outcomes After
Primary Angioplasty for Acute
Myocardial Infarction
Bruce R. Brodie, MD, Thomas D. Stuckey, MD, Charles Hansen,
Denise Muncy, RN
Primary percutaneous transluminal coronary angio-
plasty has become the preferred reperfusion strategy for
acute myocardial infarction in most institutions with in-
terventional facilities and experienced operators. The
benefit of establishing coronary reperfusion, with or
without pharmacologic therapy, before primary angio-
plasty has not been established. Consecutive patients
(n ⴝ 1,490) with acute myocardial infarction treated
with aspirin and heparin followed by primary percuta-
neous transluminal coronary angioplasty were followed
for 13 years. Follow-up angiography was obtained in
737 patients at 7.7 months. Thrombolysis In Myocardial
Infarction (TIMI) 2 to 3 flow in the infarct artery at initial
angiography was present in 18.3% of patients, and TIMI
0 to 1 flow in 81.7% of patients. Baseline variables were
similar between the 2 groups, except patients with initial
TIMI 2 to 3 flow had significantly less cardiogenic shock
(1.7% vs 9.4%, p <0.0001) and a lower incidence of
depressed ejection fraction <40% (12.6% vs 19.9%, p ⴝ
E arly trials evaluating the effectiveness of throm-
bolytic therapy combined with emergency percu-
taneous transluminal coronary angioplasty (PTCA) for
the treatment of acute myocardial infarction (AMI)
found that the combination offered no advantage over
thrombolytic therapy alone.1– 4 Following these early
trials, the strategy of combining thrombolytic therapy
with emergency PTCA fell into disfavor, and throm-
bolytic therapy and primary PTCA (without anteced-
ent thrombolytic therapy) evolved as 2 distinct and
competing reperfusion strategies for the treatment of
AMI.
Recent pilot trials have shown that platelet inhibi-
tion with abciximab in combination with low-dose
thrombolytic therapy can achieve high rates of coro-
nary reperfusion in patients with AMI.5,6 Large ran-
domized trials have also shown that abciximab and
other glycoprotein IIb/IIIa platelet inhibitors can im-
From the Department of Medicine, The Moses H. Cone Memorial
Hospital, and The LeBauer Cardiovascular Research Foundation,
Greensboro, North Carolina. This study was supported by a grant
from the LeBauer Cardiovascular Research Foundation, Greensboro,
North Carolina. Manuscript received May 24, 1999; revised manu-
script received August 9, 1999, and accepted August 11, 1999.
Address for reprints: Bruce R. Brodie, MD, 520 North Elam
Avenue, Greensboro, North Carolina 27403. E-mail: cvresearch
@aol.com.
©2000 by Excerpta Medica, Inc. All rights reserved.
The American Journal of Cardiology Vol. 85 January 1, 2000
MA, and
0.007). Procedural success was better in patients with
initial TIMI 2 to 3 flow (97.4% vs 93.8%, p ⴝ 0.02), and
catheterization laboratory events were less frequent.
Patients with initial TIMI 2 to 3 flow had lower peak
creatine kinase values (1,328 vs 2,790 IU/L, p
<0.0001), higher acute ejection fraction (54.3% vs
51.6%, p ⴝ 0.05), higher late ejection fraction (59.2% vs
54.9%, p ⴝ 0.004), and lower 30-day mortality (4.8%
vs 8.9%, p ⴝ 0.02). These data indicate that when
reperfusion occurs before primary angioplasty, out-
comes are strikingly better with less cardiogenic shock,
improved procedural outcomes, smaller infarct size, bet-
ter preservation of left ventricular function, and reduced
mortality. This should encourage new strategies to es-
tablish reperfusion before “primary” angioplasty with
“catheterization laboratory friendly” platelet inhibitors
and/or low-dose thrombolytic drugs. 䊚2000 by Ex-
cerpta Medica, Inc.
