(Circulation. 1995;92:2079-2086.)
© 1995 American Heart Association, Inc.
Articles |
A Study of Biochemical Markers of Reperfusion Early After Thrombolysis for Acute Myocardial Infarction
Presented in part at the 67th Scientific Sessions of the American Heart Association, Dallas, Tex, November 14-17, 1994.
From the Cardiology Departments of Hôpital Beaujon, Clichy (T.L.); Hôpital Bichat, Paris (P.G.S., P.A.); Hôpital Côte de Nacre, Caen (G.G.); Hôpital Central, Nancy (E.A.); Hôpital de Hautepierre, Strasbourg (J-M.M.); Hôpital la Milétrie, Poitiers (D.C.); Clinique Saint Joseph, Colmar (M.H.); Hôpital Broussais, Paris (M-C.I.); and the Biochemistry Department, Hôpital Bichat, Paris (M.D., J.B.), France.
Correspondence to Thierry Laperche, MD, Service de Cardiologie, Hôpital Beaujon, 100 Bd du Général Leclerc, 92118 Clichy Cedex, France.
 |
Abstract |
|---|
 Top Abstract IntroductionMethods Results Discussion References |
|---|
Background In acute myocardial infarction (AMI), early noninvasive identification of patients with occluded infarct-related arteries (IRAs) after thrombolysis has important prognostic and therapeutic implications. The aims of this study were to evaluate biochemical methods for the early diagnosis of patency after thrombolysis prospectively and to establish the optimal diagnostic criteria retrospectively.
Methods and Results In 97 patients with AMI treated with
thrombolytic agents 
6 hours after the onset of symptoms,
myoglobin, troponin T, creatine kinase, the MB isoenzyme and MM
isoforms of creatine kinase were measured just before
thrombolysis began and 90 minutes later. IRA patency was
assessed by means of 90-minute coronary angiography. For each
marker, compared with the expected sensitivity and specificity based on
published thresholds for the diagnosis of patency, the observed values
were consistently lower but were markedly improved in a subset
of patients treated >3 hours after the onset of symptoms. With
receiver-operator characteristic curve analysis of the
slopes of increase and relative increases in each marker over 90
minutes, the best diagnostic performance was
achieved by use of the relative increase in myoglobin, troponin T, and
MM3/MM1 creatine kinase isoforms in patients treated >3 hours after
onset (areas under the curve of 0.84, 0.83, and 0.85,
respectively).
Conclusions Effective early noninvasive diagnosis of patency after thrombolysis is possible in patients treated >3 hours after symptom onset by use of criteria derived from the relative increase over 90 minutes in plasma markers, particularly myoglobin, troponin T, and MM3/MM1 creatine kinase isoforms. The diagnostic performance of the relative increase in myoglobin appears to be less susceptible to small changes in the diagnostic threshold value.
Key Words: myocardial infarction • reperfusion • myoglobin • creatine kinase • troponin T
|
Introduction |
|---|
|
TopAbstractIntroductionMethods Results Discussion References |
|---|
During AMI, failure of thrombolysis to unblock the infarct-related vessel is associated with poor outcome.1 Both randomized and nonrandomized studies have supported the concept of emergency rescue angioplasty, which appears to have excellent short- and long-term results, notably preventing death and severe congestive heart failure.2 3 4 5 However, widespread application of rescue angioplasty requires rapid identification of patients with a persistently occluded IRA, ideally within 90 minutes of the start of thrombolytic treatment.
Clinical criteria and simple ECG parameters have limited value for the noninvasive diagnosis of myocardial reperfusion,6 although some authors have suggested that their combination may result in enhanced diagnostic performance.7 Other methods, such as continuous ST-segment monitoring and kinetic analysis of biochemical markers, may also be of value in early identification of IRA patency. The plasma kinetics of myoglobin,8 9 10 11 12 tropomyosin-binding component troponin T,11 total CK activity, CK-MB,11 and isoforms of the CK-MM isoenzyme (MM1, MM2, and MM3)8 9 13 14 appear to be the most promising biochemical markers. However, their diagnostic performance has usually been evaluated in retrospective analyses of patients undergoing coronary angiography, often performed after AMI. In addition, the thresholds suggested for the diagnosis of reperfusion were generally derived from "time-to-peak" values. This rules out early diagnosis because peak CK plasma values are reached, on average, 9±6 hours after thrombolysis; peak troponin T values, after 12±9 hours.11
This study was based on a cohort of patients who underwent 90-minute coronary angiography. The aim was to evaluate prospectively biochemical markers for the diagnosis of coronary patency early after intravenous thrombolysis for AMI. In addition, this patient cohort was used to establish optimal biochemical criteria retrospectively.
