| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
(Circulation. 1996;93:48-53.)
© 1996 American Heart Association, Inc.
Articles |
Relation Between Symptom Duration Before Thrombolytic Therapy and Final Myocardial Infarct Size
From the University of Washington, Seattle (M.H.R., C.M., M.D.C., W.D.W.); Duke University, Durham, NC (G.S.W.); and Memorial Medical Center, Long Beach, Calif (R.H.S.).
 |
Abstract |
|---|
 Top Abstract IntroductionMethods Results Discussion References |
|---|
Background Myocardial salvage is most likely to occur when thrombolytic therapy is administered within 4 to 6 hours of the onset of symptoms of myocardial infarction. The impact of delays within this early time period on final myocardial infarct size are unknown. The purpose of this study was to quantitate the relation between final myocardial infarct size and duration of symptoms before initiation of thrombolytic therapy in patients treated within 6 hours of symptom onset.
Methods and Results The findings from patients in four prospective randomized trials of thrombolytic therapy were combined for analysis. The study population consisted of 432 patients presenting within 6 hours of onset of symptoms of first acute myocardial infarction who met ECG criteria that allowed estimation of myocardial area at risk before treatment with thrombolytic therapy and who had thallium-201 myocardial infarct–size measurements performed several weeks after infarction. ECG analysis revealed no difference in myocardium at risk for infarction as a function of duration of symptoms before initiation of thrombolytic therapy. In contrast, univariate and multivariate analysis showed that final infarct size was highly dependent on duration of symptoms before initiation of therapy. Each 30-minute increase in symptom duration before thrombolytic therapy was associated with an increase in infarct size of 1% of the myocardium. Final infarct size in patients treated 4 to 6 hours after symptom onset was indistinguishable from patients who did not receive thrombolytic therapy.
Conclusions These findings suggest that for patients treated within 4 to 6 hours of the onset of symptoms, there is a progressive decline in the extent of myocardium salvaged as the duration of symptoms before therapy increases. These results support efforts to minimize the time delay between symptom onset and initiation of reperfusion therapy in all eligible patients.
Key Words: myocardial infarction • thrombolysis • reperfusion
|
Introduction |
|---|
|
TopAbstractIntroductionMethods Results Discussion References |
|---|
Reduction of infarct size is a central aim of thrombolytic therapy in patients with acute myocardial infarction.1 2 3 There is evidence from animal models that final infarct size is very sensitive to the duration of ischemia before reperfusion, with little salvage of myocardium realized if reperfusion is accomplished more than 2 hours after coronary occlusion.4 5 6 In human studies, the effect of the duration of symptoms before therapy on resulting infarct size (myocardial salvage) has been difficult to measure. This has been in part because of the use of indirect measures of infarct size, such as ejection fraction or myocardial enzyme release, but also because of the relative paucity of patients treated within the first 2 hours of symptom onset.3 7 8 The available data suggest that although there may be some survival benefit from later reperfusion therapy,9 10 11 relatively little salvage of myocardium occurs in patients treated more than 4 to 6 hours after symptom onset.12 13 14 It has not been well demonstrated how dependent infarct size is on duration of symptoms if therapy is given within this 4- to 6-hour threshold for myocardial salvage. Such information has important implications for the optimal treatment of patients who present early in the course of acute myocardial infraction. To address this question, we pooled data from four prospective studies of thrombolytic therapy in which final infarct size was quantitatively determined in a single nuclear medicine core laboratory.15 16 17 18 The patient group included 345 individuals treated an average of 2.4±1.4 hours after symptom onset, as well as 87 reference patients who did not receive thrombolytic therapy. The relation between final infarct size and time delay between symptom onset and initiation of thrombolytic therapy was determined.
|
Methods |
|---|
|
TopAbstractIntroductionMethods Results Discussion References |
|---|
Patients
Patient data from four studies of thrombolytic therapy were combined for analysis: the Western Washington Randomized Trial of Intracoronary Streptokinase in Acute Myocardial Infarction,15 the Western Washington Intravenous Streptokinase in Acute Myocardial Infarction Trial,16 the Western Washington Myocardial Infarction Registry and Emergency Department Tissue Plasminogen Activator Treatment Study,17 and the Myocardial Infarction Triage and Intervention Trial.18 All analyzed patients presented within 6 hours of onset of symptoms of acute myocardial infarction, had ST elevation on ECG, and had no contraindications to thrombolytic therapy. In the two older studies,15 16 patients were randomized to thrombolysis with streptokinase or standard therapy without thrombolysis. In the two more recent trials,17 18 recombinant tissue plasminogen activator (rt-PA) was used in all patients.