(Am J Cardiol 2000;85:13–18)
prove outcomes with both elective and emergency
coronary intervention.7–12 This has renewed interest in
the use of pharmacologic therapy to establish coronary
reperfusion before emergency PTCA to help improve
outcomes in patients with AMI.
The purpose of this study was to evaluate whether
patients with AMI, who achieve coronary reperfusion
before coronary intervention with primary PTCA,
have outcomes superior to patients without reperfu-
sion before coronary intervention.
METHODS
Study population: The study population consisted
of 1,490 consecutive patients with AMI treated with
primary PTCA without prior thrombolytic therapy by
1 cardiology group at our institution from 1984 to
1997. The patient selection criteria have been previ-
ously described.13 Patients were included in the study
only if the electrocardiogram was “diagnostic,” with
ST-segment elevation of ⱖ1 mm in ⱖ2 contiguous
leads (or reciprocal ST depression of ⱖ1 mm in leads
V1 and V2), or left bundle branch block. Primary
PTCA has been the preferred reperfusion strategy at
our institution since 1984, and of all patients with
AMI seen at our institution with diagnostic electro-
cardiograms during the study period, approximately
70% received primary PTCA, 10% thrombolytic ther-
0002-9149/00/$–see front matter 13
PII S0002-9149(99)00598-6
apy (usually given at a referring hospital before trans-
fer), and 20% received no reperfusion therapy, usually
because of late presentation, resolution of symptoms,
or comorbid disease.14
Treatment protocol: Patients were given 5,000 to
10,000 U of heparin intravenously and 325 mg of
chewable aspirin in the emergency department and
transferred promptly to the catheterization laboratory.
Reperfusion was established mechanically with pri-
mary PTCA without antecedent use of thrombolytic
therapy. After the interventional procedure, heparin
was continued for 48 hours, adjusted to achieve an
activated partial thromboplastin time 2 to 3 times the
control value. Beta blockers and nitrates were admin-
istered at the discretion of the operator and became
standard treatment in the last 4 years of the study.
Coronary stents were used in 182 patients during the
last 3 years of the study and abciximab was used in 73
patients during the last 2 years of the study.
Data collection and angiographic follow-up: Data
were obtained from reviews of catheterization labora-
tory logs and hospital charts and have been entered
into an ongoing database of patients with AMI treated
with primary PTCA since 1984. Posthospital clinical
follow-up was obtained by reviews of hospital and
office charts and telephone contacts. Follow-up cath-
eterization and angiography were performed routinely
during the first 3 years of the study and during par-
ticipation in several clinical trials (the Primary Angio-
plasty Registry in 1990 to 1991, the second Primary
Angioplasty in Myocardial Infarction [PAMI-2] trial
in 1993 to 1994, and the PAMI stent pilot trial in 1995
to 1996).15–17 Otherwise, follow-up catheterization
was performed for recurrent ischemic symptoms or
after abnormal functional testing.
Coronary flow on the initial (preintervention) cor-
onary angiogram was assessed visually by the opera-
tor and classified according to the Thrombolysis In
Myocardial Infarction (TIMI) trial grading system on
a scale of 0 to 3.18 Left ventricular ejection fractions
were calculated from tracing contours of right anterior
oblique cineangiograms using the area-length method
with correction for the right anterior oblique projec-
tion.19
Definitions: Cardiogenic shock occurring before in-
tervention was defined as hypotension (systolic blood
pressure ⬍85 mm Hg) not from hypovolemia, and
associated with severe left ventricular dysfunction or
right ventricular infarction. Congestive heart failure
occurring before intervention was defined clinically as
the presence of tachypnea, pulmonary rales, summa-
tion gallop, and/or jugular venous distention (3 of 4),
or radiographically with evidence of pulmonary con-
gestion. Time to treatment was defined as the time
from the onset of symptoms until balloon inflation.
