| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
From The Terrence Donnelly Heart Centre, Division of Cardiology, St
Michael's Hospital, University of Toronto, Toronto, Canada (S.G.G.,
A.L.); Duke University Medical Center, Durham, NC (N.M.W., G.S.W., C.B.G.,
R.M.C.); George Washington University Medical Center, Washington, DC (A.M.R.);
Favaloro Institute, Buenos Aires, Argentina (A.B.); Cleveland Clinic
Foundation, Cleveland, Ohio (E.B.S., E.J.T.); Thorax Center, Rotterdam, The
Netherlands (M.L.S.); and Department of Medicine, University of Alberta,
Edmonton, Canada (P.W.A.).
Correspondence to Shaun G. Goodman, MD, St Michael's Hospital, Division of Cardiology, 30 Bond St, Room 7–049 Queen, Toronto, Ontario, Canada M5B 1W8. E-mail goodmans{at}smh.toronto.on.ca
Methods and Results—We examined 12-lead ECG, coronary
anatomy, left ventricular function, and mortality
among 2046 patients with ST-segment elevation infarction from the
Global Utilization of Streptokinase and Tissue Plasminogen
Activator for Occluded Coronary Arteries
angiographic subset to gain further insight into the pathophysiology
and prognosis of Q- versus non–Q-wave infarction in the
thrombolytic era. Non–Q-wave infarction developed in
409 patients (20%) after thrombolytic therapy.
Compared with Q-wave patients, non–Q-wave patients were more likely to
present with lesser ST-segment elevation in a nonanterior location.
The infarct-related artery in non–Q-wave patients was more likely to
be nonanterior (67% versus 58%, P=.012) and distally
located (33% versus 39%, P=.021). Early (90-minute,
77% versus 65%, P=.001) and complete (54% versus
44%, P<.001) infarct-related artery patency was
greater among the non–Q-wave group. Non–Q-wave patients had better
global (ejection fraction, 66% versus 57%; P<.0001)
and regional left ventricular function (10 versus 24
abnormal chords, P=.0001). In-hospital, 30-day, 1-year,
and 2-year (6.3% versus 10.1%, P=.02) mortality rates
were lower among non–Q-wave patients.
Conclusions—The excellent prognosis among the subgroup of
patients who develop non–Q-wave infarction after
thrombolysis is related to early, complete, and
sustained infarct-related artery patency with resultant limitation of
left ventricular infarction and dysfunction.
Autopsy and coronary angiographic studies in the
prethrombolytic era suggest that non–Q-wave MI is
associated with less frequent coronary occlusion and a higher
incidence of collaterals to the infarct-related
artery.2 3 4 5 6 7 8 However,
pathophysiological insights gained from these
angiographic studies are limited by small patient numbers, selection
bias,4 8 and delayed timing of
evaluation.4 5 6 7
Although the incidence of non–Q MI appears to be
increasing,9 10 systematic evaluation of the
impact of thrombolytic therapy on the subsequent
development of non–Q-wave MI has been limited.11
Furthermore, the prognosis of non–Q-wave MI patients after
thrombolysis remains uncertain, with the majority of
studies not reporting on clinical outcome. Controversy exists among the
few trials stratifying patients by predischarge ECG subsets, with some
suggesting similar outcome12 13 14 and others
describing significantly lower early15 16 and
late15 16 17 mortality among non–Q- versus Q-wave
MI patients.
Accordingly, we examined coronary anatomy, left
ventricular function, and mortality among the GUSTO-I
angiographic subset18 to gain further insight
into the pathophysiology and prognosis of these two ECG categories of
MI.
Patient Population
The GUSTO-I angiographic substudy consisted of 2431 patients from 75
North American, European, and Australian hospitals. Patients later
excluded from the ECG analysis included those (1) without a
baseline or follow-up ECG (n=135), (2) whose follow-up ECG was obtained
<24 hours after thrombolytic administration (n=138),
(3) who experienced reinfarction before a follow-up ECG was obtained
(n=75), and (4) with confounding ECG factors that did not allow for an
assessment of Q-wave MI (example, left bundle-branch block, paced
rhythm, poor-quality ECG) (n=37). The remaining 2046 patients were
included in this posthoc analysis (Fig 1
Angiography
Multivessel disease was defined as >75% stenosis in at
least two vessels. Infarct related artery patency was defined as (1)
open vessels (TIMI flow grades 2 and 3 combined) and (2) complete
reperfusion (TIMI grade 3 flow). Infarct-related artery reocclusion was
defined as TIMI grade 0 or 1 flow at follow-up in patients who had
grade 2 or 3 flow at 90 minutes.