|
Methods |
|---|
|
TopAbstractIntroductionMethods Results Discussion References |
|---|
Patient Selection
Ninety-seven patients referred to seven cardiology departments within 6 hours of MI were enrolled. All gave informed consent to participate in the study, which was approved by the ethics committee of the Hôpital Saint-Louis, Paris, France. Eligibility criteria were AMI occurring <6 hours previously and in-hospital treatment with intravenous thrombolytic agents. Eligibility for thrombolytic therapy was based on the following conventional criterion: prolonged chest pain (>30 minutes) resistant to nitrates that was associated with ST-segment elevation
0.1 mV in two limb leads or 0.2 mV in two contiguous
precordial leads. The thrombolytic agent was RTPA
in 56 patients, streptokinase in 34 patients, RTPA and streptokinase in
6 patients, and RTPA and urokinase in 1 patient. None of the patients
had severe renal failure or musculoskeletal disease that could
interfere with biochemical results. One patient received an electric
countershock before initiation of thrombolytic therapy. All
patients underwent coronary angiography 90 minutes after the
start of the treatment to ascertain the patency status of the IRA,
which was graded according to the TIMI score and determined on the
first contrast injection.15 Patency was defined as TIMI
grade 3 flow in the IRA (group A).16 17 Patients with
TIMI
grade flow 2 were considered to have occluded arteries (group B). All
angiograms were recorded on 35-mm cinefilm or super VHS videotapes.
Analysis was performed in a core laboratory by two independent
experienced angiographers blinded to all biochemical information.
Biochemical Analysis
Blood samples were obtained just before
thrombolysis
began and 90 minutes later. Venous blood (10 mL) was collected in two
Vacutainer tubes: one containing 150 U lithium heparinate for
measurement of myoglobin, troponin T, and CK-MB; the other, EDTA for
measurement of CK-MM isoforms. EDTA avoids carboxypeptidase hydrolysis
of C-terminal lysine residues in vitro, which converts CK-MM3 to CK-MM2
and CK-MM1.18 19 The tubes were immediately
centrifuged for 5 minutes at 1900g, and plasma was
divided into aliquots and immediately stored at -20°C pending
further analysis.
Myoglobin was determined by use of an automated latex-enhanced immunonephelometric technique (Behring nephelometer analyzer BNA, N-Latex Myoglobin). The measurement range of myoglobin was 24 to 396 µg/L, and samples >396 µg/L were automatically diluted. The upper limit of normal was 90 µg/L. The analyzer processed a single specimen in <15 minutes.
Plasma CK activity was measured at 37°C on a multiparametric analyzer (Hitachi 737, Boehringer Mannheim Corp) with CK-NAC reagents (Enzyline, BioMerieux). Results were obtained in 10 minutes. The normal range was 20 to 195 IU/L.
CK-MB mass was measured with a microparticle enzyme immunoassay (Opus CK-MB test module for use with the Opus automated analyzer, Behring). The upper limit of normal was 6 µg/L, and the time required to process a single specimen was 20 minutes.
CK-MM3, CK-MM2, and CK-MM1 in plasma samples were separated and revealed by use of rapid, high-voltage electrophoresis on an automated analyzer (Rep, Helena Laboratories). The individual isoforms of CK-MM were expressed as percentages of the total area under the absorbent profile contributed by each isoform. The MM3-to-MM1 ratio was also computed. The assay took 30 minutes.
Troponin T was measured with an ELISA (Boehringer Mannheim Corp). The upper limit of normal was 0.2 µg/L; the measurement range was 0.2 to 15 µg/L. The assay was completed semiautomatically within 90 minutes.
For all these biochemical markers, within- and between-day coefficients of variation ranged from 1.9% to 5.9% and from 2.7% to 7.6%, respectively.
For each marker, the slope of increase 90 minutes after thrombolysis was calculated as follows: slope=T90-T0/90 (international units, micrograms, or percent per liter per minute, as appropriate; T90 is the value at 90 minutes and T0 is the value before thrombolysis) and the relative increase was calculated as relative increase=T90-T0/T0.
Statistical Analysis
All continuous variables are expressed
as mean±SD. Groups
were compared by means of 
2 analysis for
categorical variables and by the Mann-Whitney test for numerical
variables.
For each biochemical marker, the sensitivity and specificity
of each
threshold for the diagnosis of patency at 90 minutes were determined by
use of published
thresholds.9 10 11 12 20
Because the diagnosis
had to be obtained within 90 minutes of the start of
thrombolysis, criteria involving the time to peak value of
a biochemical marker and rates of rise over periods >90 minutes were
not used. For all comparisons, values of P.05 were
considered significant.