To minimize the number of factors confounding the estimation of infarct size, patients with a prior history of myocardial infarction, those who died before or failed to have follow-up nuclear studies performed, and those in whom the Aldrich ECG score (see "ECGs") could not be calculated were excluded from the study. The age, gender, duration of chest pain before therapy, systolic blood pressure, heart rate, and year of patient enrollment were gathered prospectively and were available for each patient.
ECGs
Initial pretreatment ECGs for all eligible patients were
analyzed by investigators who were blinded to the patients'
clinical presentation, hospital course, and radionuclide
infarct size. The location of each patient's infarct was recorded
as anterior (ST elevation in leads V1 through
V4) or inferior (leads II, III, and aVF). In
each ECG lead, the presence or absence and magnitude of ST elevation
and ST depression were noted, as well as the presence of T-wave
inversion or abnormal Q waves as defined by Selvester et
al.19 These values were used to calculate the Aldrich
score. The Aldrich score is a quantitative estimate of the
percentage of myocardium at risk, or the amount of
myocardium that would be expected to be infarcted if
thrombolytic therapy were not administered. The score is
calculated for anterior infarction by use of the formula: 3[1.5(number
of leads with ST elevation)-0.4]. For inferior
infarction, the formula is 3[0.6(sum of ST elevation in Leads II, III,
and aVF)+2.0].20 This method has been validated by
comparison with final infarct size as measured by the Selvester method
in patients not receiving reperfusion therapy.20 21
Radionuclide Studies
There were 1138 patients enrolled in the
four trials, 293 of
whom were excluded because of previous myocardial infarction and 150
because ECG abnormalities precluded calculation of the Aldrich
score. Of the remaining 695 patients, 432 (62% of all eligible
patients) survived and had resting quantitative thallium-201
tomographic measurement of infarct size performed a mean of 52±43 days
after therapy. Infarct-size measurements were performed at a
single, central, nuclear medicine laboratory at the Seattle Veterans
Administration Hospital. The studies were read by investigators who
were unaware of the details of treatment and hospital course.
Quantitative perfusion defect-size (infarct-size) determination
was performed by use of image acquisition and processing methods that
have been reported and validated previously.22
Statistical Analysis
Two-tailed Student's t
test and linear
regression were used to assess the statistical significance of the
univariate correlation between individual patient clinical
and ECG characteristics and infarct size. Multivariate
stepwise linear regression was used to select independent predictors of
infarct size. ANOVA was used to test the association between
infarct-size measurements and time from symptom onset to treatment.
The method of Tukey was used to compare selected subgroups based on
time to treatment.
|
Results |
|---|
|
TopAbstractIntroductionMethods Results Discussion References |
|---|
Baseline Patient Characteristics
Baseline characteristics of the 345 patients who received thrombolytic therapy and the 87 control patients are shown in Table 1
. Age, sex, initial heart rate,
systolic blood pressure, and ECG characteristics, including the
Aldrich-score prediction of infarct size, were similar in all
four contributing studies. Mean duration of symptoms before
thrombolytic therapy became progressively shorter with each
study, with an overall mean delay until treatment of 2.4±1.4 hours.
Because the control patients all came from the two older studies, the
time from symptom onset to hospital admission in the control patients
was about 25 minutes longer than for the treated patients. Otherwise,
treatment and control patients were similar with respect to
baseline characteristics.
|
Infarct Size
The Aldrich score was used to assess whether
there was an
association between duration of symptoms before initiation of
thrombolytic therapy and amount of myocardium
at risk. A weak negative correlation was observed
(r=-.10,
P=.03), suggesting that patients who were treated later were
at risk for somewhat smaller infarcts than those who were treated
earlier in their hospital course. In contrast, there was a positive
correlation between larger final infarct size and a longer duration of
symptoms before initiation of therapy (r=.25,
P<.0001). Other variables that had a significant
positive correlation with larger infarct size included several that
were derived from the initial ECG, including number of abnormal Q
waves, sum of ST elevation, sum of ST depression, and Aldrich score
(Table 2). Although some of the correlation coefficients
in Table 2 were highly statistically significant, it should be
recognized that the strength of association between infarct size and
significant covariates was moderate, with no coefficient exceeding
.30.
|
Stepwise linear regression was used to identify predictors of final
infarct size as measured by thallium-201 imaging in 323 treatment
patients for whom complete information was available (Table 3).