ECG Classification
Patients with evidence of prior MI on the baseline ECG were included
because ST-segment elevation and careful comparison of the new MI
location on the follow-up ECG allowed localization of the index
infarct.
Clinical Follow-up
Statistical Analysis
Qualifying ECG Findings
Cardiac Catheterization Findings
Complete infarct-related artery patency (TIMI grade 3 flow) was
significantly greater among the non–Q-wave group (54% versus 44%,
P<.001). Early (90-minute) infarct-related artery patency
(TIMI grade 2 or 3 flow) was significantly greater among the
non–Q-wave group (77% of 195 versus 65% of 790 patients,
respectively; P=.001; Table 3
Five hundred eighteen patients had a patent infarct-related artery 90
minutes after treatment and underwent follow-up angiography at 5 to 7
days. Patients who subsequently developed a non–Q-wave MI had less
reocclusion: overall reocclusion was 0.8% in the 119 patients who
evolved a non–Q-wave MI compared with 6.3% of 399 patients who later
developed a Q-wave MI (P=.015; Table 3
Left Ventricular Function
Regional function in the infarct zone was also significantly better
among non–Q-wave MI patients (median, -1.78 versus -2.84 SDs/chord;
P<.0001). In addition, non–Q-wave MI patients had fewer
abnormal chords (median, 10 versus 24 chords; P=.0001), and
more of these patients showed preserved wall motion than did the Q-wave
MI patients (44% versus 19%, P<.0001).
Consistent with the patency data, the left
ventricular ejection fraction, end-systolic volume
index, regional function in the infarct zone, number of normal chords,
and number of patients with preserved wall motion was greater at all
four angiographic time frames among non–Q-wave MI patients.
Furthermore, in patients who underwent both 90-minute and 5- to 7-day
follow-up study, better global (eg, median ejection fraction at 90
minutes: 66% versus 58% and 5 to 7 days: 68% versus 57%) and
regional (eg, median infarct zone motion at 90 minutes: -1.84 versus
-2.95 SDs/chord; 5 to 7 days: -1.27 versus -2.56 SDs/chord) left
ventricular function was seen among the non–Q-wave
group.
Clinical Outcomes
After adjustment for differences in baseline characteristics and other
prognostic determinants of survival (eg, time to
thrombolytic treatment, thrombolytic
strategy) in a multivariable model, non–Q-wave MI was a
significant independent predictor of lower 2-year mortality (odds
ratio, 0.61; 95% confidence interval, 0.38 to 0.97;
P=.044).
The use of in-hospital coronary
revascularization procedures was similar among the
non–Q- and Q-wave groups (42% versus 44%, P=.45);
coronary angioplasty accounted for the majority of cases (33%
versus 36%). Thirty-day and 1-year mortality rates were similar among
the non–Q-wave MI patients, regardless of whether they underwent
in-hospital coronary revascularization
(1.7% versus 1.7% and 4.1% versus 4.7%, respectively).
Cardiogenic shock and congestive heart failure were less frequent in
the non–Q- versus the Q-wave group (1.5% versus 4.8%,
P<.001; and, 11% versus 15%, P=.013,
respectively). Rates of reinfarction (0.5% versus 0.2%,
P=.35), recurrent ischemia (19% versus 16%,
P=.29), and stroke (1.2% versus 1.3%, P=.85),
were similar among the two groups.
Although autopsy and coronary angiographic studies in the
prethrombolytic era supported the view of earlier
reperfusion in non–Q-wave MI, <375 non–Q-wave MI patients were
evaluated within 24 hours of the course of their
MI.4 8 In addition, the
pathophysiological insight gained from earlier
observational angiographic studies was limited by selection bias. For
example, the decision to proceed with angiography was usually
clinically based; thus, patients included in these studies may not
represent the spectrum of those who develop non–Q-wave MI. A
strength of the present study was the systematic, protocol-driven
evaluation of angiographic end points at defined times after
presentation.
