CLINICAL STUDY
Mechanisms behind the prognostic value of troponin T in unstable coronary artery disease: a FRISC II substudy
Bertil Lindahl, MD, PhD*,
Erik Diderholm, MD*,
Bo Lagerqvist, MD, PhD*,
Per Venge, MD, PhD ,
Lars Wallentin, MD, PhD* the FRISC II Investigators
* Department of Cardiology, Uppsala, Sweden
Department of Clinical Chemistry, University Hospital, Uppsala, Sweden
Manuscript received February 5, 2001;
revised manuscript received May 1, 2001,
accepted June 25, 2001.
Reprint requests and correspondence: Dr. Bertil Lindahl, Department of Cardiology, University Hospital, S-751 85 Uppsala, Sweden
bertil.lindahl{at}card.uas.lul.se
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Abstract
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OBJECTIVES
This study was designed to elucidate possible mechanisms for the prognostic value of troponin T (tnT).
BACKGROUND
The reasons for the adverse prognosis associated with elevation of troponins in unstable coronary artery disease are poorly understood.
METHODS
Patients enrolled in the Fast Revascularization during InStability in CAD (FRISC-II) trial were included. Clinical characteristics, findings at echocardiography and coronary angiography, and prognosis were evaluated in relation to different tnT levels.
RESULTS
Absence of significant coronary stenosis was more frequent and three-vessel disease or left main stem stenosis was less frequent in patients without, compared with, detectable tnT. The occurrence of visible thrombus increased with rising levels of tnT. In the group with the highest levels of tnT, occlusion of the left circumflex artery was more common than in the three other tnT groups, as was a left ventricular ejection fraction below 0.45. The one-year risk of death in the noninvasive arm of the study increased by increasing levels of tnT (1.6% to 4.6%), whereas the risk of myocardial infarction showed an inverted U-shaped curve and was lower in the lowest (5.5%) and highest (8.4%) tnT groups than in the two intermediate groups (17.5% and 16.2%).
CONCLUSIONS
Any detectable elevation of tnT raises the probability of significant coronary stenosis and thrombus formation and is associated with an increased risk of reinfarction and death. However, at a more pronounced elevation of troponin, a higher proportion of patients has a persistent occlusion of the culprit vessel and reduced left ventricular function, associated with a high mortality but a modest risk of reinfarction.
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Abbreviations and Acronyms
| | CAD | = coronary artery disease | | ECG | = electrocardiogram | | FRISC-II | = Fast Revascularization during InStability in CAD | | MI | = myocardial infarction | | TIMI | = Thrombolysis In Myocardial Infarction | | tnT | = troponin T |
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The value of troponin T (tnT) or I for risk stratification in unstable coronary artery disease (CAD), that is, non–ST-segment elevation myocardial infarction (MI) and unstable angina, is well established (1–3). However, the reasons for the adverse prognosis associated with elevations of troponin are not fully understood. The troponins are sensitive and specific markers for myocardial necrosis (4), which might occur in unstable CAD as a result of persistent or transient thrombotic vessel occlusion at the site of plaque rupture or erosion (5). Furthermore, small areas of myocardial necrosis
caused by microembolizations from the thrombus, occluding arterioles and capillaries downstream, might be an alternative or contributory cause of minor elevations of troponin in unstable CAD (6). Recently, it has been shown (7,8) that patients with unstable CAD and elevated tnT or I had more widespread CAD than those without elevated tnT or I and more often had complex lesion characteristics and visible thrombus in the culprit vessel (7,9,10). The aim of the present study was to further elucidate the mechanisms behind the prognostic value of tnT in a large cohort of patients with unstable CAD.
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Methods
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Patients and study design.
The present study was a substudy of the FRISC-II (Fast Revascularization during InStability in CAD) trial (11,12). In brief, the FRISC-II was a prospective, multicenter trial in which 2,457 patients were randomized to a noninvasive or an invasive strategy. Furthermore, within each arm patients were randomized to 90 days treatment with low molecular weight heparin, dalteparin or placebo.
Inclusion criteria were symptoms of myocardial ischemia associated with ST-depression, T-wave inversion or elevation of available cardiac markers. Major exclusion criteria were raised risk of bleeding, angioplasty performed within past six months, waiting list for coronary revascularization procedure, previous open-heart surgery, other severe cardiac disease, renal insufficiency (serum creatinine >150 µg/l) or other severe illness.
Written consent was obtained from all patients and the protocol was approved by all local ethics committees.
Randomized treatment.
All patients were initially treated with either subcutaneous dalteparin or by intravenous infusion of standard heparin. The patients were randomized within 48 h after the start of open-label dalteparin or standard heparin. From randomization all patients received dalteparin subcutaneously (120 U/kg) twice daily until the early invasive procedure and for at least five days in the noninvasive arm. After this initial treatment, patients received twice-daily subcutaneous injections of either dalteparin in a dose adjusted for weight and gender (5,000 to 7,500 U) or placebo for three months.
The early invasive strategy required coronary angiography and, if appropriate, revascularization within seven days from start of open-label dalteparin. The noninvasive strategy included coronary angiography only in patients with refractory symptoms, severe ischemia at a predischarge symptom-limited exercise test, or severe angina or MI during follow-up.
The patient flow in the present substudy is outlined in Figure 1.
Blood samples for biochemical markers.
At randomization ethylenediamine tetraacetate-plasma samples were obtained from 2,329 patients (95%) and stored frozen at –70°C for central analysis of tnT with a third-generation tnT assay on an Elecsys 2010 (13). The analytical range extends from 0.01 to 25 µg/l and the upper reference level, defined as the 99th percentile of healthy controls, is below the lower limit of the analytical range. At our laboratory the intra-assay CV was 7.9% (n = 19) and interassay CV was 11.2% (n = 8) at the low end of the analytical range (tnT = 0.037 µg/l).
The patients were divided in four groups based on tnT levels: the first group consisted of all patients without measurable tnT (<0.01 µg/l, n = 623) and the others of the first, second and third tertile, respectively, of the remaining patients (0.01 to 0.17 µg/l, n = 570; 0.18 to 0.63 µg/l, n = 569; and >0.63 µg/l, n = 567).
ECG and echocardiogram.