For each marker studied, ROC curves were constructed by plotting sensitivity against (1-specificity) for both the slope and the relative increase in the plasma value.21 The best compromise between sensitivity and specificity was determined graphically.
|
Results |
|---|
|
TopAbstractIntroductionMethods Results Discussion References |
|---|
We enrolled 97 patients (82 men, 15 women) in this study. Mean age was 59±12 years. Mean time from the onset of symptoms to thrombolytic therapy was 212±97 minutes (range, 25 to 360 minutes). Forty-nine patients were treated >3 hours after the onset of symptoms. Angiography at 90 minutes showed that IRA was patent in 45 patients (group A), while TIMI flow grade was
2 in 52 patients
(group B) (TIMI flow grade 0 to 1 in 35 patients; grade 2 in 17
patients). Table 1
summarizes the clinical
characteristics of these patients. There were no significant
differences between the groups in terms of sex, age, location of MI, or
thrombolytic regimen. Likewise, the IRA distribution was
similar in the two groups. However, there was a nonsignificant trend
toward a longer delay before treatment in patients with occluded
arteries (P=.07). This was associated with statistically
higher baseline myoglobin values in these patients (Table 2).
|
|
Slopes of increase at 90 minutes did not differ between the groups, regardless of the marker studied. Relative increases at 90 minutes were consistently higher in group A than in group B, a difference that reached statistical significance for myoglobin, troponin T, and CK-MM3/CK-MM1 isoforms.
Prospective Validation of Published Thresholds for the Diagnosis
of IRA
Table 3 summarizes the observed sensitivity and
specificity of several published thresholds for the diagnosis of
IRA patency 90 minutes after the start of
thrombolysis.9 10 11 12 20
For each biochemical
marker, the observed values in this study were consistently
lower than those reported in retrospective analyses. Switching
patients with TIMI grade 2 IRA flow from group B to group A resulted in
consistently increased specificity but inconsistent
changes in sensitivity (Table 3).
|
Stratification According to Time to Treatment
The diagnostic
performance of all the markers
was markedly improved when patients were stratified according to the
time until treatment and when the analysis was restricted to
those patients treated >3 hours after the onset of symptoms (Table
4).
|
Retrospective Analysis of Biochemical Markers
For each
biochemical marker, we performed ROC curve
analyses of the slope of increase and the relative increase at
90 minutes. These curves were constructed for the whole cohort and for
the subset of patients treated >3 hours after the onset of symptoms
(Fig 1). Areas under the curves ranged from 0.56 to
0.85; the largest were those of the relative increases in myoglobin,
troponin T, and CK-MM3/CK-MM1 isoforms in patients treated >3 hours
after onset, which were high and very similar (0.83, 0.84, and 0.85,
respectively). Criteria based on CK or CK-MB isoforms had lower
sensitivity and specificity. For each marker, a cutoff value above
which patency of the infarct vessel is likely was determined from the
ROC curves through an attempt to identify the best compromise between
sensitivity and specificity (Table 5). For each marker
except CK-MM3 isoforms, the relative rates of increase in plasma values
consistently yielded better results than slopes of
increase.
|
|
Fig 2 shows the sensitivity and specificity of
the
relative increase in each biochemical marker for the prediction of
patency, according to the threshold value used for patients treated >3
hours after onset. The diagnostic performance of
myoglobin was less susceptible than that of troponin T to changes in
the threshold value: an elevation from 6.8 to 9 (a 1.3-fold increase)
of the threshold value of the relative increase in troponin T resulted
in a loss of sensitivity of 17 points (89% to 72%) and no gain in
specificity (83%). When the myoglobin threshold value was increased
1.3-fold (from 3 to 4), sensitivity and specificity did not change;
however, when the threshold value increased from 3 to 6 (2-fold) there
was a loss of sensitivity of 11 points (79% to 68%) but an increase
in specificity (82% to 84%). Finally, although the relative increase
in CK-MM3/CK-MM1 appeared to have good diagnostic
performance, it was extremely susceptible to changes in the
threshold value: a 1.3-fold increase (from 2 to 2.6) resulted in an
increase in specificity (87% to 96%) but a loss of sensitivity (68%
to 62%).