Variables considered for entry in the model are
listed in Table 2
. Time to treatment was an important predictor
of
infarct size, and it was the second variable to enter the model.
The positive association between time to treatment and infarct size was
such that a 29-minute increase in time to treatment was associated with
an absolute increase of 1% in infarct size. It is important to
recognize that other factors were also independently predictive of
final infarct size: number of abnormal Q waves on admission ECG (the
first variable to enter the model), sum of ST elevation on
admission ECG, anterior infarct location, sum of ST depression, and
male sex. Together, all six variables explained 22%
(r=.47) of the variation in infarct size. Time to therapy
remained an important predictor of larger infarct size when year of
therapy and use of rt-PA were included in the analysis.
|
Fig
1 shows the Aldrich-score estimation of
myocardium at risk and actual final infarct size by
thallium-201 tomography as a function of duration of symptoms before
initiation of thrombolytic therapy in treated patients as
well as in 87 comparable patients who did not receive
thrombolytic therapy. Pretreatment estimates of
myocardium at risk are similar for each time interval,
again suggesting minimal influence of time to therapy on amount of
myocardium at risk. The strong association between duration
of symptoms before therapy and resulting final infarct size is
depicted. Patients treated within 1 hour after symptom onset had
infarcts 40% as large as those treated 4 to 6 hours after symptom
onset; patients treated after intermediate time periods had infarcts of
intermediate size. There was no statistical difference in final infarct
size between patients treated 4 to 6 hours after symptom onset and
those who did not receive thrombolytic therapy. Figs 2 and
3 show that this relation between
time to treatment and resulting infarct size is present in both
anterior and inferior infarction.
|
|
|
Thrombolytic Agent
Nearly all patients treated within 2 hours
of symptom onset
received rt-PA; therefore, no assessment can be made of the role of
streptokinase in limiting infarct size when given in this very early
time period. Results of multivariate analysis
showed that a shorter duration of symptoms before therapy remained an
independent predictor of smaller infarct size for both drugs.
|
Discussion |
|---|
|
TopAbstractIntroductionMethods Results Discussion References |
|---|
Limitation of Infarct Size
Our analysis demonstrates that a shorter duration of symptoms before initiation of thrombolytic therapy is associated with a smaller final infarct size in patients treated within 4 hours of symptom onset. Each 30-minute delay in initiating thrombolytic therapy was associated with an increase in infarct size equal to 1% of the myocardium. This finding was independent of both clinical and ECG variables indicative of infarct location and myocardium at risk. The observation that final infarct size becomes progressively larger as the interval from symptom onset to therapy increases suggests that in this time frame (within 6 hours of onset of symptoms), myocardial salvage is not an all-or-nothing phenomenon but instead is highly dependent on duration of symptoms before therapy. Thus, to minimize infarct size, continuing efforts should be made to reduce the time from symptom onset to initiation of thrombolytic therapy in patients presenting within 6 hours of symptom onset. There is evidence that such optimization of myocardial salvage may translate into reduced mortality.8 In the Fibrinolytic Therapy Trialists' Collaborative Group study of 58 600 patients enrolled in randomized trials of thrombolytic therapy, there was a strong linear relation between lower mortality and shorter duration of symptoms before therapy in patients treated within 6 hours of symptom onset.11 This progressively increasing mortality benefit that results from earlier therapy in patients treated relatively soon after symptom onset may well be the result of improved myocardial salvage.