The admission (qualifying) 12-lead electrocardiograms (ECGs) were evaluated at a core laboratory. Rhythm, presence and location of pathological Q-waves, ST-segment depression ( 0.05 mV) and T-wave inversion were recorded.
Echocardiograms were obtained in 1,867 (80%) of the patients before discharge and always before any invasive procedure. All echocardiograms were evaluated centrally and the left ventricular ejection fraction was visually assessed. A depressed systolic left ventricular function was considered present when the ejection fraction was below 0.45.
Coronary angiogram.
In 1,142 (98.4%) of the 1,161 patients randomized to an invasive policy and with tnT determined at randomization, a coronary angiogram was performed at a median of four days (25th to 75th percentile; 3 to 5 days) from admission (Fig. 1). The coronary angiograms were evaluated locally according to a detailed protocol and without knowledge of tnT status. The coronary vessels were divided in 16 segments (14) and degree of stenosis, Thrombolysis In Myocardial Infarction (TIMI) flow grade and any visible thrombus were noted in each of these segments. A 50% diameter obstruction in at least one of the segments in the respective vessel area (right coronary, left anterior descending and left circumflex artery) was considered significant in respect of the traditional one-, two- or three-vessel disease. Also for the left main artery, a 50% diameter stenosis was considered significant. The evaluator of the coronary angiogram was urged to identify and localize the culprit lesion to a single segment, which was possible in 652 patients (56%).
Clinical end points.
The relation between tnT levels and clinical outcome at 12 months was evaluated in the noninvasive arm of the study (Fig. 1). The noninvasive arm was chosen because of the marked influence of an invasive strategy on subsequent events (11,12). The randomization to three months of dalteparin versus placebo was not considered, as it did not influence the long-term outcome (11). The clinical end points used in the present analysis were total death, MI and revascularization (due to incapacitating or recurrent symptoms or severe ischemia at the exercise test). Details about the follow-up and evaluation procedures and definitions have been published elsewhere (11,12).
Statistics.
Differences in proportions were evaluated by chi-square test. The Kruskal-Wallis one-way analysis of variance was used to test the equality of distributions in the four tnT groups.
Adjusted relative risk ratios and 95% confidence intervals in relation to tnT levels were calculated for occurrence of depressed left ventricular ejection fraction and findings at coronary angiography, respectively, by multiple logistic regression analysis. To identify independent predictors of death and MI, respectively, multiple logistic regression analyses were applied, forcing all the tested variables into the models.
For all statistical analyses a significant difference was considered to exist at the p < 0.05 levels. All calculations were done with the SPSS system 10.0 (SPSS Inc., Chicago, Illinois).
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Results
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Clinical data, echocardiogram and tnT.
The blood sample for analysis of tnT was obtained at randomization, which took place in median 38.6 h (25th to 75th percentile, 26.8 to 54.0 h) from onset of last episode of chest pain. Seventy-three percent, 58% and 47% of the patients had a tnT level 0.01, 0.1 and 0.2 µg/l, respectively.
The clinical characteristics at inclusion according to tnT levels are shown in Table 1. The patients with, compared to without, detectable tnT were older and more often had ST-segment depression and abnormal Q-waves on admission ECG. The proportion of men increased by increasing levels of tnT. In contrast, the proportion of patients with a history of stable angina, previous angioplasty and use of aspirin, beta blockade and other cardiovascular drugs decreased with increasing levels of tnT. There was no significant association between tnT levels and traditional risk factors (except for cholesterol level), previous MI, pharmacologically treated congestive heart failure or chest pain at rest.
A left ventricular ejection fraction below 0.45 was significantly more common, also after adjusting for several possible confounders, in the group with the highest levels of tnT (>0.63 µg/l) compared with every other tnT group (Table 2A and B).
Coronary angiography and tnT in the invasive arm.
The proportion of patients without significant stenosis was higher and the proportion of three-vessel disease or left main stem stenosis was lower in patients without, compared to with, detectable tnT. However, among patients with detectable tnT there was no relation between severity of CAD and the level of tnT. In contrast, the occurrence of visible thrombus and TIMI flow 0 to 1 in at least one vessel gradually increased by rising levels of tnT (Table 3A). The same patterns were found irrespective of gender, although the absolute numbers differed; that is, among men and women with tnT <0.01 µg/l, no significant stenosis could be demonstrated in 26% and 43%, respectively, and among those with tnT 0.01 µg/l in 4.4% and 14.3%, respectively. The demonstrated associations between the tnT level and the severity of CAD, occurrence of visible thrombus and TIMI flow grade were consistent also after adjusting for several possible confounders (Table 3B).
Among those with tnT <0.01, 0.01 to 0.17, 0.18 to 0.63 and >0.63 µg/l, the proportions of patients with total or subtotal occlusion (TIMI flow 0 or 1) of a culprit lesion in the left circumflex artery territory, were 4%, 4%, 12% and 22% (p < 0.001), respectively. The corresponding figures for the left anterior descending artery territory were 8%, 10%, 12% and 12% (p = 0.62) and for the right coronary artery territory 7%, 5%, 8% and 9% (p = 0.48).
Prognosis and tnT.
The frequency of death, MI, revascularization and the combined end point death/MI at 12 months in relation to the different tnT levels in the noninvasive group are shown in Table 4. The risk of death showed a trend to a gradual increase by increasing levels of tnT. However, the risk of MI, revascularization and the composite of death and MI were lowest in the lowest, modest in the highest and highest in the two intermediate tnT groups (Fig. 2).
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Figure 2 Death and myocardial infarction (MI) rate at 12 months, respectively, in relation to troponin T (tnT) levels.
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The prognostic value of tnT regarding death and MI, respectively, was evaluated in models using multivariate logistic regression analysis (Table 5). After adjustment for age, gender, diabetes, hypertension, a history of stable angina or previous MI and ST-segment depression, patients with a tnT 0.17 µg/l had an approximately tripled risk of death compared with patients without any myocardial damage, and there was a trend to increased risk also among those with only a minor myocardial damage (tnT 0.01 to 0.17 µg/l). Somewhat differently, the relative risk of MI was also significantly and substantially elevated in patients with tnT 0.01 to 0.17 µg/l as tnT 0.18 to 0.63 µg/l. However, the risk of MI in patients with the largest myocardial damage (tnT >0.63 µg/l) was not significantly higher than in patients without detectable myocardial damage.