|
|
Discussion |
|---|
|
TopAbstractIntroductionMethods Results Discussion References |
|---|
Rationale of the Study
This study was aimed at prospectively validating noninvasive criteria of coronary artery patency on the basis of biochemical markers. IRA patency early after thrombolysis has a strong beneficial impact on short- and long-term outcome that does not appear to be entirely related to improved left ventricular function.1 22 Early identification of patients with persistent occlusion after thrombolysis during AMI also is important because it can pave the way for rescue interventions such as rescue percutaneous transluminal coronary angioplasty4 5 or repeated thrombolysis.23 24 25 Finally, it may be used as a surrogate end point for angiographic demonstration of patency in future clinical studies of reperfusion therapy. Coronary angiography has several limitations as a gold standard method for assessing reperfusion that are related primarily to the frequent fluctuations in coronary patency early after thrombolysis,26 absence of assessment of patency between 0 and 90 minutes, protective role of collateral circulation (which cannot be routinely quantified by angiography27 28 ), and no-reflow phenomenon. Therefore, angiography is an appropriate method for studying coronary patency rather than reperfusion. However, considering the fact that angiographic patency has been demonstrated to have an important prognostic impact1 29 30 and because there currently is no validated substitute for angiographic patency as a gold standard, we relied on coronary angiography for validation of our biochemical results. We thus focused on early biochemical indexes, obtained within 90 minutes, and not criteria based on the time required to reach the peak plasma value of biochemical markers (several hours generally are required before a diagnosis can be established).
Prospective Study
The first part of this study showed that,
when studied
prospectively, the diagnostic performance
(sensitivity and specificity) of biochemical criteria for patency did
not match that in previous studies. This discrepancy between the value
of a diagnostic threshold defined by retrospective
examination of a patient cohort and its prospective validation is not
surprising, especially when the small number of patients with
persistent occlusion in some studies is
considered.9 10 12 20 In
addition, the
diagnostic value of some methods may be particularly
sensitive to changes in the threshold value.11 All
previous studies defined patency as TIMI grade 2 and 3 flow in the IRA.
It has recently been shown that patients with TIMI grade 2 flow in the
IRA at the end of thrombolysis have a worse prognosis than
patients with TIMI grade 3 flow; as a result, only the latter is
currently considered to define successful thrombolysis in
terms of artery patency.16 17 However, this
difference in
the definition of infarct-vessel patency relative to previous
studies does not appear to influence the results because switching
patients with TIMI grade 2 flow from the occlusion to the patency group
led to only a mild increase in specificity and inconsistent
changes in sensitivity. Finally, although the biochemical methods we
used are standard and widely used, there were subtle differences in the
methods for CK-MM isoforms and CK-MB isoenzyme determination between
our study and previous work (related mainly to the use of mass rather
than activity measurements for CK-MB isoenzymes20 ).
However, this probably will not have a substantial impact on the
results and does not explain any of the differences observed for other
markers.
Diagnostic performance improved when the analysis was restricted to patients treated >3 hours after the onset of symptoms but failed to reach reported sensitivity and specificity values, regardless of the criteria used to define patency (including or excluding patients with TIMI grade 2 flow in the IRA). It must be pointed out that the better results for patients treated relatively late cannot account for the better diagnostic performance reported in the literature because in most reports10 11 the time until treatment approximated that in our study.
Retrospective Study
Using the same patient cohort, we
evaluated the
diagnostic performance of each biochemical marker
by means of ROC curve analysis. In the overall cohort, the
diagnostic performance of most markers was
acceptable; the areas under the curve ranged from 0.56 to 0.72 (values
>0.5 are not due to chance). However, as in the prospective
analysis, the diagnostic performance of all
the markers was markedly better in patients treated >3 hours after
onset, with areas under the curve ranging from 0.63 to 0.85. This
probably resulted because plasma values of the markers studied start to
rise about 3 hours after symptom onset (1 to 4 hours for myoglobin, 3
to 12 hours for troponin T and CK-MB isoenzymes, and 1 to 6 hours for
CK-MM isoforms31 ). These methods are nonetheless useful in
clinical practice because the mean time until admission or treatment
initiation in recent studies of thrombolytic therapy was
close to 3 hours32 33 and because the proven value of
late
(up to 12 hours) thrombolytic therapy34 will
probably lead to increased use of this approach between 6 and 12 hours
after onset. Early biochemical diagnosis of IRA patency after
thrombolysis is thus possible in patients treated >3 hours
after onset. On the basis of the area under ROC curves, the best makers
were myoglobin, troponin T, and CK-MM3/CK-MM1 isoforms, which had very
similar diagnostic performance (area under the
curves of the relative increase were 0.84, 0.83, and 0.85,
respectively).
Determination of Diagnostic Thresholds
For each marker, a
cutoff value above which patency of the infarct
vessel is likely was determined from the ROC curves (Table 5
).
When noninvasive diagnosis of patency is used to
triage patients with suspected failure of thrombolysis to
angiography and angioplasty, high specificity is important to avoid
overlooking patients who require rescue angioplasty. However, this must
be combined with good sensitivity to avoid a large number of
unnecessary coronary angiographies in patients with patent
IRAs. The compromise chosen may vary with the clinical situation
(patient's age or extent of the infarct) and availability of emergency
coronary angiography, which may differ from center to
center.