Methodological Considerations
Past efforts to determine the
relation between duration of
symptoms of acute myocardial infarction before initiation of
thrombolytic therapy and resulting infarct size have been
limited both by the methods used to estimate infarct size and by the
population of patients studied. Mortality is not a specific marker of
infarct size after thrombolytic therapy, because treatment
may affect mortality through mechanisms other than myocardial
salvage.1 2 3 7 The
inaccuracy of ejection fraction and
segmental wall motion as indexes of infarct size has been
recognized increasingly.7 The relation between infarct
size and ejection fraction can be obscured by stunning or hibernation
adjacent to the infarct region and by hyperkinesis of unaffected
regions of the left ventricle. Analysis of segmental wall
motion improves the accuracy of these measures of infarct
size23 but if performed too early is subject to error due
to myocardial stunning. Enzyme release has been used to measure infarct
size in several studies13 14 but is an indirect
estimate
dependent on assumptions regarding the kinetics of enzyme release and
clearance. ECG-based measures of final infarct size have also been
used24 25 but have been shown to be inaccurate in
patients
treated with thrombolytic therapy.26 Although
chronically ischemic myocardium may still cause
some error, direct estimation of infarct size by measuring perfusion
defect size with single photon emission computed tomography avoids most
of these problems.27 Two aspects of our protocol would
minimize error as a result of chronic ischemia. First, we
performed rest injections, thereby eliminating any effects due to
preceding exercise-induced worsened relative hypoperfusion. Second,
overestimation of infarct size as a result of resting ischemia
in peri-infarct regions has been shown to be minimized by waiting a
mean of 8 weeks after infarction, whether or not patients were treated
initially with thrombolytic therapy.28 29
Despite the advantages of our methods, our model explained only 22% of the observed variability in final infarct size. This finding is most likely the result of not being able to include variables indicative of whether thrombolytic therapy, once administered, was actually successful in achieving prompt and long-lasting recanalization of the infarct-related artery. A patient treated very early who does not achieve reperfusion or who has reocclusion with infarction 24 hours later will contribute significantly to the lack of precision of the model. Furthermore, in patients who do achieve long-lasting infarct artery patency, time to therapy, although an important clinical variable, does not directly measure time to reperfusion, which is probably the critical variable in predicting early myocardial salvage.
Bassand et
al27 used quantitative single photon emission
computed tomography to estimate infarct size and showed that overall
thrombolytic therapy reduced infarct size compared with
treatment with heparin, but these investigators did not examine the
relation between duration of symptoms before therapy and eventual
infarct size. To our knowledge, this is the first study to use these
methods to estimate infarct size, to show a relation between duration
of symptoms and myocardial salvage, and to delineate the time window
for salvage. Christian et al30 used sestamibi computed
tomography imaging to measure myocardium at risk and
infarct size in patients treated a mean of 4.7 hours after symptom
onset, but they were unable to demonstrate a direct correlation between
duration of symptoms and infarct size despite eliminating patients who
did not have successful reperfusion. Given our finding that myocardial
salvage occurs primarily in groups of patients treated relatively soon
after symptom onset, with little salvage observed in those treated
after 4 hours of symptoms, it is not surprising that in the study of
relatively late therapy by Christian et al30 infarct size
was more dependent on measures of collateral flow and factors affecting
the myocardium at risk than on duration of symptoms. In the
present study, patients were treated a mean of 2.4 hours after
symptom onset, including 12% treated within 1 hour of their first
symptoms. As a result, the effect of duration of symptoms before
therapy on infarct size was much more prominent. Although we did not
have direct tomographic measurements of the amount of
myocardium at risk, which was a limitation of this study,
we were able to estimate myocardium at risk by using the
Aldrich score, other clinical indicators of myocardium
at risk, and comparison with untreated controls. The Aldrich score
alone appears to somewhat overestimate infarct size in
inferior infarction (Fig 3) and, although more accurate, to
overestimate size in anterior infarction (Fig
2).21 The
reasons for the inaccuracy of the Aldrich score are unclear. The
score is most valuable to our study in that it shows no trend toward
increasing or decreasing myocardium at risk as a function
of duration of symptoms before initiation of thrombolytic
therapy.