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Table 5 Multivariate Logistic Regression Analyses Regarding Death and MI at 12 Months, Respectively, in the Noninvasive Group (n = 1,148)
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The influence of the left ventricular ejection fraction on the predictive values of any tnT elevation (tnT 0.01 µg/l) was studied in the subgroup of 961 patients with an echocardiogram obtained. The relative risk ratio for death at 12 months decreased from 2.01 to 1.73 after adjustment for the left ventricular ejection fraction (/<0.45), whereas the relative risk ratio for MI was virtually unchanged after adjustment (from 2.52 to 2.45).
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Discussion
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The unique design of the present study gave specific advantages in attempts to further elucidate the possible mechanisms for the prognostic value of troponin concerning mortality and myocardial (re-)infarctions in unstable CAD. The relation between tnT and baseline characteristics, ECG findings and left ventricular ejection fraction could be reliably evaluated in the large cohort of the whole trial. The relation between the tnT level and the coronary lesions and blood flow could be evaluated in the half of the population randomized to an early coronary angiogram. Finally, the prognostic information in tnT and other factors could be evaluated without the influence of early revascularization procedures in the other half of the population randomized to the noninvasive arm of the study, which mainly reflected the "natural course" of the coronary lesions and their consequences in unstable CAD.
Prognosis and tnT.
The mortality among patients without elevation of tnT was low, in accordance with previous studies (2,3). The one-year mortality of 1.6% in patients without any measurable tnT elevation was close to the annual mortality of 1.7% found in patients with stable angina pectoris (15). However, at any sign of myocardial damage there was a strong trend to an increased mortality in accordance with previous findings (2). The relation between the tnT level and the risk of subsequent MI showed a somewhat different pattern. The one-year risk of MI was lowest in the group without detectable tnT, 5.5%, which is approximately twice as high as the annual rate of MI found in patients with stable angina pectoris (15). In the two intermediate tnT groups the rate of MI during follow-up was substantially higher, 16.2% to 17.5%, indicating a severely unstable coronary lesion as the underlying condition. However, rather unexpectedly, the rate of re-MI in those with the highest levels of tnT was only 8.4%, which was only marginally higher than in those without any tnT elevation. The one-year rate of reinfarction in this group resembles the one-year reinfarction rate of 6.4% after a Q-wave infarction in the Framingham heart study (16). Thus, the risk of myocardial (re-)infarction in relation to tnT level showed an inverted U-shaped curve in the present study (Fig. 2), that has not previously been described. However, in retrospect, the same association between tnT level and risk of MI could be seen in the FRISC-1 trial (2). The proportion of patients requiring a revascularization procedure during follow-up in the four tnT groups showed a similar inverted U-shaped curve. This finding supports the concept of a more unstable coronary lesion in the two intermediate groups than in the lowest and highest tnT groups.
Clinical characteristics, tnT and risk of future events.
Several baseline variables known to be associated with an increased risk of new coronary events differed in relation to tnT levels. Patients without elevation of tnT were somewhat younger, more often women and less likely to have ST-segment depression at the admission ECG. However, there was no consistent pattern that indicated that patients with elevated tnT constituted a more sick population; on the contrary, several factors known to be associated with an increased risk of adverse events, such as previous angina, antianginal medication and higher cholesterol levels, were more common in patients without elevation of tnT, in accordance with some (10), but not all, previous studies (17). Thus, it is unlikely that the relation between the tnT levels and baseline characteristics is a major determinant of the prognostic value of tnT, especially as tnT remained an independent prognostic factor in multivariate analysis.
Coronary angiogram, tnT and risk of future events.
The extent of CAD is a major determinant of the prognosis in unstable CAD, with a very low risk of cardiac events in patients without significant obstructions (18) and the highest risk in those with three-vessel or left main disease (19). Furthermore, complex lesions, occurrence of visible thrombus and decreased TIMI flow grade have been associated with the risk of death and MI (20). Only a few studies have evaluated findings at coronary angiography in relation to troponin levels in patients with unstable CAD (7–10). In the present study, the largest so far, there were significant relations between the tnT level and the extent and type of coronary lesions and coronary blood flow. In this large cohort it was possible to demonstrate that these relations remained after adjustment for differences in baseline variables, excluding the possibility that these relations were merely a reflection of such differences. Despite a clinical diagnosis of unstable CAD in all patients, 26% of the men and 43% of the women without any measurable elevation of tnT (<0.01 µg/l) did not have significant coronary stenosis. In contrast, in men and women with tnT elevation and thus myocardial damage, 4% and 14%, respectively, had no significant obstruction, which is close to the figures in patients with non–ST-elevation MI in the GUSTO IIb study, 4.2% and 9.1%, respectively (21). The gender difference might be explained by differences in thrombotic activity as well as in the underlying substrate of coronary thrombosis between the sexes (22,23). Patients with any sign of myocardial damage more often had three-vessel disease or left main stem stenosis (35% to 40%) than did those without detectable tnT (23%). These findings are in accordance with previous smaller studies showing more frequent triple-vessel and left main coronary artery involvement in patients with elevated troponin (7,8). Thus, the relation between the tnT levels and the extent of CAD might explain some of the prognostic value of elevated tnT levels.
Coronary thrombus, tnT and risk of future events.
By increasing levels of tnT there was a graded rise, from 3% to 16%, in occurrence of visible intracoronary thrombus, in accordance with the study of Heeschen et al. (10). The incidences of visible intracoronary thrombi in patients with tnT <0.01 µg/l were very low (<3%) in our study as well as in their study (10), and comparable to patients with stable angina pectoris (2%) (24). However, it should be emphasized that visual evaluation of coronary angiograms from patients with unstable CAD is associated with a substantial underestimate of the occurrence of intracoronary thrombi in comparison to intracoronary angioscopy (25). Therefore, the occurrence of intracoronary thrombi at increasing tnT levels probably is considerably larger than apparent in the current study. Thus, the relation between tnT and remaining thrombi at the coronary lesions might be one explanation for the relation between tnT level and risk of early (re-)infarction.
Coronary occlusion, tnT and risk of future events.