Most previous studies have focused on slopes of increase; in this study, particularly with myoglobin, troponin T, and CK-MM3/CK-MM1 isoforms, threshold values had better diagnostic performance when established from relative increases. The fact that relative increases take into account the basal value of the marker may explain in part their superiority over slopes of increase.
The
diagnostic performance achieved by the relative
increases in troponin T at 90 minutes (threshold of 6.8: sensitivity,
89%; specificity, 83%), myoglobin (threshold of 4: sensitivity, 79%;
specificity, 82%), and CK-MM3/CK-MM1 isoforms (threshold of 2:
sensitivity, 68%; specificity, 87%) appears high enough to allow
clinicians to comfortably rely on biochemical diagnosis in deciding
whether to undertake emergency and rescue angioplasties. However, the
sensitivity and specificity of the myoglobin threshold were less
susceptible to changes in the cutoff value: with troponin T and
CK-MM3/CK-MM1 isoforms, a 1.3-fold increase in the threshold value led
to a large loss of sensitivity (Fig 2). Therefore, myoglobin
may be the
marker of choice for noninvasive diagnosis of patency after
thrombolysis. It must be emphasized, however, that these
retrospectively defined criteria now require prospective
validation.
The time necessary to obtain the results of each test is important in clinical practice.35 However, rapid methods are already available36 37 or will become available within months38 for most criteria for clinical use.
Conclusions
This study shows that early noninvasive
identification of patients
with failed thrombolysis is possible with biochemical
criteria. In this prospective study, the actual diagnostic
performance of most markers did not match the results obtained
in retrospective analyses of previously published cohorts.
However, diagnostic performance was markedly
improved when analysis was restricted to patients receiving
thrombolysis >3 hours after symptom onset and when
criteria derived from the relative increase in plasma values over the
first 90 minutes were used. In this patient subset, the
diagnostic performance of myoglobin, troponin T,
and CK-MM3/CK-MM1 isoforms was good and very similar (areas under ROC
curves, 0.84, 0.83, and 0.85, respectively). However, the
diagnostic performance of the relative increase in
plasma myoglobin appears to be less susceptible to changes in the
threshold value used.
|
Selected Abbreviations and Acronyms |
|---|
|
|
Acknowledgments |
|---|
This work was supported by the Délégation à la Recherche Clinique, Assistance Publique-Hôpitaux de Paris. We thank Véronique Benard for her excellent secretarial assistance.
|
Footnotes |
|---|
A complete list of investigators participating in the Prospective Evaluation of Reperfusion Markers (PERM) Study Group is given in the "Appendix."
The following made up the PERM Study Group.
Coordination
Principal investigators: Thierry Laperche,
MD, Hôpital
Beaujon, Clichy, and P. Gabriel Steg, MD, Hôpital Bichat,
Paris.
Biochemistry core laboratory: Joëlle Benessiano, PhD, Monique Dehoux, PhD, and Fouzi Mestari, PhD, Hôpital Bichat, Paris.
Angiography core laboratory: Pierre Aubry, MD, Dominique Himbert, MD, and Jean-Michel Juliard, MD, Hôpital Bichat, Paris; Damien Coisne, MD, Hôpital la Milétrie, Poitiers; and Serge Makowski, MD, Hôpital Broussais, Paris.
Statistical consultant: Jean-Louis Golmard, Département de Biomathématiques et Unité INSERM U 436, Hôpital de la Pitié Salpétrière, Paris.
Scientific Analysis Committee: Marie-Claude Aumont, MD, Hôpital Bichat, Paris; René Gourgon, MD, Hôpital Beaujon, Clichy; Gilles Grollier, MD, Hôpital de la Côte de Nacre, Caen; Jean-Pierre Monassier, MD, Hôpital de Mulhouse, Mulhouse; and Paul-Etienne Valère, MD, Hôpital Bichat, Paris.
Study Sites
Groupe Hospitalier
Bichat-Beaujon, Paris: P. Gabriel Steg, MD
(principal investigator); and Pierre Aubry, MD; Hakim Benamer, MD;
Alain Cohen-Solal, MD; Dominique Himbert, MD; and Jean-Michel Juliard,
MD (coinvestigators).
Hôpital de la Côte de Nacre, Caen: Gilles Grollier, MD (principal investigator), and Sabine Fradin, PhD, and Benoît Valette, MD (coinvestigators).
Hôpital Central, Nancy: Etienne Aliot, MD (principal investigator); and Christian de Chillou, MD, and Gérard Ethévenot, MD (coinvestigators).