Early angiographic data in the thrombolytic era are
limited to a secondary analysis of 2634 patients with first MI
in the TIMI-II trial, 29.1% of whom evolved a non–Q-wave MI by day
2.14 At 18 to 48 hours after
thrombolysis, a greater percentage of non–Q-wave MI
patients had an open infarct-related artery (TIMI flow grades 2 or 3),
complete infarct-related artery reperfusion (TIMI grade 3 flow), and
predischarge resting left ventricular ejection fraction
(based on radionuclide ventriculography) of >55%. Differences between
that substudy and the current analysis include the exclusion of
patients >76 years of age and those with prior myocardial MI,
restriction of cardiac catheterization findings to the
subgroup of patients assigned to an invasive strategy, and the delayed
timing (mean, >30 hours)26 of angiography after
the start of thrombolytic therapy.
Despite the favorable angiographic and left ventricular
function differences seen among the non–Q-wave MI patients in the
TIMI-II substudy, similar rates of early and 1-year mortality and
reinfarction were seen in the two groups. In contrast, the current
analysis showed a trend toward lower early mortality among
patients who developed a non–Q-wave, and a significant difference was
evident at 1 and 2 years.
Other studies describing the outcome of non–Q- and Q-wave MI patients
after thrombolytic therapy for ST-segment elevation MI
are presented in Table 4
The differences observed between the studies of non–Q- versus Q-wave
survival likely relate to differences in patient selection (eg, age
exclusion, prior MI exclusion), time from chest pain onset to
initiation of thrombolytic therapy, and differences in
post-thrombolytic treatment strategies (eg, use of
adjunctive intravenous heparin, particularly among patients
who received alteplase, and coronary
revascularization).
In addition, multiple classifications and different time frames for
infarct type stratification have been used; the ECG criteria for
diagnosis of non–Q- and Q-wave MI have never been standardized. The
simple screening criteria we used in this analysis have been
validated with quantitative anatomic analysis and are easily
applied by the clinician at the bedside. The optimal timing of ECG
classification of non–Q- and Q-wave MI
post-thrombolysis is also
controversial27 ; perhaps, as Matetzky et
al17 suggest, the prognostic value of this ECG
stratification is best demonstrated at a later (predischarge) rather
than an earlier (24 hours) time after thrombolysis.
Although the rate of in-hospital coronary
revascularization was high (43%), this is
comparable to that seen in the TIMI-II study, and one of the major
findings in that study was a similar rate of reinfarction and death in
the non–Q-wave group, regardless of the treatment strategy assigned.
Finally, short- and long-term mortality rates were similar among
non–Q-wave MI patients in the current analysis regardless of
whether they underwent in-hospital
revascularization.
Another novel finding of this study is the more frequent finding of a
more distal location of the culprit stenosis within the
infarct-related artery: only 33% of patients in the non–Q-wve group
experienced MI from an occlusion of the left main, proximal left
anterior descending, left circumflex, or right coronary artery.
In addition to the more common finding of right coronary artery
and left circumflex culprit involvement, this more distal location
within the infarct-related artery could account for the more frequent
incidence of non–Q-wave MI given that a smaller (and possibly
electrocardiographically silent) left ventricular territory
is at risk.
Study Limitations
Although this post hoc analysis does provide explanatory
pathophysiological mechanisms for the development
of non–Q-wve MI after thrombolysis, most patients who
sustain a non–Q-wave MI do not present with ECG changes (eg,
ST-segment elevation or left bundle-branch block) that would lead the
physician at the bedside to administer thrombolytic
therapy.28 There is evidence that patients
without ST-segment elevation, particularly those with significant
ST-segment depression16 29 (who often develop a
non–Q-wave), have a much worse prognosis than patients with ST-segment
elevation who receive
thrombolysis.30 Finally, although
patients with ST-segment elevation who evolve non–Q-wave MI are an
important subgroup, they represent <50% of the overall
non–Q-wave population.16
Conclusions
Received June 5, 1997;
revision received October 3, 1997;
accepted October 10, 1997.
© 1998 American Heart Association, Inc.