In the present study there was also a relation between the tnT level and impairment of coronary blood flow, in accordance with Heeschen et al. (10). This was due mainly to a rise in occurrence of total or subtotal occlusions by increasing levels of tnT. The high incidence of total or subtotal occlusions, especially of the circumflex artery or its branches, in the group with the highest tnT levels suggests that many of the patients in this group might have had a "transmural" infarction that was undetected by the standard 12-lead ECG on admission (26). The higher rate of completed infarctions at the highest tnT levels might explain the lower risk of reinfarction and lower need for revascularization, in analogy with the lower risk of reinfarction in patients after a Q-wave compared with a non–Q-wave infarction (17).
Left ventricular ejection fraction, tnT and risk of future events.
The left ventricular function has a major impact on mortality (27). The tnT level has been shown to correlate with infarct size (28) and left ventricular ejection fraction (29). A depressed left ventricular ejection fraction at the echocardiogram was significantly more common in the group with the highest tnT levels (>0.63 µg/l) in the present study (Table 2A). This relation also remained after adjustment for baseline variables possibly associated with a depressed left ventricular function (Table 2B), indicating that the lower ejection fraction in the group with the highest tnT levels was indeed a result of the myocardial damage associated with the index event. Thus, the increased mortality found at a tnT level >0.63 µg/l might be a consequence of myocardial damage large enough to cause a decreased left ventricular function. However, left ventricular dysfunction was no explanation for the increased risk of death in patients with only minor elevations of tnT. Thus, the association between a minor tnT elevation and future mortality probably is related to the raised risk of reinfarction.
Study limitations.
One limitation of the present study is that tnT was determined only at randomization, at a median of 38.6 h from onset of last episode of chest pain. However, because tnT levels remain elevated for 10 to 14 days in patients with myocardial necrosis (30), very few false negative results should have occurred. It is also important to recognize that tnT was determined with the new third-generation assay, which has slightly different properties, such as a lower upper reference level, compared with the second-generation assay.
Another limitation of the study is that the coronary angiograms were not assessed centrally. However, the evaluation was performed according to a predefined protocol. The striking similarities regarding the occurrence of coronary thrombus and TIMI flow grade in the present study, as in the previous study by Heeschen et al. (10) with central evaluation, corroborate our results.
Conclusions and clinical implications.
These results, together with previous experiences, suggest that much of the prognostic value of troponins in unstable CAD can be attributed to underlying severe coronary stenosis, culprit lesion thrombosis, downstream embolization with microinfarction and, in some patients, total coronary occlusion and a large MI. The group without any tnT elevation consists partly of patients without significant atherosclerotic CAD, whose symptoms often have noncardiac causes, and partly of patients with CAD, whose symptoms might be caused by an increase of oxygen demand or a decrease in oxygen supply unrelated to coronary thrombosis. At any detectable elevation of tnT the probability of significant coronary stenosis is considerably raised, and there is an increased likelihood of an unstable plaque with thrombus and downstream microembolization and impairment of coronary flow, all factors associated with a raised risk of reinfarction and death. However, with a more pronounced elevation of troponin, a higher proportion of patients will have a persistent occlusion of the culprit coronary vessel associated with reduced left ventricular function, resembling a Q-wave infarction with a high mortality but lower risk of reinfarction.
These results also give a reasonable explanation of why treatment with coagulation or platelet inhibition, which reduces the risk of thromboembolic events, is protective mainly in patients with elevated troponin (31–33).
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Footnotes
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This study was supported by Pharmacia, the Upjohn Company and the Swedish Heart and Lung Foundation.
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References
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|---|
1. Hamm CW, Ravkilde J, Gerhardt W, et al. The prognostic value of serum troponin T in unstable angina. N Engl J Med. 1992;327:146–150[Medline]
2. Lindahl B, Venge P, Wallentin L. Relation between troponin T and the risk of subsequent cardiac events in unstable coronary artery disease. Circulation. 1996;93:1651–1657[Abstract/Free Full Text]
3. Lüscher MS, Thygesen K, Ravkilde J, Heickendorff L. Applicability of cardiac troponin T and I for early risk stratification in unstable coronary artery disease. Circulation. 1997;96:2578–2585[Abstract/Free Full Text]
4. Bhayana V, Henderson AR. Biochemical markers of myocardial damage. Clin Biochem. 1995;28:1–29[CrossRef][Medline]
5. Falk E, Shah PK, Fuster V. Coronary plaque disruption. Circulation. 1995;92:657–671[Free Full Text]
6. Topol EJ, Yadav JS. Recognition of the importance of embolization in atherosclerotic vascular disease. Circulation. 2000;101:570–580[Free Full Text]
7. Jurlander B, Farhi ER, Banas JJ, et al. Coronary angiographic findings and troponin T in patients with unstable angina pectoris. Am J Cardiol. 2000;85:810–814[CrossRef][Medline]
8. Janorkar S, Koning R, Eltchaninoff H, Andres H, Lavoinne A, Cribier A. Relation between serum cardiac troponin I values and severity of clinical, electrocardiographic and quantitative angiographic features in unstable angina. Indian Heart J. 1999;51:31–34[Medline]
9. Benamer H, Steg PG, Benessiano J, et al. Elevated cardiac troponin I predicts a high-risk angiographic anatomy of the culprit lesion in unstable angina. Am Heart J. 1999;137:815–820[CrossRef][Medline]
10. Heeschen C, van Den Brand MJ, Hamm CW, Simoons ML. Angiographic findings in patients with refractory unstable angina according to troponin T status. Circulation. 1999;100:1509–1514[Abstract/Free Full Text]