Hôpital de Hautepierre, Strasbourg: Jean-Marie Mossard, MD (principal investigator), and André Sacrez, MD (coinvestigator).
Hôpital la Milétrie, Poitiers: Damien Coisne, MD (principal investigator), and José Allal, MD (coinvestigator).
Clinique Saint Joseph, Colmar: Michel Hanssen, MD (principal investigator), and Jean-Marc Boulenc, MD, and Olivier Katz, MD (coinvestigators).
Hôpital Broussais, Paris: Marie-Christine Iliou, MD (principal investigator).
Received March 14, 1995; revision received May 8, 1995; accepted May 13, 1995.
|
References |
|---|
|
TopAbstractIntroductionMethods Results Discussion References |
|---|
-
The GUSTO Angiographic Investigators. The
effects of tissue plasminogen activator,
streptokinase, or both on coronary-artery patency,
ventricular function, and survival after acute myocardial
infarction. N Engl J Med. 1993;329:1615-1622.
[Abstract/Free Full Text]
-
Califf RM, Topol EJ, Stack RS, Ellis SG, George BS,
Kereiakes DJ, Samaha JK, Worley SJ, Anderson JL, Harrelson-Woodlief L,
Wall TC, Phillips HR, Abbottsmith CW, Candela RJ, Flanagan WH, Sasahara
AA, Mantell SJ, Lee KL, for the TAMI Study Group. Evaluation of
combination thrombolytic therapy and timing of cardiac
catheterization in acute myocardial infarction.
Circulation. 1991;83:1543-1556.
[Abstract/Free Full Text]
-
Ellis SG, Van der Werf F, Ribeiro-Da-Silva E, Topol
EJ. Present status of rescue coronary angioplasty:
current polarization of opinion and randomized trials.
J Am Coll Cardiol. 1992;19:681-686. [Abstract]
-
The CORAMI Study Group. Outcome of attempted
rescue coronary angioplasty after failed
thrombolysis for acute myocardial infarction.
Am J Cardiol. 1994;74:172-174. [Medline]
[Order article via Infotrieve]
-
Ellis SG, Ribeiro da Silva E, Heyndrickx G, Talley JD,
Cernigliaro C, Steg PG, Spaulding C, Nobuyoshi M, Erbel R, Vassanelli
C, Topol EJ, for the RESCUE Investigators. Randomized comparison
of rescue angioplasty with conservative management of patients with
early failure of thrombolysis for acute anterior myocardial
infarction. Circulation. 1994;90:2280-2284.
[Abstract/Free Full Text]
-
Califf RM, O'Neill W, Stack RS, Aronson L, Mark DB,
Mantell S, George BS, Candela RJ, Kereiakes DJ, Abbottsmith C, Topol
EJ, for the TAMI Study Group. Failure of simple clinical
measurements to predict perfusion status after intravenous
thrombolysis. Ann Intern Med. 1988;108:658-662.
-
Kircher BJ, Topol EJ, O'Neill W, Pitt B.
Prediction of infarct coronary artery
recanalization after intravenous
thrombolytic therapy. Am J Cardiol. 1987;59:513-515. [Medline]
[Order article via Infotrieve]
-
Ellis AK, Little T, Masud AR, Liberman HA, Morris DC,
Klocke FJ. Early noninvasive detection of successful reperfusion
in patients with acute myocardial infarction.
Circulation. 1988;78:1352-1357.
[Abstract/Free Full Text]
-
Laperche T, Steg PG, Benessiano J, Dehoux M, Juliard
JM, Himbert D, Gourgon R. Patterns of myoglobin and MM creatine
kinase isoforms release early after intravenous
thrombolysis or direct percutaneous
transluminal coronary angioplasty for acute myocardial
infarction, and implications for the early non invasive diagnosis of
reperfusion. Am J Cardiol. 1992;70:1129-1134. [Medline]
[Order article via Infotrieve]
-
Abendschein DR, Ellis AK, Eisenberg PR, Klocke FJ,
Sobel BE, Jaffe AS. Prompt detection of coronary
recanalization by analysis of rates of
change of concentrations of macromolecular markers in plasma.
Coron Artery Dis. 1991;2:201-212.
-
Zabel M, Hohnloser SH, Köster W, Prinz M, Kasper
W, Just H. Analysis of creatine kinase, CK-MB,
myoglobin, and troponin T time-activity curves for early assessment
of coronary artery reperfusion after intravenous
thrombolysis. Circulation. 1993;87:1542-1550.