Clinical Investigation and Reports
Non–Q-Wave Versus Q-Wave Myocardial Infarction After Thrombolytic Therapy
Angiographic and Prognostic Insights From the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries–I Angiographic Substudy
Abstract
Top
Abstract
Introduction
Methods
Results
Discussion
References
Background—Although the
stratification of patients with myocardial infarction into ECG subsets
based on the presence or absence of new Q waves has important clinical
and prognostic utility, systematic evaluation of the impact of
thrombolytic therapy on the subsequent development and
prognosis of non–Q-wave infarction has been limited to date.
Key Words: infarction • electrocardiography • thrombolysis • catheterization • prognosis
Introduction
Top
Abstract
Introduction
Methods
Results
Discussion
References
The stratification of
patients with acute MI into ECG subsets by abnormal new Q waves has
important clinical and prognostic use. Studies in the
prethrombolytic era have shown lower in-hospital
mortality among patients with non–Q-wave MI. Despite a better initial
prognosis, non–Q-wave MI patients had more frequent infarct extension
and reinfarction, resulting in a similar or worse long-term prognosis
compared with those with Q-wave MI.1
Methods
Top
Abstract
Introduction
Methods
Results
Discussion
References
Randomization and Treatment Strategies
The entry criteria for enrollment into
GUSTO-I19 and the GUSTO-I angiographic
substudy18 have been described in detail.
Briefly, patients with chest pain for <6 hours and ST-segment
elevation compatible with acute MI were randomized to one of four
treatment strategies for reperfusion: (1) streptokinase with
subcutaneous heparin, (2) streptokinase with intravenous
heparin, (3) alteplase given in an accelerated manner with
intravenous heparin, or (4) streptokinase and alteplase
with intravenous heparin. All patients received aspirin
and, for those without a contraindication, intravenous
followed by oral atenolol therapy. All other medications and the use of
coronary revascularization were left to the
discretion of the investigator.
Patients in the GUSTO-I angiographic
substudy18 were randomly assigned to cardiac
angiography at one of four times after the initiation of
thrombolysis: 90 minutes, 180 minutes, 24 hours, or 5
to 7 days. The group undergoing angiography at 90 minutes underwent
repeat study after 5 to 7 days, allowing for analysis of
reocclusion and ventricular function at uniform times after
therapy. 
).
View larger version (23K):
[in a new window]
Figure 1. Disposition of patients; overall TIMI grade 3
infarct-related artery flow rates; and 30-day, 1-year, and 2-year
mortality rates.
The protocol and core laboratory procedures of the angiographic
substudy have been described in detail.18
Briefly, the infarct-related artery was identified through assessment
of the initial ECG, ventriculographic location of contractile
abnormality, and presence of stenosis or thrombus in the
corresponding artery. Flow in the infarct-related artery was determined
during the initial injection of contrast agent and graded as described
in the TIMI trial.20 Coronary collateral
score was grade 0, no angiographic filling of the infarct vessel distal
to occlusion; grade 1, faint opacification or small fragments of the
distal vessel visualized; grade 2, visualization of more than half of
the estimated length of the distal vessel, although less opacified than
a normal vessel of equal caliber; or grade 3, entire distal vessel wall
visualized and densely opacified. Ventricular volumes and
ejection fraction were calculated by the area-length
method.21 Global left ventricular
function was assessed by left ventricular ejection fraction
and end-systolic volume index. Regional function was measured
according to the method of Sheehan and Dodge22
and expressed as the number of abnormal chords in the infarct zone
(defined by >2 SDs below the norm) and by the mean magnitude of
depressed infarct-zone chords. Preserved wall motion was defined by all
infarct-zone chords being normal. Patients who underwent angioplasty
before the follow-up study at 5 to 7 days were excluded from the
analysis of reocclusion.
A Q-wave MI was based on a follow-up ECG performed 
24 hours
after the initiation of thrombolysis. The determination
of Q- and non–Q-wave ECG patterns was made by experienced readers
without knowledge of the angiographic findings at the ECG Core
Laboratory (Duke University); they used the Selvester QRS screening
criteria for Q-wave (or Q-wave–equivalent)
MI23 24 : (1) Q wave of 30 ms in aVF
(inferior); (2) Q wave of 40 ms in I and aVL (lateral);
(3) Q wave of 40 ms in two of V4 through
V6 (apical); (4) R wave of 40 ms in
V1 (posterior); (5) any Q wave in
V2 (anterior); and (5) R wave 
0.1 mV and 10 ms
in lead V2 (anterior).