11. Invasive compared with noninvasive treatment in unstable coronary-artery disease: FRISC II prospective randomised multicentre study. FRagmin and Fast Revascularisation during InStability in coronary artery disease Investigators. Lancet. 1999;354:708–715[CrossRef][Medline]
12. Wallentin L, Lagerqvist B, Husted S, Kontny F, Stahle E, Swahn E. Outcome at 1 year after an invasive compared with a noninvasive strategy in unstable coronary artery disease: the FRISC II invasive randomised trial. FRISC II Investigators. Fast Revascularisation during Instability in coronary artery disease. Lancet. 2000;356:9–16[CrossRef][Medline]
13. Hallermayer K, Klenner D, Vogel R. Use of recombinant human cardiac Troponin T for standardization of third generation Troponin T methods. Scand J Clin Lab Invest. 1999;230(Suppl):128–131
14. Austen WG, Edwards JE, Frye RL, et al. A reporting system on patients evaluated for coronary artery disease. Report of the Ad Hoc Committee for Grading of Coronary Artery Disease, Council on Cardiovascular Surgery, American Heart Association. Circulation. 1975;51(Suppl):5–40[Medline]
15. Rehnqvist N, Hjemdahl P, Billing E, et al. Effects of metoprolol vs. verapamil in patients with stable angina pectoris. The Angina Prognosis Study in Stockholm (APSIS). Eur Heart J. 1996;17:76–81[Abstract/Free Full Text]
16. Berger CJ, Murabito JM, Evans JC, Anderson KM, Levy D. Prognosis after first myocardial infarction. Comparison of Q-wave and non–Q-wave myocardial infarction in the Framingham Heart Study. JAMA. 1992;268:1545–1551[Abstract/Free Full Text]
17. Stubbs P, Collinson P, Moseley D, Greenwood T, Noble M. Prospective study of the role of cardiac troponin T in patients admitted with unstable angina. Br Med J. 1996;313:262–264[Abstract/Free Full Text]
18. Lichtlen PR, Bargheer K, Wenzlaff P. Long-term prognosis of patients with anginalike chest pain and normal coronary angiographic findings. J Am Coll Cardiol. 1995;25:1013–1018[Abstract]
19. Sharma GV, Deupree RH, Luchi RJ, Scott SM. Identification of unstable angina patients who have favorable outcome with medical or surgical therapy (eight-year follow-up of the Veterans Administration Cooperative Study). Am J Cardiol. 1994;74:454–458[CrossRef][Medline]
20. Freeman MR, Williams AE, Chisholm RJ, Armstrong PW. Intracoronary thrombus and complex morphology in unstable angina. Relation to timing of angiography and in-hospital cardiac events. Circulation. 1989;80:17–23[Abstract/Free Full Text]
21. Hochman JS, Tamis JE, Thompson TD, et al. Sex, clinical presentation, and outcome in patients with acute coronary syndromes. N Engl J Med. 1999;341:226–232[CrossRef][Medline]
22. Conlan MG, Folsom AR, Finch A, et al. Associations of factor VIII and von Willebrand factor with age, race, sex, and risk factors for atherosclerosis: the Atherosclerosis Risk In Communities (ARIC) study. Thromb Haemost. 1993;70:380–385[Medline]
23. Farb A, Burke AP, Tang AL, et al. Coronary plaque erosion without rupture into a lipid core. A frequent cause of coronary thrombosis in sudden coronary death. Circulation. 1996;93:1354–1363[Abstract/Free Full Text]
24. Ahmed WH, Bittl JA, Braunwald E. Relation between clinical presentation and angiographic findings in unstable angina pectoris, and comparison with that in stable angina. Am J Cardiol. 1993;72:544–550[CrossRef][Medline]
25. de Feyter PJ, Ozaki Y, Baptista J, et al. Ischemia-related lesion characteristics in patients with stable or unstable angina. A study with intracoronary angioscopy and ultrasound. Circulation. 1995;92:1408–1413[Abstract/Free Full Text]
26. Boden WE, Gibson RS, Schechtman KB, et al. ST segment shifts are poor predictors of subsequent Q wave evolution in acute myocardial infarction. A natural history study of early non-Q wave infarction. Circulation. 1989;79:537–548[Abstract/Free Full Text]
27. St. John Sutton M, Pfeffer MA, Plappert T, et al. Quantitative two-dimensional echocardiographic measurements are major predictors of adverse cardiovascular events after acute myocardial infarction. The protective effects of captopril. Circulation. 1994;89:68–75[Abstract/Free Full Text]
28. Wagner I, Mair J, Fridrich L, et al. Cardiac troponin T release in acute myocardial infarction is associated with scintigraphic estimates of myocardial scar. Coron Artery Dis. 1993;4:537–544[Medline]
29. Rao AC, Collinson PO, Canepa-Anson R, Joseph SP. Troponin T measurement after myocardial infarction can identify left ventricular ejection of less than 40%. Heart. 1998;80:223–225[Abstract/Free Full Text]
30. Katus HA, Remppis A, Neumann FJ, et al. Diagnostic efficiency of troponin T measurements in acute myocardial infarction. Circulation. 1991;83:902–912[Abstract/Free Full Text]
31. Lindahl B, Venge P, Wallentin L. Troponin T identifies patients with unstable coronary artery disease who benefit from long term antithrombotic protection. J Am Coll Cardiol. 1997;29:43–48[Abstract]
32. Heeschen C, Hamm CW, Goldmann B, Deu A, Langenbrink L, White HD. Troponin concentrations for stratification of patients with acute coronary syndromes in relation to therapeutic efficacy of tirofiban. PRISM Study Investigators. Platelet Receptor Inhibition in Ischemic Syndrome Management. Lancet. 1999;354:1757–1762[CrossRef][Medline]
33. Hamm CW, Heeschen C, Goldmann B, et al. Benefit of abciximab in patients with refractory unstable angina in relation to serum troponin T levels. N Engl J Med. 1999;340:1623–1629[CrossRef][Medline]
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J. T. Saunders, V. Nambi, J. A. de Lemos, L. E. Chambless, S. S. Virani, E. Boerwinkle, R. C. Hoogeveen, X. Liu, B. C. Astor, T. H. Mosley, et al.
Cardiac Troponin T Measured by a Highly Sensitive Assay Predicts Coronary Heart Disease, Heart Failure, and Mortality in the Atherosclerosis Risk in Communities Study
Circulation,
April 5, 2011;
123(13):
1367 - 1376.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. S. Jolly, H. Shenkman, D. Brieger, K. A. Fox, A. T. Yan, K. A. Eagle, P. G. Steg, K.-D. Lim, A. Quill, S. G. Goodman, et al.
Quantitative troponin and death, cardiogenic shock, cardiac arrest and new heart failure in patients with non-ST-segment elevation acute coronary syndromes (NSTE ACS): insights from the Global Registry of Acute Coronary Events
Heart,
February 1, 2011;
97(3):
197 - 202.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
G. Biondi-Zoccai, A. Abbate, and G. Sangiorgi
It's never too early! Evidence for rushing your acute coronary patients to the cath lab
Eur. Heart J.,
January 1, 2011;
32(1):
13 - 15.