Procedural success was defined as the achievement of
⬍50% residual narrowing in the infarct-related artery
at the PTCA site with TIMI 2 to 3 flow. Catheteriza-
tion laboratory adverse events before or after interven-
tion included (1) ventricular fibrillation requiring elec-
trical cardioversion, (2) cardiopulmonary arrest de-
fined as the loss of blood pressure or respiration
14 THE AMERICAN JOURNAL OF CARDIOLOGY姞 VOL. 85
requiring external cardiac compression or intubation
with assisted ventilatory support, and (3) prolonged
hypotension defined as systolic blood pressure ⬍85
mm Hg requiring treatment with intraaortic balloon
counterpulsation or intravenous pressor agents. Non-
fatal reinfarction was defined as recurrent chest pain
with or without electrocardiographic ST changes as-
sociated with a secondary increase in the creatine
kinase and MB fraction. Recurrent ischemia was de-
fined as recurrent ischemic chest pain without rein-
farction requiring intervention with repeat PTCA or
bypass surgery. Late target vessel revascularization
after hospital discharge was defined as repeat coronary
intervention of the infarct-related artery or coronary
bypass surgery occurring within 6 months of the acute
infarction. Restenosis was defined as ⬎50% luminal
diameter narrowing at the PTCA site by visual assess-
ment at follow-up angiography. The restenosis rate
was defined as the number of patients with angio-
graphically documented restenosis divided by the total
number of patients.
Statistical analysis: Statistical comparisons were
performed using the chi-square statistic for categorical
variables and Student’s unpaired t test for continuous
variables. Multiple logistic regression was used to
assess the relation between predictor variables and
30-day mortality. The differences in late cardiac sur-
vival across categories of discrete predictor variables
were examined with Kaplan-Meier survival curves
and their associated log-rank test statistics. Multivari-
able analyses of predictors of late cardiac survival
were performed using Cox proportional-hazards re-
gression models. All analyses were performed with
SAS (SAS Institute Inc., Cary, North Carolina) and
SPSS, (SPSS, Chicago, Illinois) statistical software.
RESULTS
Initial (preintervention) TIMI flow: Most patients had
totally occluded infarct arteries on initial (preinterven-
tion) angiography with TIMI 0 flow in 74.8%, TIMI 1
flow in 8.3%, TIMI 2 flow in 8.1%, and TIMI 3 flow
in 8.8% of patients. TIMI 0 to 1 flow was present in
1,214 patients (81.7%) and TIMI 2 to 3 flow in 272
patients (18.3%). Four patients had missing data.
Baseline variables: Baseline variables in patients
with TIMI 0 to 1 versus TIMI 2 to 3 flow in the infarct
artery on initial angiography are listed in Table I.
Patients with initial TIMI 2 to 3 flow presented earlier
were more likely to be ⬎70 years old, and had a much
lower incidence of cardiogenic shock and depressed
left ventricular function (ejection fraction ⬍40%).
Procedural outcomes: Procedural outcomes by ini-
tial TIMI flow are shown in Table II. Patients with
initial TIMI 2 to 3 flow had a higher procedural
success rate and fewer catheterization laboratory ad-
verse events than patients with initial TIMI 0 to 1
flow. Patients with initial TIMI 2 to 3 flow also had
fewer adjunctive treatments with intraaortic balloon
counterpulsation or temporary transvenous pacemaker
insertion.