A potential limitation of this study is bias produced by the exclusion of 263 otherwise eligible patients in the contributing studies from the analysis because they did not have follow-up radionuclide studies. Patients did not have infarct-size measurements for two main reasons: either they died before scheduled follow-up, or they refused follow-up, usually because of the distance they lived from the core laboratory.22 Comparison of excluded patients with included patients reveals that those excluded were treated after a longer duration of symptoms (3.2±1.7 versus 2.4±1.4 hours, P<.0001) but had similar Aldrich scores on presentation (19.7±8.3 versus 18.7±8.5, P=.21). Because these patients were treated later, and because many of the deaths probably represent failure of thrombolytic therapy, one would expect that their exclusion would result in an underestimation of the final infarct size, predominantly in patients treated relatively late after symptom onset. Thus, if we had been able to include these patients, we might have expected an even stronger correlation between longer duration of symptoms before thrombolytic therapy and larger final infarct size.
Implications for Health Policy
The Myocardial Infarction
Triage and Intervention (MITI)
trial18 and the European Myocardial Infarction
Project31 trial showed that prehospital administration
of thrombolytic therapy is feasible and probably indicated
when there are delays of 90 minutes or more from prehospital assessment
to hospital treatment. In addition, these studies showed that emergency
department– and hospital-based causes of delays in initiation of
therapy can be effectively overcome when prehospital identification of
candidates for thrombolytic therapy is performed by use of
clinical checklists and prehospital ECGs. Patients randomized to
in-hospital therapy in MITI experienced a delay of only 20 minutes
from arrival in the emergency department to initiation of
therapy.18 It is hoped that the demonstration of a
progressive increase in infarct size as the time from symptom onset to
initiation of thrombolytic therapy increases, even in
patients treated relatively early in the course of acute myocardial
infarction, will provide renewed urgency to efforts to eliminate
avoidable delays in initiation of thrombolytic therapy.
Summary
Determinants of final myocardial infarction size were
examined in
patients who received thrombolytic therapy within 6 hours
of symptom onset. A variety of clinical and ECG variables were
tested, and a shorter duration of symptoms before therapy was found to
be a strong independent predictor of smaller infarct size regardless of
infarct location. The relation between final infarct size and duration
of symptoms before therapy suggested no distinct time threshold for
complete myocardial salvage but instead a continuous relation between
duration of symptoms before therapy and final infarct size. Therapy
that was started 4 to 6 hours after symptom onset was not associated
with significant reductions in infarct size compared with untreated
patients. Continued efforts to shorten the time from development of
symptoms of acute myocardial infarction to provision of reperfusion
therapy are warranted, especially in patients presenting within 6
hours of symptom onset.
|
Acknowledgments |
|---|
This work was supported in part by grant RO1-HL-38454 from the National Heart, Lung, and Blood Institute. The authors would like to thank all of the physicians and nurses who participated in the Western Washington and MITI trials that form the basis of the present study, as well as Susan Shattuc, MS, for preparation of the figures.
|
Footnotes |
|---|
Reprint requests to W. Douglas Weaver, MD, MITI Coordinating Center, University of Washington Medical Center, 1910 Fairview Ave E, Ste 205, Seattle, WA 98102.
Received July 8, 1994; revision received June 8, 1995; accepted August 8, 1995.
|
References |
|---|
|
TopAbstractIntroductionMethods Results Discussion References |
|---|
-
Braunwald E. Myocardial reperfusion,
limitation of infarct size, reduction of left ventricular
dysfunction, and improved survival: should the paradigm be
expanded? Circulation. 1989;79:441-444.
[Free Full Text]
-
Califf RM, Topol EJ, Gersh BJ. From myocardial
salvage to patient salvage in acute myocardial infarction: the role of
reperfusion therapy. J Am Coll Cardiol. 1989;14:1382-1388. [Medline]
[Order article via Infotrieve]
-
Gersh BJ, Anderson JL. Thrombolysis
and myocardial salvage: results of clinical trials and the animal
paradigm—paradox or predictable?
Circulation. 1993;88:296-305.
[Free Full Text]
-
Reimer KA, Jennings RB. The `wavefront
phenomenon' of myocardial ischemic cell death, II: transmural
progression of necrosis within the framework of ischemic bed
size (myocardium at risk) and collateral flow.
Lab Invest. 1979;40:633-644. [Medline]
[Order article via Infotrieve]
-
Flameng W, Lesaffre E, Vanhaecke J.
Determinants of infarct size in non-human primates.