In-hospital recurrent ischemia, congestive heart
failure, nonfatal stroke, cardiogenic shock, nonfatal reinfarction,
revascularization, and mortality were documented in
all patients. In addition, 30-day, 1-year, and 2-year mortality rates
were recorded, with complete follow-up available in 95.4% of the
patients.
Descriptive statistics (percentages for discrete variables;
medians with 25th and 75th percentiles for continuous variables)
were generated for baseline characteristics and for ECG, angiographic,
and clinical outcomes. Comparison of baseline characteristics and
clinical outcomes between patient groups was carried out using
likelihood-ratio 
2 or Fisher's exact tests
for differences in proportions of categorical variables, and
Wilcoxon rank sum tests was used for differences in median
values of continuous variables. Kaplan-Meier estimates were used to
obtain survival rates at 1 and 2 years, and curve comparisons were made
using the log-rank test. A modified, backward elimination logistic
regression model25 was used for prediction of
2-year mortality. The presence of non–Q-wave MI was added to this
model, which contains the variables found to be predictive of
30-day mortality in the overall GUSTO-I trial: age, height, weight,
systolic blood pressure, Killip class, heart rate, infarct
location, previous MI, time to treatment, diabetes, smoking status
(current and former), thrombolytic strategy, previous
bypass surgery, hypertension, and previous cerebrovascular disease.
Final data analysis was performed at Duke University; 2-year
survival analysis was performed at the George Washington
University Medical Center.
Results
Top
Abstract
Introduction
Methods
Results
Discussion
References
Characteristics of Post-thrombolytic Non–Q- Versus
Q-Wave MI Groups
Of the 2046 patients in this analysis, 409 (20%)
developed a non–Q-wave MI. Follow-up ECGs were acquired 6.9 (4.2,
10.0) and 7.4 (4.3, 10.8) days after thrombolysis in
the non–Q- and Q-wave groups, respectively (P=.12).
Comparison of the baseline characteristics of patients in the non–Q-
and Q-wave groups revealed similar age and coronary artery
disease risk factor profiles (Table 1).
Non-Q-wave MI patients were more likely to be female and to have a
history of smoking. Presentation characteristics revealed
similar pretreatment heart rate, blood pressure, Killip class, and time
from chest pain onset to thrombolytic administration.
Maximal CK and CK-MB values were significantly lower among the non–Q-
versus the Q-wave group: median of 742 versus 1853 IU
(P=.0001) and 79 versus 159 IU (P=.0001),
respectively. The 20% rate of non–Q-wave MI development did not
differ by thrombolytic regimen received.
View this table:
[in a new window]
Table 1. Patient Characteristics
ECG indicators of infarct severity were fewer and of less
magnitude in non–Q- compared with Q-wave MI patients: the median
number of leads with ST-segment elevation of 0.1 mV was 3 (3, 5)
versus 4 (3, 6) leads (P=.0001); and the median of the
maximal ST-segment elevation in any lead was 0.2 (0.1, 0.3) versus 0.3
(0.2, 0.4) mV (P=.0001). Non–Q-wave MI patients were more
likely to present with ST-segment elevation in an
inferior (63% versus 56%) or other (4% versus 2%)
location compared with more frequent anterior ST-elevation in the
Q-wave group (34% versus 42%; overall P=.012).
Patients with non–Q-wave MI were more likely to have an
angiographic infarct-related lesion in the right coronary or
left circumflex artery than were Q-wave MI patients (Table 2). Non–Q-wave MI patients were less
likely to have a proximal site of occlusion (left main, proximal left
anterior descending, circumflex, or right coronary artery) than
were Q-wave MI patients (33% versus 39%, P=.021). Patients
with non–Q-wave compared with Q-wave MI were less likely to have
multivessel disease (34% versus 39%, P=.103), particularly
among those in whom the circumflex was the infarct-related artery (26%
versus 42%). There was no difference in the frequency of identifiable
collaterals between the non–Q- and Q-wave groups.
View this table:
[in a new window]
Table 2. Coronary Angiographic Findings ). Angiograms obtained >180 minutes
after the start of therapy showed consistently greater overall
patency among the non–Q-wave group; however, these differences were
not statistically significant. The non–Q wave group also showed a
trend toward a lower median residual percent diameter stenosis
of the infarct-related artery.