Hospital outcomes: Hospital outcomes are shown in
Table III. Mortality at 30 days was significantly less in
JANUARY 1, 2000
 TABLE I Baseline Variables by Initial (preintervention) TIMI TABLE III Hospital and Late Outcomes by Initial
flow (preintervention) TIMI Flow
Initial TIMI Flow Initial TIMI Flow

TIMI 0–1 TIMI 2–3 TIMI 0–1 TIMI 2–3

Variable (n ⫽ 1,214) (n ⫽ 272) p Value Outcomes (n ⫽ 1,214) (n ⫽ 272) p Value

Hospital outcomes
Age ⱖ70 yrs 255 (21.0) 73 (26.8) 0.04 30-day mortality 108 (8.9) 13 (4.8) 0.02
Age (yrs) (mean ⫾ SD) 59.5 ⫾ 11.6 60.6 ⫾ 12.8 0.18 Reinfarction 40 (3.3) 7 (2.6) 0.54
Women 369 (30.4) 78 (28.7) 0.58 (nonfatal)
Diabetes 171 (14.1) 45 (16.5) 0.30 Recurrent ischemia 29 (2.4) 12 (4.4) 0.07
Prior infarction 229 (18.9) 56 (20.6) 0.51 Peak creatine 2,790 ⫾ 2,730 1,328 ⫾ 1,529 ⬍0.0001
Prior bypass surgery 64 (5.3) 10 (3.7) 0.27 kinase (U/L)
Anterior infarction 492 (40.5) 103 (37.9) 0.42 Peak MB 187 ⫾ 155 108 ⫾ 127 ⬍0.0001
Cardiogenic shock 114 (9.4) 5 (1.8) ⬍0.0001 fraction (ng/ml)
Congestive heart failure 80 (6.6) 12 (4.4) 0.18 Late clinical
3-vessel CAD 274 (22.6) 54 (19.9) 0.33 outcomes
Acute EF ⬍40%* 215 (19.9) 32 (12.6) 0.007 Late mortality 76 (6.3) 17 (6.3) 0.99
Time to treatment ⬍2 hr 125 (10.3) 48 (17.6) 0.0006 Late reinfarction 43 (3.5) 19 (7.0) 0.01
Time to treatment (hr) 5.3 ⫾ 6.1 4.6 ⫾ 6.3 0.09 Late target vessel 218 (18.0) 57 (21.0) 0.25
(mean ⫾ SD) revascularization
*Acute ejection fraction data for 1,333 patients (TIMI 0 to 1 [n ⫽ 1,080]; Late angiographic
TIMI 2 to 3 [n ⫽ 253]). outcomes
Values are expressed as number of patients (%), unless otherwise noted. Restenosis 323 (26.6) 72 (26.5) 0.96
EF ⫽ ejection fraction. Reocclusion 114 (9.5) 11 (4.0) 0.004
Acute EF (%)* 51.6 ⫾ 12.8 54.3 ⫾ 13.4 0.05
Follow-up EF (%) 54.9 ⫾ 13.1 59.2 ⫾ 14.2 0.004
Improvement EF (%) 3.3 ⫾ 11.8 4.9 ⫾ 10.5 0.16
TABLE II Procedural Outcomes by Initial (preintervention) TIMI *Paired ejection fraction data were available in 606 patients (TIMI 0 to 1
Flow [n ⫽ 491], TIMI 2–3 [n ⫽ 115]).
Initial TIMI Flow Values are expressed as number of patients (%) or mean ⫾ SD.
Abbreviation as in Table I.
TIMI 0–1 TIMI 2–3
Outcomes (n ⫽ 1,214) (n ⫽ 272) p Value

Procedural success 1,139 (93.8) 265 (97.4) 0.02

Catheterization laboratory 3.6 years. Late mortality (after 30 days) was similar in
adverse events patients with initial TIMI 0 to 1 and TIMI 2 to 3 flow.
Ventricular fibrillation 118 (9.7) 9 (3.3) 0.0006 The frequency of late reinfarction was significantly
Cardiopulmonary arrest 77 (6.3) 8 (2.9) 0.03
Prolonged hypotension 28 (2.3) 5 (1.8) 0.64 higher in patients with initial TIMI 2 to 3 flow. Pa-
Adjunctive treatment tients with late reinfarction had lower values of crea-
Intraaortic balloon 190 (15.7) 22 (8.1) 0.001 tine kinase-MB fraction with the index infarction
counterpulsation (134 ⫾ 98 vs 174 ⫾ 155, p ⫽ 0.003). There was no
Temporary pacemaker 267 (22.0) 35 (12.9) 0.007
difference between groups in late target vessel revas-
Values are expressed as number of patients (%). cularization.