[Abstract/Free Full Text]
-
Abe S, Arima S, Nomoto S, Maruyma I, Miyata M,
Yamaguchi H, Okino H, Yamashita T, Atsuchi Y, Tahara M, Nakao S, Tanaka
H. Early detection of coronary reperfusion by rapid
assessment of plasma myoglobin. Int J Cardiol. 1993;38:33-40. [Medline]
[Order article via Infotrieve]
-
Abe S, Nomoto K, Arima S, Miyata M, Yamashita T,
Kawataki M, Maruyama I, Toda H, Okino H, Atsuchi Y, Tahara M, Nakao S,
Tanaka H, Suzuki T. Detection of reperfusion 30 and 60 minutes
after coronary recanalization by a rapid
new assay of creatine kinase isoforms in acute myocardial
infarction. Am Heart J. 1993;125:649-656. [Medline]
[Order article via Infotrieve]
-
Puleo PR, Perryman MB, Bresser MA, Rokey R, Pratt CM,
Roberts R. Creatine kinase isoform analysis in the
detection and assessment of thrombolysis in man.
Circulation. 1987;75:1162-1169.
[Abstract/Free Full Text]
-
Chesebro JH, Knatterud G, Roberts R, Borer J, Cohen LS,
Dalen J, Dodge HT, Francis CK, Hillis D, Ludbrook P, Markis JE, Mueller
H, Passamani ER, Powers ER, Rao AK, Robertson T, Ross A, Ryan TJ, Sobel
BE, Willerson J, Williams DO, Zaret BL, Braunwald E.
Thrombolysis in Myocardial Infarction (TIMI) trial
phase I: a comparison between intravenous tissue
plasminogen activator and
intravenous streptokinase: clinical findings through
hospital discharge. Circulation. 1987;76:142-154.
[Abstract/Free Full Text]
-
Anderson JL, Karagounis LA, Becker LC, Sorensen SG,
Menlowe RL, for the TEAM-3 Investigators. TIMI perfusion grade 3
but not grade 2 results in improved outcome after
thrombolysis for myocardial infarction: ventriculographic,
enzymatic, and electrocardiographic evidence from the TEAM-3
study. Circulation. 1993;87:1829-1839.
[Abstract/Free Full Text]
-
Stadius ML. Angiographic monitoring of
reperfusion therapy for acute myocardial infarction: TIMI grade 3
perfusion is the goal. Circulation. 1993;87:2055-2057.
[Free Full Text]
-
Perryman MB, Knell JD, Roberts R.
Carboxypeptidase-catalyzed hydrolysis of C-terminal lysine:
mechanism for in vivo production of multiple forms of creatine
kinase in plasma. Clin Chem. 1984;30:662-664.
[Abstract/Free Full Text]
-
Panteghini M. Serum isoforms of creatine kinase
isoenzymes. Clin Biochem. 1988;21:211-218. [Medline]
[Order article via Infotrieve]
-
Garabedian HD, Gold HK, Yasuda T, Johns JA, Finkelstein
DM, Gaivin RJ, Cobbaert C, Leinbach RC, Collen D. Detection of
coronary artery reperfusion with creatine kinase-MB
determinations during thrombolytic therapy: correlation
with acute angiography. J Am Coll Cardiol. 1988;11:729-734. [Abstract]
-
Hanley JA, McNeil BJ. The meaning and use of the
area under a receiver operator characteristic (ROC) curve.
Radiology. 1982;143:29-36.
[Abstract/Free Full Text]
-
White HD, Cross DB, Elliott J, Norris RM, Yee T.
Long-term prognostic importance of patency of the
infarct-related coronary artery after
thrombolytic therapy for acute myocardial
infarction. Circulation. 1994;89:61-67.
[Abstract/Free Full Text]
-
White HD, Cross DB, Williams BF, Norris RM.
Safety and efficacy of repeat thrombolytic treatment
after acute myocardial infarction. Br Heart J. 1990;64:177-181.
[Abstract/Free Full Text]
-
Simoons M, Arnout J, van den Brand M, Nyssen K,
Verstraete M. Retreatment with alteplase for early signs of
reocclusion after thrombolysis: the European Cooperative
Study Group. Am J Cardiol. 1993;71:524-528. [Medline]
[Order article via Infotrieve]
-
White HD, Cross DB, Williams BF, Norris RM, Woo KS,
Hamer AW, Elliott JM, Ormiston JA. `Rescue'
thrombolysis with intracoronary tissue
plasminogen activator for failed
intravenous thrombolysis with streptokinase for
acute myocardial infarction. Am J Cardiol. 1995;75:172-174. [Medline]
[Order article via Infotrieve]
-
Hackett D, Davis G, Chierchia S, Maseri A.