Basic Res Cardiol. 1990;85:392-403. [Medline]
[Order article via Infotrieve]
-
Reimer KA, Heide RSV, Richard VJ. Reperfusion
in acute myocardial infarction: effect of timing and modulating factors
in experimental models. Am J Cardiol. 1993;72:13G-21G. [Medline]
[Order article via Infotrieve]
-
Califf RM, Harrelson-Woodlief L, Topol EJ. Left
ventricular ejection fraction may not be useful as an end
point of thrombolytic therapy comparative trials.
Circulation. 1990;82:1847-1853.
[Abstract/Free Full Text]
-
Lincoff AM, Topol EJ. Illusion of
reperfusion: does anyone achieve optimal reperfusion during acute
myocardial infarction? Circulation. 1993;88:1361-1374.
[Abstract/Free Full Text]
-
EMERAS (Estudio Multicéntrico Estreptoquinasa
Repúblicas de Américas del Sur) Collaborative Group.
Randomised trial of late thrombolysis in patients
with suspected acute myocardial infarction. Lancet. 1993;342:767-772. [Medline]
[Order article via Infotrieve]
-
The LATE Investigators. Assessment of
thrombolytic efficacy (LATE) study with alteplase 6-24
hours after onset of acute myocardial infarction.
Lancet. 1993;342:759-766. [Medline]
[Order article via Infotrieve]
-
Fibrinolytic Therapy Trialists' (FTT) Collaborative
Group. Indications for fibrinolytic therapy in suspected acute
myocardial infarction: collaborative overview of early mortality and
major morbidity results from all randomized trials of more than 1000
patients. Lancet. 1994;343:311-322. [Medline]
[Order article via Infotrieve]
-
Koren G, Weiss AT, Hasin Y, Appelbaum D, Weber S,
Rozenman Y, Lotan C, Mosseri M, Sapozinkov D, Luria MH, Gotsman MS.
Prevention of myocardial damage in acute myocardial
ischemia by early treatment with intravenous
streptokinase. N Engl J Med. 1985;313:1384-1389. [Abstract]
-
ISAM Study Group. A prospective trial of
streptokinase in acute myocardial infarction (ISAM): mortality,
morbidity, and infarct size at 21 days. N Engl
J Med. 1986;314:1465-1471. [Abstract]
-
Simoons ML, Serruys PW, Van Den Bran M, Res J, Verheugt
FW, Krauss XH, Remme WJ, Bar F, De Zwaan C, Van Der Laarse A, Vermeer
F, Lubsen J. Early thrombolysis in acute myocardial
infarction: limitation of infarct size and improved survival.
J Am Coll Cardiol. 1986;7:717-728. [Abstract]
-
Kennedy JW, Ritchie JL, Davis KB, Fritz JK.
Western Washington randomized trial of intracoronary
streptokinase in acute myocardial infarction. N
Engl J Med. 1983;309:1477-1482. [Abstract]
-
Kennedy JW, Martin GV, Davis KB, Maynard C, Stadius M,
Sheehan FH, Ritchie JL. The western Washington
intravenous streptokinase in acute myocardial infarction
randomized trial. Circulation. 1988;77:345-352.
[Abstract/Free Full Text]
-
Althouse R, Maynard C, Cerqueira MD, Olsufka M, Ritchie
JL, Kennedy JW. The western Washington infarction registry and
emergency department tissue plasminogen
activator treatment trial. Am J Cardiol. 1990;66:1298-1303. [Medline]
[Order article via Infotrieve]
-
Weaver WD, Cerqueria M, Hallstrom AP, Litwin PE, Martin
JS, Kudenchuck PJ, Eisenberg M, for the MITI Project Group.
Early treatment with thrombolytic therapy: results
from the myocardial infarction, triage and intervention
pre-hospital trial. JAMA. 1993;270:1211-1216. [Abstract]
-
Selvester RH, Wagner GS, Hindeman NB. The
Selvester QRS scoring system for estimating myocardial infarct size:
the development and application of the system. Arch
Intern Med. 1985;145:1877-1881. [Medline]
[Order article via Infotrieve]
-
Aldrich HR, Wagner NB, Boswick J, Corsa AT, Jones
MG, Grande P, Lee K, Wagner GS. Use of initial ST-segment
deviation for prediction of final electrocardiographic size of acute
myocardial infarcts. Am J Cardiol. 1988;61:749-753. [Medline]
[Order article via Infotrieve]
-
Clemmensen P, Grande P, Aldrich HR, Wagner GS.