Kaplan-Meier survival curves comparing late car-
diac survival (including 30-day survival) in patients
patients with initial TIMI 2 to 3 flow. There was no with TIMI 2 to 3 flow versus TIMI 0 to 1 flow are
significant difference in the incidence of nonfatal re- shown in Figure 1. The 30-day mortality benefit seen
infarction. The incidence of recurrent ischemia was in patients with initial TIMI 2 to 3 flow persisted and
slightly higher in patients with initial TIMI 2 to 3 remained significant at late follow-up. When the effect
flow. Both creatine kinase and MB fraction were sig- of initial TIMI flow was adjusted for differences in
nificantly lower in patients with initial TIMI 2 to 3 baseline variables by Cox regression, TIMI 0 to 1 flow
flow. was no longer a significant independent predictor of
When the effect of TIMI flow on 30-day mortality late cardiac mortality (RR 1.03, 95% confidence in-
was adjusted by logistical regression for differences in terval 0.67 to 1.58).
baseline variables (all categorical variables in Table Late angiographic outcomes: Follow-up angiogra-
I), initial TIMI 0 to 1 flow was no longer a significant phy was obtained in 737 patients (49.6%) at a mean
independent predictor (odds ratio 1.16, 95% confi- follow-up time of 7.7 ⫾ 10.8 months. A comparison
dence interval 0.55 to 2.44). When cardiogenic shock of baseline variables in patients with and without
and acute ejection fraction ⬍40% were excluded from follow-up angiography is shown in Table IV. Older
the model, initial TIMI 0 to 1 flow was a significant patients, women, and patients with cardiogenic shock,
predictor of 30-day mortality (odds ratio 2.00, 95% congestive heart failure, and 3-vessel coronary artery
confidence interval 1.06 to 3.70). disease were less likely to undergo follow-up angiog-
Late clinical outcomes: Late clinical outcomes are raphy.
shown in Table III. Clinical follow-up was obtained in Late angiographic outcomes are shown in Table
98.7% of patients at a mean follow-up time of 4.2 ⫾ III. Restenosis occurred with similar frequency in

CORONARY ARTERY DISEASE/CORONARY REPERFUSION BEFORE PRIMARY ANGIOPLASTY 15

 FIGURE 1. Kaplan-Meier sur-
vival curves comparing late
cardiac survival (including 30-
day survival) in patients with
initial TIMI 2 to 3 flow versus
TIMI 0 to 1 flow. Patients with
initial TIMI 2 to 3 flow had
significantly better late cardiac
survival. The numbers of pa-
tients entering each 2-year
interval are shown adjacent to
the curves.