Intermittent coronary occlusion in acute myocardial
infarction. N Engl J Med. 1987;317:1055-1059. [Abstract]
-
Ito H, Tomooka T, Sakai N, Yu H, Higashino Y, Fujii K,
Masuyama T, Kitabatake A, Minamino T. Lack of myocardial
perfusion immediately after successful thrombolysis: a
predictor of poor recovery of left ventricular function in
anterior myocardial infarction.
Circulation. 1992;85:1699-1705.
[Abstract/Free Full Text]
-
Sabia PJ, Powers ER, Ragosta M, Sarembock IJ, Burwell
LR, Kaul S. An association between collateral blood flow and
myocardial viability in patients with recent myocardial
infarction. N Engl J Med. 1992;327:1825-1831. [Abstract]
-
Braunwald E. The open-artery theory is alive
and well again. N Engl J Med. 1993;329:1650-1652.
[Free Full Text]
-
Kennedy JW. Optimal management of acute
myocardial infarction requires early and complete reperfusion.
Circulation. 1995;91:1905-1907.
[Free Full Text]
-
Adams JE III, Abendschein DR, Jaffe AS.
Biochemical markers of myocardial injury: is MB creatine kinase
the choice for the 1990s? Circulation. 1993;88:750-763.
[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]
-
The GUSTO Investigators. An international
randomized trial comparing four thrombolytic strategies for
acute myocardial infarction. N Engl J Med. 1993;329:673-682.
[Abstract/Free Full Text]
-
LATE Study Group. Late 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]
-
Roberts R, Kleiman NS. Earlier diagnosis and
treatment of acute myocardial infarction necessitates the need for a
`new diagnostic mind-set.'
Circulation. 1994;89:872-881.
[Abstract/Free Full Text]
-
Abendschein DR, Fontanet HL, Nohara R. Optimized
preservation of isoforms of creatine kinase MM isoenzyme in plasma
specimens and their rapid quantification by semi-automated
chromatofocusing. Clin Chem. 1990;36:723-727.
[Abstract/Free Full Text]
-
Mair J, Artner-Dworzak E, Lechleitner P, Morass B,
Smidt J, Wagner I, Dienstl F, Puschendorf B. Early diagnosis of
acute myocardial infarction by a newly developed rapid
immunoturbidimetric assay for myoglobin. Br Heart J. 1992;68:462-468.
-
Katus HA, Müller-Bardorf M, Hallermayr K, Borgya
A, Maier J, Mattusch F, Remppis A, Scheffold T. Development and
characterization of an improved rapid enzyme immunoassay for cardiac
troponin T. J Am Coll Cardiol. 1994;23:77A.
This article has been cited by other articles:
 |
|
 |
|
  P. G. Steg, L. Francois, B. Iung, D. Himbert, P. Aubry, P. Charlier, H. Benamer, L. J. Feldman, and J.-M. Juliard Long-term clinical outcomes after rescue angioplasty are not different from those of successful thrombolysis for acute myocardial infarction Eur. Heart J., September 2, 2005; 26(18): 1831 - 1837. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Kitagawa, T. Yamazaki, T. Akiyama, M. Sugimachi, K. Sunagawa, and H. Mori Microdialysis separately monitors myocardial interstitial myoglobin during ischemia and reperfusion Am J Physiol Heart Circ Physiol, August 1, 2005; 289(2): H924 - H930. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. A. de Lemos and E. Braunwald ST segment resolution as a tool for assessing the efficacy of reperfusion therapy J. Am. Coll. Cardiol., November 1, 2001; 38(5): 1283 - 1294. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. E. Goldman and M. J. Eisenberg Identification and Management of Patients with Failed Thrombolysis after Acute Myocardial Infarction Ann Intern Med, April 4, 2000; 132(7): 556 - 565. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. J. Tanasijevic, C. P. Cannon, E. M. Antman, D. R. Wybenga, G. A. Fischer, C. Grudzien, C. M. Gibson, J. W. Winkelman, E. Braunwald, and for the TIMI 10B Investigators Myoglobin, creatine-kinase-MB and cardiac troponin-I 60-minute ratios predict infarct-related artery patency after thrombolysis for acute myocardial infarction: Results from the thrombolysis in myocardial infarction study (TIMI) 10B J. Am. Coll. Cardiol., September 1, 1999; 34(3): 739 - 747. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. Frostfeldt, G. Ahlberg, G. Gustafsson, G. Helmius, B. Lindahl, A. Nygren, A. Siegbahn, E. Swahn, P. Venge, and L. Wallentin Low molecular weight heparin (dalteparin) as adjuvant treatment to thrombolysis in acute myocardial infarction--a pilot study: Biochemical Markers in Acute Coronary Syndromes (BIOMACS II) J. Am. Coll. Cardiol., March 1, 1999; 33(3): 627 - 633. [Abstract] [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||