Evaluation of formulas for estimating the final size of acute
myocardial infarcts from quantitative ST-segment elevation on the
initial standard 12-lead ECG. J
Electrocardiol. 1991;24:77-83. [Medline]
[Order article via Infotrieve]
-
Cerqueira MD, Maynard C, Ritchie JL, Davis KB, Kennedy
JW. Long-term survival in 618 patients from the western
Washington streptokinase in myocardial infarction trials.
J Am Coll Cardiol. 1992;20:1452-1459. [Abstract]
-
Sheehan FH, Mathey DG, Schofer J, Dodge HT, Bolson EL.
Factors that determine recovery of left ventricular
function after thrombolysis in patients with acute
myocardial infarction. Circulation. 1985;71:1121-1128.
[Abstract/Free Full Text]
-
Hogg KJ, Lees KR, Hornung RS, Howie CA, Dunn FG, Hillis
WS. Electrocardiographic evidence of myocardial salvage after
thrombolysis in acute myocardial infarction.
Br Heart J. 1989;61:489-495.
[Abstract/Free Full Text]
-
Clemmensen P, Grande P, Saunamaki K, Pedersen F,
Svendsen JH, Wagner N, Granborg J, Madsen JK, Haedersdal C, Wagner GS.
Effect of intravenous streptokinase on the relation
between initial ST-predicted size and final QRS-estimated size of acute
myocardial infarcts. J Am Coll Cardiol. 1990;16:1252-1257. [Abstract]
-
Christian TF, Clements IP, Behrenbeck T, Huber KC,
Chesebro JH, Gersh BJ, Gibbons RJ. Limitations of the
electrocardiogram in estimating infarction size after
acute reperfusion therapy for acute myocardial infarction.
Ann Intern Med. 1991;114:264-270.
-
Bassand JP, Machecourt J, Cassagnes J, Anguenot T,
Lusson R, Borel E, Peycelon P, Wolf E, Ducellier D, for the APISIM
Study Investigators. Multicenter trial of
intravenous anisoylated plasminogen
streptokinase activator complex (APSAC) in acute myocardial
infarction: effects on infarct size and left ventricular
function. J Am Coll Cardiol. 1989;13:988-997. [Abstract]
-
Schwartz JS, Ponto RA, Forstrom LA, Bache RJ.
Decrease in thallium-201 image defect size after permanent
coronary occlusion. Am Heart J. 1983;106:1083-1088.
-
De Coster PM, Melin JA, Detry JM, Brasseur LA, Beckers
C, Col J. Coronary artery reperfusion in acute
myocardial infarction: assessment by pre- and postintervention
thallium-201 myocardial perfusion imaging. Am J
Cardiol. 1985;55:889-895. [Medline]
[Order article via Infotrieve]
-
Christian TF, Schwartz RS, Gibbons R.
Determinants of infarct size in reperfusion therapy for acute
myocardial infarction. Circulation. 1992;86:81-90.
[Abstract/Free Full Text]
-
The European Myocardial Infarction Project Group.
Prehospital thrombolytic therapy in patients with
suspected acute myocardial infarction. N Engl J
Med. 1993;329:383-389.