[Full Text]
[PDF]
|
|
|
|
|
|
|
G. Ganesha Babu, J. Malcolm Walker, D. M. Yellon, and D. J. Hausenloy
Peri-procedural myocardial injury during percutaneous coronary intervention: an important target for cardioprotection
Eur. Heart J.,
January 1, 2011;
32(1):
23 - 31.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. A. de Lemos, M. H. Drazner, T. Omland, C. R. Ayers, A. Khera, A. Rohatgi, I. Hashim, J. D. Berry, S. R. Das, D. A. Morrow, et al.
Association of Troponin T Detected With a Highly Sensitive Assay and Cardiac Structure and Mortality Risk in the General Population
JAMA,
December 8, 2010;
304(22):
2503 - 2512.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. Ardissino, D. Lina, and F. Notarangelo
Chapter 44 Non-ST-elevation acute coronary syndromes
The ESC Textbook of Acute and Intensive Cardiac Care,
December 1, 2010;
1(1):
med-9780199584314-chapter - med-9780199584314-chapter.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
E. Swahn, J. Alfredsson, and S. Sederholm Lawesson
Chapter 48 Gender considerations in acute coronary syndromes
The ESC Textbook of Acute and Intensive Cardiac Care,
December 1, 2010;
1(1):
med-9780199584314-chapter - med-9780199584314-chapter.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
C. Eek, B. Grenne, H. Brunvand, S. Aakhus, K. Endresen, O. A. Smiseth, T. Edvardsen, and H. Skulstad
Strain echocardiography predicts acute coronary occlusion in patients with non-ST-segment elevation acute coronary syndrome
Eur Heart J Cardiovasc Imaging,
July 1, 2010;
11(6):
501 - 508.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
H. W. Kim, A. Farzaneh-Far, and R. J. Kim
Cardiovascular Magnetic Resonance in Patients With Myocardial Infarction: Current and Emerging Applications
J. Am. Coll. Cardiol.,
January 5, 2010;
55(1):
1 - 16.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
P. Venge, N. Johnston, B. Lindahl, and S. James
Normal Plasma Levels of Cardiac Troponin I Measured by the High-Sensitivity Cardiac Troponin I Access Prototype Assay and the Impact on the Diagnosis of Myocardial Ischemia
J. Am. Coll. Cardiol.,
September 22, 2009;
54(13):
1165 - 1172.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
K. M. Eggers, B. Lagerqvist, P. Venge, L. Wallentin, and B. Lindahl
Prognostic Value of Biomarkers During and After Non-ST-Segment Elevation Acute Coronary Syndrome
J. Am. Coll. Cardiol.,
July 21, 2009;
54(4):
357 - 364.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
F. S. Apple, S. W. Smith, L. A. Pearce, and M. M. Murakami
Assessment of the Multiple-Biomarker Approach for Diagnosis of Myocardial Infarction in Patients Presenting with Symptoms Suggestive of Acute Coronary Syndrome
Clin. Chem.,
January 1, 2009;
55(1):
93 - 100.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. Jeremias, N. S. Kleiman, D. Nassif, W.-H. Hsieh, M. Pencina, K. Maresh, M. Parikh, D. E. Cutlip, R. Waksman, S. Goldberg, et al.
Prevalence and Prognostic Significance of Preprocedural Cardiac Troponin Elevation Among Patients With Stable Coronary Artery Disease Undergoing Percutaneous Coronary Intervention: Results From the Evaluation of Drug Eluting Stents and Ischemic Events Registry
Circulation,
August 5, 2008;
118(6):
632 - 638.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
F. S. Apple, S. W. Smith, L. A. Pearce, R. Ler, and M. M. Murakami
Use of the Centaur TnI-Ultra Assay for Detection of Myocardial Infarction and Adverse Events in Patients Presenting With Symptoms Suggestive of Acute Coronary Syndrome
Clin. Chem.,
April 1, 2008;
54(4):
723 - 728.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
Authors/Task Force Members, J.-P. Bassand, C. W. Hamm, D. Ardissino, E. Boersma, A. Budaj, F. Fernandez-Aviles, K. A.A. Fox, D. Hasdai, E. M. Ohman, et al.
Guidelines for the diagnosis and treatment of non-ST-segment elevation acute coronary syndromes: The Task Force for the Diagnosis and Treatment of Non-ST-Segment Elevation Acute Coronary Syndromes of the European Society of Cardiology
Eur. Heart J.,
July 1, 2007;
28(13):
1598 - 1660.
[Full Text]
[PDF]
|
|
|
|
|
|
|
NACB WRITING GROUP MEMBERS, D. A. Morrow, C. P. Cannon, R. L. Jesse, L. K. Newby, J. Ravkilde, A. B. Storrow, A. H.B. Wu, and R. H. Christenson
National Academy of Clinical Biochemistry Laboratory Medicine Practice Guidelines: Clinical Characteristics and Utilization of Biochemical Markers in Acute Coronary Syndromes
Circulation,
April 3, 2007;
115(13):
e356 - e375.
[Full Text]
[PDF]
|
|
|
|
|
|
|
NACB WRITING GROUP MEMBERS, D. A. Morrow, C. P. Cannon, R. L. Jesse, L. K. Newby, J. Ravkilde, A. B. Storrow, A. H.B. Wu, R. H. Christenson, NACB COMMITTEE MEMBERS, et al.
National Academy of Clinical Biochemistry Laboratory Medicine Practice Guidelines: Clinical Characteristics and Utilization of Biochemical Markers in Acute Coronary Syndromes
Clin. Chem.,
April 1, 2007;
53(4):
552 - 574.