DISCUSSION
TABLE IV Baseline Variables in Patients With and Without
Findings of the study: Our study documents superior
Follow-Up Angiography
outcomes in patients who achieve TIMI 2 to 3 flow
Follow-Up No Follow-Up before intervention with primary PTCA. Patients with
Angiography Angiography
Variable (n ⫽ 737) (n ⫽ 749) p Value
initial TIMI 2 to 3 flow have a significantly lower
incidence of cardiogenic shock and severely depressed
Age ⱖ70 yrs 131 (17.8) 197 (26.3) ⬍0.0001 acute left ventricular function. This likely occurs be-
Age (yrs) (mean ⫾ SD) 57.8 ⫾ 11.5 61.5 ⫾ 11.9 ⬍0.0001
Women 198 (26.9) 249 (33.2) 0.007 cause of preservation of flow to the infarct zone with
Diabetes 102 (13.8) 114 (15.2) 0.45 consequent preservation of myocardial viability. Pa-
Prior infarction 139 (18.9) 146 (19.5) 0.76 tients with initial TIMI 2 to 3 flow have higher pro-
Prior bypass surgery 33 (4.5) 41 (5.5) 0.38 cedural success rates, fewer catheterization laboratory
Anterior infarction 293 (39.8) 302 (40.3) 0.82
Cardiogenic shock 28 (3.8) 91 (12.1) ⬍0.0001 events, and a reduced need for adjunctive treatment
Congestive heart failure 31 (4.2) 61 (8.1) 0.002 with intraaortic balloon counterpulsation or temporary
3-vessel CAD 129 (17.5) 199 (26.6) ⬍0.0001 transvenous pacemaker insertion. These improved
Acute EF ⬍40%* 118 (17.1) 129 (20.1) 0.15 procedural outcomes may be related to the fact that an
Time to treatment ⬍2 h 97 (13.2) 76 (10.1) 0.07
Time to treatment (h) 4.7 ⫾ 5.1 5.5 ⫾ 6.9 0.01 initially open infarct artery often makes the primary
(mean ⫾ SD) PTCA procedure technically less difficult and also
*Acute ejection fraction data for 1,333 patients (follow-up angiography,
may reduce the incidence of reperfusion arrhythmias
n ⫽ 692; no follow-up angiography, n ⫽ 641). that sometimes occur when a closed infarct artery is
Values are expressed as number of patients (%) unless otherwise noted. suddenly reperfused.
Abbreviation as in Table I. Patients with initial TIMI 2 to 3 flow also have
smaller infarct size and better preservation of left
ventricular function, as evidenced by lower peak cre-
patients with initial TIMI 0 to 1 and TIMI 2 to 3 flow. atine kinase values and higher acute and follow-up
Reocclusion at follow-up angiography was signifi- ejection fractions. Thirty-day mortality was signifi-
cantly less frequent in patients with initial TIMI 2 to 3 cantly lower in patients with initial TIMI 2 to 3 flow,
flow. and this mortality benefit persisted into late follow-up.
Of 737 patients with follow-up angiography, 606 The mortality benefit in patients who had reperfusion
patients had paired acute and follow-up left ventricu- before intervention is likely due to multiple factors
lar angiograms that were adequate for ejection fraction including a decreased incidence of cardiogenic shock,
measurements. The effects of initial TIMI flow on smaller infarct size, better preservation of left ventric-
acute and follow-up ejection fraction in patients with ular function, and better procedural results.
paired ejection fraction data are shown in Table III. An interesting paradoxical finding in this study is
Acute and follow-up ejection fraction were signifi- that patients with initial TIMI 2 to 3 flow had a lower
cantly higher in patients with initial TIMI 2 to 3 flow. incidence of late reocclusion of the infarct artery, yet
Improvement in ejection fraction was also greater in a higher incidence of late reinfarction. It may be that
patients with TIMI 2 to 3 flow, but the difference was reinfarction was more easily detected in patients with
not statistically significant. initial TIMI 2 to 3 flow, because these patients had

16 THE AMERICAN JOURNAL OF CARDIOLOGY姞 VOL. 85 JANUARY 1, 2000

smaller infarct size, better preservation of left ventric-
ular function, and probably had more viable myocar-
dium. This may also explain the higher incidence of
in-hospital recurrent ischemia in patients with initial
TIMI 2 to 3 flow. This concept is supported by the fact
that patients with reinfarction did have lower creatine
kinase-MB fraction values with the index infarction.
Other studies documenting benefit of reperfusion be-
fore primary angioplasty: Investigators from the recent
stent PAMI trial evaluated the effect of infarct artery
patency before intervention on outcomes with primary
PTCA.20 Patients with TIMI 2 to 3 flow versus TIMI
0 to 1 flow on initial angiography had lower mortality
(1.7% vs 4.3%, p ⫽ 0.02), higher acute ejection frac-
tion (49.5% vs 47.1%, p ⫽ 0.002), and slightly higher
procedural success rates (95.3% vs 93.1%, p ⫽ 0.16).