[Abstract/Free Full Text]
This article has been cited by other articles:
 |
|
 |
|
  E. Bjorklund, U. Stenestrand, J. Lindback, L. Svensson, L. Wallentin, B. Lindahl, and on behalf of the RIKS-HIA Investigators Pre-hospital thrombolysis delivered by paramedics is associated with reduced time delay and mortality in ambulance-transported real-life patients with ST-elevation myocardial infarction Eur. Heart J., May 2, 2006; 27(10): 1146 - 1152. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Part 4: Adult Basic Life Support Circulation, December 13, 2005; 112(24_suppl): IV-19 - IV-34. [Full Text] [PDF]
|
|
|
|
 |
|
 G. Tarantini, L. Cacciavillani, F. Corbetti, A. Ramondo, M. P. Marra, E. Bacchiega, M. Napodano, C. Bilato, R. Razzolini, and S. Iliceto Duration of Ischemia Is a Major Determinant of Transmurality and Severe Microvascular Obstruction After Primary Angioplasty: A Study Performed With Contrast-Enhanced Magnetic Resonance J. Am. Coll. Cardiol., October 4, 2005; 46(7): 1229 - 1235. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L Price, P Keeling, G Brown, D Hughes, and A Barton A qualitative study of paramedics' attitudes to providing prehospital thrombolysis Emerg. Med. J., October 1, 2005; 22(10): 738 - 741. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Johanson, Y. Fu, S. G. Goodman, M. Dellborg, P. W. Armstrong, M. W. Krucoff, L. Wallentin, and G. S. Wagner A dynamic model forecasting myocardial infarct size before, during, and after reperfusion therapy: an ASSENT-2 ECG/VCG substudy Eur. Heart J., September 1, 2005; 26(17): 1726 - 1733. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. G. Rosenfeld, A. Lindauer, and B. G. Darney Understanding Treatment-Seeking Delay in Women with Acute Myocardial Infarction: Descriptions of Decision-Making Patterns Am. J. Crit. Care., July 1, 2005; 14(4): 285 - 293. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. Bjorklund, B. Lindahl, P. Johanson, T. Jernberg, A.-M. Svensson, P. Venge, L. Wallentin, M. Dellborg, and the ASSENT-2 and ASSENT-PLUS study groups Admission Troponin T and measurement of ST-segment resolution at 60 min improve early risk stratification in ST-elevation myocardial infarction Eur. Heart J., January 2, 2004; 25(2): 113 - 120. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y Birnbaum and B J Drew The electrocardiogram in ST elevation acute myocardial infarction: correlation with coronary anatomy and prognosis Postgrad. Med. J., September 1, 2003; 79(935): 490 - 504. [Abstract] [Full Text]
|
|
|
|
|
|
P. Widimsky, T. Budesinsky, D. Vorac, L. Groch, M. Zelizko, M. Aschermann, M. Branny, J. St'asek, P. Formanek, and on behalf of the 'PRAGUE' Study Group Investigator Long distance transport for primary angioplasty vs immediate thrombolysis in acute myocardial infarction: Final results of the randomized national multicentre trial--PRAGUE-2 Eur. Heart J., January 1, 2003; 24(1): 94 - 104. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Fu, S. Goodman, W.-C. Chang, F. Van de Werf, C. B. Granger, and P. W. Armstrong Time to Treatment Influences the Impact of ST-Segment Resolution on One-Year Prognosis: Insights From the Assessment of the Safety and Efficacy of a New Thrombolytic (ASSENT-2) Trial Circulation, November 27, 2001; 104(22): 2653 - 2659. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P Chareonthaitawee, R J Gibbons, R S Roberts, T F Christian, and R Burns The impact of time to thrombolytic treatment on outcome in patients with acute myocardial infarction Heart, August 1, 2000; 84(2): 142 - 148. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A J O. Ophuis, F W Bar, F Vermeer, W Janssen, P A Doevendans, R J Haest, W R Dassen, and H J J Wellens Angiographic assessment of prospectively determined non-invasive reperfusion indices in acute myocardial infarction Heart, August 1, 2000; 84(2): 164 - 170. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Widimsky, L. Groch, M. Zelizko, M. Aschermann, F. Bednar, and H. Suryapranata Multicentre randomized trial comparing transport to primary angioplasty vs immediate thrombolysis vs combined strategy for patients with acute myocardial infarction presenting to a community hospital without a catheterization laboratory. The PRAGUE Study Eur. Heart J., May 2, 2000; 21(10): 823 - 831. [Abstract] [PDF]
|
|
|
|
|
|
T. Noda, S. Minatoguchi, K. Fujii, M. Hori, T. Ito, K. Kanmatsuse, M. Matsuzaki, T. Miura, H. Nonogi, M. Tada, et al. Evidence for the delayed effect in human ischemic preconditioning: Prospective multicenter study for preconditioning in acute myocardial infarction J. Am. Coll. Cardiol., December 1, 1999; 34(7): 1966 - 1974. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Effect of time from onset to coming under care on fatality of patients with acute myocardial infarction: effect of resuscitation and thrombolytic treatment Heart, August 1, 1998; 80(2): 114 - 120. [Abstract] [Full Text]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||