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. A. Waxman, S. Hecht, J. Schappert, and G. Husk
A Model for Troponin I as a Quantitative Predictor of In-Hospital Mortality
J. Am. Coll. Cardiol.,
November 7, 2006;
48(9):
1755 - 1762.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M Heras, H Bueno, A Bardaji, A Fernandez-Ortiz, H Marti, J Marrugat, and on behalf of the DESCARTES Investigators
Magnitude and consequences of undertreatment of high-risk patients with non-ST segment elevation acute coronary syndromes: insights from the DESCARTES Registry
Heart,
November 1, 2006;
92(11):
1571 - 1576.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. K. James, J. Lindback, J. Tilly, A. Siegbahn, P. Venge, P. Armstrong, R. Califf, M. L. Simoons, L. Wallentin, and B. Lindahl
Troponin-T and N-Terminal Pro-B-Type Natriuretic Peptide Predict Mortality Benefit From Coronary Revascularization in Acute Coronary Syndromes: A GUSTO-IV Substudy
J. Am. Coll. Cardiol.,
September 19, 2006;
48(6):
1146 - 1154.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
W. L. Miller, K. N. Garratt, M. F. Burritt, R. J. Lennon, G. S. Reeder, and A. S. Jaffe
Baseline troponin level: key to understanding the importance of post-PCI troponin elevations
Eur. Heart J.,
May 1, 2006;
27(9):
1061 - 1069.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
T. W. Wallace, S. M. Abdullah, M. H. Drazner, S. R. Das, A. Khera, D. K. McGuire, F. Wians, M. S. Sabatine, D. A. Morrow, and J. A. de Lemos
Prevalence and Determinants of Troponin T Elevation in the General Population
Circulation,
April 25, 2006;
113(16):
1958 - 1965.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
B. Zethelius, N. Johnston, and P. Venge
Troponin I as a Predictor of Coronary Heart Disease and Mortality in 70-Year-Old Men: A Community-Based Cohort Study
Circulation,
February 28, 2006;
113(8):
1071 - 1078.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
F. S. Apple, R. Ler, A. Y. Chung, M. J. Berger, and M. M. Murakami
Point-of-Care i-STAT Cardiac Troponin I for Assessment of Patients with Symptoms Suggestive of Acute Coronary Syndrome,
Clin. Chem.,
February 1, 2006;
52(2):
322 - 325.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Rajappa and A. Sharma
Biomarkers of Cardiac Injury: An Update
Angiology,
November 1, 2005;
56(6):
677 - 691.
[Abstract]
[PDF]
|
|
|
|
|
|
|
M. Thielmann, P. Massoudy, M. Neuhauser, S. Knipp, M. Kamler, J. Piotrowski, K. Mann, and H. Jakob
Prognostic Value of Preoperative Cardiac Troponin I in Patients With Non-ST-Segment Elevation Acute Coronary Syndromes Undergoing Coronary Artery Bypass Surgery
Chest,
November 1, 2005;
128(5):
3526 - 3536.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. De Servi, M. Mariani, G. Mariani, and A. Mazzone
C-Reactive Protein Increase in Unstable Coronary Disease: Cause or Effect?
J. Am. Coll. Cardiol.,
October 18, 2005;
46(8):
1496 - 1502.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. T. Roe, E. D. Peterson, Y. Li, C. V. Pollack Jr, R. H. Christenson, W. F. Peacock, F. M. Fesmire, L. K. Newby, R. L. Jesse, J. W. Hoekstra, et al.
Relationship Between Risk Stratification by Cardiac Troponin Level and Adherence to Guidelines for Non-ST-Segment Elevation Acute Coronary Syndromes
Arch Intern Med,
September 12, 2005;
165(16):
1870 - 1876.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
T Nageh, R A Sherwood, B M Harris, and M R Thomas
Prognostic role of cardiac troponin I after percutaneous coronary intervention in stable coronary disease
Heart,
September 1, 2005;
91(9):
1181 - 1185.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
C-K Wong and H D White
Implications of the new definition of myocardial infarction
Postgrad. Med. J.,
September 1, 2005;
81(959):
552 - 555.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
B. Lindahl, J. Lindback, T. Jernberg, N. Johnston, M. Stridsberg, P. Venge, and L. Wallentin
Serial analyses of N-terminal pro-B-type natriuretic peptide in patients with non-ST-segment elevation acute coronary syndromes: A Fragmin and fast Revascularisation during InStability in coronary artery disease (FRISC)-II substudy
J. Am. Coll. Cardiol.,
February 15, 2005;
45(4):
533 - 541.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
G. Landesberg, M. Mosseri, V. Shatz, I. Akopnik, M. Bocher, M. Mayer, H. Anner, Y. Berlatzky, and C. Weissman
Cardiac troponin after major vascular surgery: The role of perioperative ischemia, preoperative thallium scanning, and coronary revascularization
J. Am. Coll. Cardiol.,
August 4, 2004;
44(3):
569 - 575.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
G. E. Ross, F. N. Bever, Z. Uddin, L. Devireddy, and J. M. Gardin
Common Scenarios to Clarify the Interpretation of Cardiac Markers
J Am Osteopath Assoc,
April 1, 2004;
104(4):
165 - 176.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
K. Okamatsu, M. Takano, S. Sakai, F. Ishibashi, R. Uemura, T. Takano, and K. Mizuno
Elevated Troponin T Levels and Lesion Characteristics in Non-ST-Elevation Acute Coronary Syndromes
Circulation,
February 3, 2004;
109(4):
465 - 470.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Panteghini, F. Pagani, K.-T. J. Yeo, F. S. Apple, R. H. Christenson, F. Dati, J. Mair, J. Ravkilde, and A. H.B. Wu
Evaluation of Imprecision for Cardiac Troponin Assays at Low-Range Concentrations
Clin. Chem.,
February 1, 2004;
50(2):
327 - 332.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. C. Lin, F. S. Apple, M. M. Murakami, and R. V. Luepker
Rates of Positive Cardiac Troponin I and Creatine Kinase MB Mass among Patients Hospitalized for Suspected Acute Coronary Syndromes
Clin. Chem.,
February 1, 2004;
50(2):
333 - 338.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
T. Jernberg, B. Lindahl, A. Siegbahn, B. Andren, G. Frostfeldt, B. Lagerqvist, M. Stridsberg, P. Venge, and L. Wallentin
N-terminal pro-brain natriuretic peptide in relation to inflammation, myocardial necrosis, and the effect of an invasive strategy in unstable coronary artery disease
J. Am. Coll. Cardiol.,
December 3, 2003;
42(11):
1909 - 1916.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. Prasad, V. Mathew, D. R Holmes Jr., and B. J Gersh
Current management of non-ST-segment-elevation acute coronary syndrome: reconciling the results of randomized controlled trials
Eur. Heart J.,
September 1, 2003;
24(17):
1544 - 1553.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. A. Barrabes, J. Figueras, C. Moure, J. Cortadellas, and J. Soler-Soler
Prognostic Value of Lead aVR in Patients With a First Non-ST-Segment Elevation Acute Myocardial Infarction
Circulation,
August 19, 2003;
108(7):
814 - 819.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
E. Giannitsis and H. A. Katus
99th Percentile and Analytical Imprecision of Troponin and Creatine Kinase-MB Mass Assays: An Objective Platform for Comparison of Assay Performance
Clin. Chem.,
August 1, 2003;
49(8):
1248 - 1249.