These results are consistent with the results of our
study, although late clinical and angiographic fol-
low-up were not reported.
The Plasminogen Activator Angioplasty Compati-
bility Trial Investigators randomized patients with
AMI to low-dose thrombolytic therapy versus pla-
cebo, followed by emergency PTCA.21 The investiga-
tors found that patients who achieved TIMI grade 3
flow on initial angiography (whether spontaneous or
after thrombolytic therapy) had significantly better left
ventricular function at 7 days.
There are also data from early studies documenting
greater improvement in left ventricular ejection frac-
tion in patients with patent infarct arteries on initial
angiography before treatment with thrombolytic ther-
apy or primary PTCA.22–24
Clinical significance: If patients with an open versus
a closed infarct artery on initial angiography before
intervention with primary PTCA have superior out-
comes, there may be renewed interest in developing
new strategies to establish reperfusion before “prima-
ry” PTCA. The combination of thrombolytic therapy
followed by emergency PTCA has been theoretically
an attractive reperfusion strategy for AMI. Unfortu-
nately early studies—including the Thrombolysis and
Angioplasty in Myocardial Infarction trial, the Euro-
pean Cooperative Study Group trial, and the TIMI IIb
trial—found that emergency PTCA after tissue plas-
minogen activator (tPA) offered no advantage over
tPA alone, and suggested that the combination of tPA
and PTCA may be harmful.1–3 The lack of synergism
between tPA and PTCA in these early trials may have
been related to several factors. Thrombolytic therapy
is associated with a procoagulant effect and with
platelet activation, both of which may complicate cor-
onary intervention.25–27 In addition, these studies were
performed in the 1980s when PTCA equipment and
experience were less developed and before the advent
of stents and platelet inhibitors.
Recent experience with the platelet glycoprotein
IIb/IIIa inhibitors has renewed interest in the possibil-
ity of combining early pharmacologic treatment of
AMI with emergency PTCA. Pilot trials have shown
that abciximab in combination with low-dose throm-
bolytic therapy can achieve very high rates of TIMI 3
flow in the infarct artery at 60 and 90 minutes.5,6
CORONARY ARTERY DISEASE/CORONARY REPERFUSION BEFORE PRIMARY ANGIOPLASTY
Several large, prospective, randomized trials have also
shown that abciximab and other platelet inhibitors can
significantly improve outcomes with both elective and
emergency coronary intervention.7–12 If platelet inhib-
itors and/or low-dose thrombolytic therapy can estab-
lish early coronary reperfusion, and if these agents are
synergistic with coronary intervention, the combina-
tion of pharmacologic treatment and PTCA may pro-
vide superior outcomes compared with either throm-
bolytic therapy alone or primary PTCA alone. The
results of the current study should encourage new
trials to evaluate the effectiveness of using pharmaco-
logic therapy to establish coronary reperfusion before
emergency or “primary” PTCA. If these trials prove
successful, the 2 reperfusion strategies—pharmaco-
logic and mechanical—may come together once
again.
Study limitations: Our study has several limitations.
Initial TIMI flow was assessed visually by the opera-
tor rather than by core laboratory analysis. Angio-
graphic follow-up studies were available in a limited
number of patients (50%). There are differences in
baseline variables between patients with and without
follow-up angiography, and the late angiographic out-
comes may not be representative of our entire patient
population. Finally, our data represent an observa-
tional experience from 1 institution.
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Lee KL, Pitt B, Stack RS, O’Neill WW. A randomized trial of immediate vs.
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Schmidt W, Thery C, Vahanian A, Willems GM, Arnold AER, De Bono DP,
Dougherty SC, Lambertz H, Meier B, Raynaud P, Sanz GA, Serruys PW, Uebis
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