View this table:
[in a new window]
Table 3. Coronary and Left Ventricular
Angiographic Findings 
).
Non–Q-wave MI patients had significantly better global left
ventricular function, as indicated by greater median left
ventricular ejection fraction, than did Q-wave MI patients
(66% versus 57%, P<.0001, Table 3). In addition,
end-systolic volume index was significantly lower among the
non–Q-wave group (median 21 versus 27 mL/m2,
P=.0001).
Compared with the Q-wave group, there was a trend toward lower
in-hospital mortality among the non–Q-wave group (1.5% versus 3.0%,
P=.067); this difference was maintained at 30 days (1.7%
versus 3.2%, P=.082) and achieved statistical significance
at 1 year (4.0% versus 7.0%, P=.021). Two-year mortality
was also significantly lower among the non–Q-wave group (6.4% versus
10.1%, P=.02; Fig 2).
View larger version (13K):
[in a new window]
Figure 2. Kaplan-Meier plot of 2-year survival among
patients who developed non–Q-wave (dashed line, n=409) or Q-wave
(solid line, n=1637) MI after thrombolysis.
Discussion
Top
Abstract
Introduction
Methods
Results
Discussion
References
In our study, 20% of the 2046 GUSTO-I angiographic patients who
were eligible for this secondary analysis and presented
with ST-segment elevation were classified as evolving a non–Q-wave
infarct pattern after treatment with thrombolytic
therapy. This rate of non–Q-wave development is similar to that seen
in a large ECG substudy of the overall GUSTO-I trial in which 4601 of
21 570 patients (21.3%) without ECG evidence of prior MI or other
confounding factors sustained a non–Q-wave MI.15
In contrast to patients who developed a Q wave, those who subsequently
evolved a non–Q-wave were more likely to have had early, complete, and
sustained infarct-related artery patency. These coronary
angiographic findings were associated with significantly less enzymatic
evidence of myocardial necrosis, better global and regional left
ventricular function, and improved short and long-term
survival rates. . The
improved survival among non–Q-wave MI patients in the current
angiographic substudy analysis was also found among patients
with first MI in the overall GUSTO-I study.15
Together with the findings from the LATE
substudy,16 the current angiographic substudy and
overall GUSTO-I analyses15
represent the first studies to show an improved prognosis among
patients who receive thrombolysis and subsequently
develop non–Q- compared with Q-wave MI. Furthermore, the overall
GUSTO-I analysis demonstrated the independent predictive value
of non–Q-wave MI in addition to age, infarct location, and other
important predictors of 30-day mortality.15 25
Additional features of our study include better longer-term (2-year)
survival among patients receiving thrombolysis who
evolve a non–Q wave and the independent value of a
post-thrombolytic ECG (24 hours) Q- versus non–Q wave
designation in the prediction of 2-year mortality.
View this table:
[in a new window]
Table 4. Mortality After Thrombolysis According
to Infarct Type
The current analysis was based on a follow-up ECG
performed at 24 hours after the initiation of
thrombolysis but before hospital discharge, with a
median time of 
1 week. Therefore, analysis of reinfarction
was limited because most of these events (87 of 96) occurred before a
follow-up ECG was obtained. In addition, patients who died before the
acquisition of a follow-up ECG were not included in this
analysis. Of the 385 patients (15.8%) enrolled in the GUSTO-I
angiographic study excluded from the current analysis, 102
(26.5%) died within 30 days. However, 51% of these deaths occurred
within 24 hours, and this time frame is too short to accurately assess
ECG development or provide prognostic information from a Q- or
non–Q-wave classification.
The findings from this secondary GUSTO-I angiographic
analysis indicate significant ECG, angiographic, and mortality
differences between patients who evolve a non–Q- versus Q-wave MI
after thrombolysis. The excellent prognosis among the
subgroup of patients who develop non–Q-wave MI after
thrombolytic therapy is related to early, complete, and
sustained infarct-related artery patency with resultant limitation of
left ventricular MI and dysfunction.