[Full Text]
[PDF]
|
|
|
|
|
|
|
F. S. Apple, H. E. Quist, P. J. Doyle, A. P. Otto, and M. M. Murakami
Plasma 99th Percentile Reference Limits for Cardiac Troponin and Creatine Kinase MB Mass for Use with European Society of Cardiology/American College of Cardiology Consensus Recommendations
Clin. Chem.,
August 1, 2003;
49(8):
1331 - 1336.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. A. Morrow, N. Rifai, M. S. Sabatine, S. Ayanian, S. A. Murphy, J. A. de Lemos, E. Braunwald, and C. P. Cannon
Evaluation of the AccuTnI Cardiac Troponin I Assay for Risk Assessment in Acute Coronary Syndromes
Clin. Chem.,
August 1, 2003;
49(8):
1396 - 1398.
[Full Text]
[PDF]
|
|
|
|
|
|
|
P. Venge, N. Johnston, B. Lagerqvist, L. Wallentin, and B. Lindahl
Clinical and Analytical Performance of the Liaison Cardiac Troponin I Assay in Unstable Coronary Artery Disease, and the Impact of Age on the Definition of Reference Limits. A FRISC-II Substudy
Clin. Chem.,
June 1, 2003;
49(6):
880 - 886.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. K. James, P. Armstrong, E. Barnathan, R. Califf, B. Lindahl, A. Siegbahn, M. L. Simoons, E. J. Topol, P. Venge, L. Wallentin, et al.
Troponin and C-reactive protein have different relations to subsequent mortality and myocardial infarction after acute coronary syndrome: A GUSTO-IV substudy
J. Am. Coll. Cardiol.,
March 19, 2003;
41(6):
916 - 924.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
W. E. Boden
"Routine invasive" versus "selective invasive" approaches to non-ST-segment elevation acute coronary syndromes management in the post-stent/platelet inhibition era
J. Am. Coll. Cardiol.,
February 19, 2003;
41(4_Suppl_S):
113S - 122S.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
E. J. Topol
A guide to therapeutic decision-making in patients with non-ST-segment elevation acute coronary syndromes
J. Am. Coll. Cardiol.,
February 19, 2003;
41(4_Suppl_S):
123S - 129S.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
P. Kaul, L. K. Newby, Y. Fu, V. Hasselblad, K. W. Mahaffey, R. H. Christenson, R. A. Harrington, E. M. Ohman, E. J. Topol, R. M. Califf, et al.
Troponin T and quantitative ST-segment depression offer complementary prognostic information in the risk stratification of acute coronary syndrome patients
J. Am. Coll. Cardiol.,
February 5, 2003;
41(3):
371 - 380.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
G. C. Wong, R. P. Giugliano, and E. M. Antman
Use of Low-Molecular-Weight Heparins in the Management of Acute Coronary Artery Syndromes and Percutaneous Coronary Intervention
JAMA,
January 15, 2003;
289(3):
331 - 342.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. E. Bertrand, M. L. Simoons, K. A.A. Fox, L. C. Wallentin, C. W. Hamm, E. McFadden, P. J. De Feyter, G. Specchia, and W. Ruzyllo
Management of acute coronary syndromes in patients presenting without persistent ST-segment elevation
Eur. Heart J.,
December 1, 2002;
23(23):
1809 - 1840.
[Full Text]
[PDF]
|
|
|
|
|
|
|
P J Sheridan and D C Crossman
Critical review of unstable angina and non-ST elevation myocardial infarction
Postgrad. Med. J.,
December 1, 2002;
78(926):
717 - 726.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
F. S. Apple, M. M. Murakami, R. L. Jesse, M. A. Levitt, A. K. Berger, L. A. Pearce, and P. Collinson
Near-Bedside Whole-Blood Cardiac Troponin I Assay for Risk Assessment of Patients with Acute Coronary Syndromes
Clin. Chem.,
October 1, 2002;
48(10):
1784 - 1787.
[Full Text]
[PDF]
|
|
|
|
|
|
|
G. C. Wong, D. A. Morrow, S. Murphy, N. Kraimer, R. Pai, D. James, D. H. Robertson, L. A. Demopoulos, P. DiBattiste, C. P. Cannon, et al.
Elevations in Troponin T and I Are Associated With Abnormal Tissue Level Perfusion: A TACTICS-TIMI 18 Substudy
Circulation,
July 9, 2002;
106(2):
202 - 207.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
R. A. Kerensky, M. Wade, P. Deedwania, W. E. Boden, C. J. Pepine, and Veterans Affairs Non-Q-Wave Infarction Strategies
Revisiting the culprit lesion in non-Q-wave myocardial infarction: Results from the VANQWISH trial angiographic core laboratory
J. Am. Coll. Cardiol.,
May 1, 2002;
39(9):
1456 - 1463.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. A. Goldstein
Angiographic plaque complexity: the tip of the unstable plaque iceberg
J. Am. Coll. Cardiol.,
May 1, 2002;
39(9):
1464 - 1467.
[Full Text]
[PDF]
|
|
|
|
|
|
|
F. Q. Almeda and J. E. Calvin
Troponin T in acute coronary syndromes: mechanisms and management issues
J. Am. Coll. Cardiol.,
April 17, 2002;
39(8):
1404 - 1405.
[Full Text]
[PDF]
|
|
|
|
|
|
|
B. Lindahl
Mechanisms behind the prognostic value of troponin T in unstable coronary artery disease: A FRISC II substudy: reply
J. Am. Coll. Cardiol.,
April 17, 2002;
39(8):
1405 - 1405.
[Full Text]
[PDF]
|
|
|
|
Top
Abstract
Methods