Selected Abbreviations and Acronyms
GUSTO
=
Global Utilization of Streptokinase and Tissue plasminogen
activator for Occluded coronary arteries (trial)
MI
=
myocardial infarction
TIMI
=
Thrombolysis in Myocardial Infarction (trial)
Acknowledgments
The GUSTO-I study was supported by a combined grant from Bayer
(New York), CIBA-Corning (Medfield, Mass), Genentech (South San
Francisco, Calif), ICI Pharmaceuticals (Wilmington, Del), and Sanofi
Pharmaceuticals (Paris, France). Dr Goodman was supported by a Heart
and Stroke Foundation of Canada Research Fellowship. We express our
appreciation to Deneane Boyle for her assistance in the 2-year
statistical analyses, Kathy Gates for her assistance in
coordinating this project, Steven Starr for his assistance in
coordinating the ECG analysis, Taco Baardman for his assistance
in obtaining ECGs from the non–North American centers, Patricia
Williams for her editorial assistance, and Susan Francis for her
assistance in preparation of the manuscript.
Footnotes
1 A list of participating GUSTO-I angiographic investigators is given in N Engl J Med. 1993;329:1615–1622. 
References
Top
Abstract
Introduction
Methods
Results
Discussion
References
This article has been cited by other articles:
 |
|
 |
|
  H. F.J Mannaerts, J. A van der Heide, O. Kamp, M. G Stoel, J. Twisk, and C. A Visser Early identification of left ventricular remodelling after myocardial infarction, assessed by transthoracic 3D echocardiography Eur. Heart J., April 2, 2004; 25(8): 680 - 687. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Spacek, P. Widimsky, Z. Straka, E. Jiresova, J. Dvorak, R. Polasek, I. Karel, R. Jirmar, L. Lisa, T. Budesinsky, et al. V_alue of First Day Angiography/Angioplasty I_n Evolving N_on-ST Segment Elevation Myocardial Infarction: An O_pen Multicenter Randomized Trial. The VINO Study Eur. Heart J., February 1, 2002; 23(3): 230 - 238. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Tomoda and N. Aoki Pathophysiology of Early Coronary Angioplasty with Stenting on Non-Q-Wave vs Q-Wave Myocardial Infarction Angiology, October 1, 2001; 52(10): 671 - 679. [Abstract] [PDF]
|
|
|
|
|
|
J Abdulla, B Brendorp, C Torp-Pedersen, L Kober, and on behalf of the TRACE study group Does the electrocardiographic presence of Q waves influence the survival of patients with acute myocardial infarction? Eur. Heart J., June 2, 2001; 22(12): 1008 - 1014. [Abstract] [PDF]
|
|
|
|
 |
|
 M. I. Furman, H. L. Dauerman, R. J. Goldberg, J. Yarzbeski, D. Lessard, and J. M. Gore Twenty-two year (1975 to 1997) trends in the incidence, in-hospital and long-term case fatality rates from initial q-wave and non-q-wave myocardial infarction: a multi-hospital, community-wide perspective J. Am. Coll. Cardiol., May 1, 2001; 37(6): 1571 - 1580. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. F. Wexler, A. S. Blaustein, P. W. Lavori, K. G. Lehmann, M. Wade, W. E. Boden, and for the Veterans Affairs Non-Q-Wave Infarction Str Non-Q-wave myocardial infarction following thrombolytic therapy: a comparison of outcomes in patients randomized to invasive or conservative post-infarct assessment strategies in the Veterans Affairs Non-Q-Wave Infarction Strategies In-Hospital (VANQWISH) trial J. Am. Coll. Cardiol., January 1, 2001; 37(1): 19 - 25. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Porela, H. Helenius, K. Pulkki, and L.-M. Voipio-Pulkki Epidemiological classification of acute myocardial infarction: time for a change? Eur. Heart J., October 2, 1999; 20(20): 1459 - 1464. [Abstract] [PDF]
|
|
|
|
|
|
K. A. Eagle, R. A. Guyton, R. Davidoff, G. A. Ewy, J. Fonger, T. J. Gardner, J. P. Gott, H. C. Herrmann, R. A. Marlow, W. C. Nugent, et al. ACC/AHA guidelines for coronary artery bypass graft surgery: A report of the American College of Cardiology/ American Heart Association task force on Practice Guidelines (Committee to revise the 1991 Guidelines for Coronary Artery Bypass Graft Surgery) J. Am. Coll. Cardiol., October 1, 1999; 34(4): 1262 - 1347. [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||