Original Article
Benefit of Abciximab in Patients with Refractory Unstable Angina in Relation to Serum Troponin T Levels
N Engl J Med 1999; 340:1623-1629May 27, 1999
- Abstract
Background
In patients with refractory unstable angina, the platelet glycoprotein IIb/IIIa–receptor antibody abciximab reduces the incidence of cardiac events before and during coronary angioplasty. We investigated whether serum troponin T levels identify patients most likely to benefit from therapy with this drug.
Methods
Among 1265 patients with unstable angina who were enrolled in the c7E3 Fab Antiplatelet Therapy in Unstable Refractory Angina (CAPTURE) trial, serum samples drawn at the time of randomization to abciximab or placebo were available from 890 patients; we used these samples for the determination of troponin T and creatine kinase MB levels. Patients with postinfarction angina were not included.
Results
Serum troponin T levels at the time of study entry were elevated (above 0.1 ng per milliliter) in 275 patients (30.9 percent). Among patients receiving placebo, the risk of death or nonfatal myocardial infarction was related to troponin T levels. The six-month cumulative event rate was 23.9 percent among patients with elevated troponin T levels, as compared with 7.5 percent among patients without elevated troponin T levels (P<0.001). Among patients treated with abciximab, the respective six-month event rates were 9.5 percent for patients with elevated troponin T levels and 9.4 percent for those without elevated levels. As compared with placebo, the relative risk of death or nonfatal myocardial infarction associated with treatment with abciximab in patients with elevated troponin T levels was 0.32 (95 percent confidence interval, 0.14 to 0.62; P=0.002). The lower event rates in patients receiving abciximab were attributable to a reduction in the rate of myocardial infarction (odds ratio, 0.23; 95 percent confidence interval, 0.12 to 0.49; P<0.001). In patients without elevated troponin T levels, there was no benefit of treatment with respect to the relative risk of death or myocardial infarction at six months (odds ratio, 1.26; 95 percent confidence interval, 0.74 to 2.31; P=0.47).
Conclusions
The serum troponin T level, which is considered to be a surrogate marker for thrombus formation, identifies a high-risk subgroup of patients with refractory unstable angina suitable for coronary angioplasty who will particularly benefit from antiplatelet treatment with abciximab.
Media in This Article
Figure 1
Odds Ratios for Cardiac Events Associated with Treatment with Abciximab at the Six-Month Follow-up, According to Quartile of Serum Troponin T.Figure 3
Odds Ratios for Cardiac Events Associated with Treatment with Abciximab at the Six-Month Follow-up, in Subgroups of Patients Defined According to Serum Troponin T (TnT) Level, Serum Creatine Kinase MB Fraction (CK-MB), ST-Segment Depression, and T-Wave Inversion.Article Activity
- Article
Unstable angina is a critical phase of coronary heart disease that is defined by clinical symptoms and is associated with a high risk of myocardial infarction and death.1 The underlying pathophysiologic mechanism involves rupture or erosion of atherosclerotic plaques, followed by local thrombus formation.2-4 If thrombotic material is transported downstream, focal cell necrosis will result.3 Such minor myocardial injury is detected in 20 to 40 percent of patients with unstable angina by the measurement of serum troponin T or troponin I, but rarely by measurement of serum creatine kinase.5-12 Patients with such minor myocardial injury are at increased risk for adverse outcomes — in particular, subsequent myocardial infarction or sudden death.6-15
The recent c7E3 Fab Antiplatelet Therapy in Unstable Refractory Angina (CAPTURE) trial demonstrated that treatment with the glycoprotein IIb/IIIa–receptor blocker abciximab reduced the risk of myocardial infarction in patients with refractory unstable angina, both during the 18-to-24-hour period preceding the coronary intervention and during subsequent balloon angioplasty.16 Since treatment with abciximab is directed against the formation of platelet aggregates, we postulated that such treatment might be particularly effective in patients with elevated troponin T levels due to thrombotic microembolization. Accordingly, we assessed the value of troponin T measurements taken at base line among patients in the CAPTURE study in predicting the therapeutic efficacy of abciximab.
Methods
Patients
The study population of the CAPTURE trial was composed of 1265 patients (345 women and 920 men; mean [±SD] age, 61±10 years) who were recruited from 69 centers in 12 countries between May 1993 and December 1995. All the patients had had recurrent chest pain at rest, with concomitant electrocardiographic changes (ST-segment depression, ST-segment elevation, or abnormal T waves), and had had one or more episodes of chest pain or electrocardiographic abnormalities, or both, within two hours after the initiation of therapy with intravenous heparin and nitroglycerin. The most recent episode of ischemia had to have occurred within 48 hours before randomization (mean, 8.7±6.0). Exclusion criteria were the occurrence of a recent myocardial infarction, unless serum creatine kinase (CK) enzyme activity had returned to less than two times the upper limit of normal; the need for immediate intervention; and the presence of risk factors for bleeding. All patients had evidence on coronary angiography of substantial coronary artery disease (defined by the presence of one culprit lesion suitable for angioplasty). Study medication was started within 24 hours after angiography, and percutaneous transluminal coronary angioplasty (PTCA) was scheduled to be performed 18 to 24 hours after the start of study medication. Additional electrocardiograms were recorded at enrollment; 6, 12, and 18 hours after enrollment; just before PTCA; 1, 6, and 24 hours after PTCA; at discharge; and whenever patients had recurrent chest pain. Further details have been published elsewhere.16
Patients were randomly assigned to receive a bolus injection of 0.25 mg of abciximab (ReoPro, Centocor, Leiden, the Netherlands, and Eli Lilly, Indianapolis) per kilogram of body weight, followed by a continuous infusion at a rate of 10 μg per minute, or to receive a matching placebo. Treatment was started within two hours after randomization and continued until one hour after the completion of PTCA.
During hospitalization and the six-month follow-up period, all events were recorded, including death, nonfatal myocardial infarction, repeated PTCA, and coronary bypass surgery. Myocardial infarction was diagnosed during the index hospital stay, which included the angioplasty procedure, when the level of CK activity was more than three times the upper limit of normal in at least two samples or when new, clinically significant Q waves were detected in two or more continuous electrocardiographic leads. Myocardial infarction after discharge was diagnosed on the basis of CK values exceeding two times the upper limit of normal or the detection of new, significant Q waves in two or more continuous leads. With respect to rates of cardiac events, four time points were considered: the period before PTCA (up to 36 hours after randomization), 72 hours after randomization (including up to 36 hours after PTCA), 30 days after randomization, and 6 months after randomization.
Analytic Techniques
All serum samples were stored at –20°C or lower and transported to a central laboratory, where they were stored at –80°C until they were analyzed. Quantitative determination of the cardiac markers (troponin T and creatine kinase MB fraction [CK-MB]) was performed at the research laboratory of the University of Hamburg by technicians who were unaware of the patients' histories and the assigned treatments.
Serum cardiac troponin T was measured with a one-step enzyme immunoassay that uses magnetic particles carrying the monoclonal antibody and chemiluminescence (Elecsys 2010, Boehringer Mannheim, Mannheim, Germany). The lower limit of detection in this assay was 0.01 ng per milliliter, and the threshold value for the diagnosis (the diagnostic cutoff point) was 0.10 ng per milliliter.17 The interassay coefficient of variation was 6.7 percent at a level of 0.12 ng per milliliter and 4.1 percent at 0.56 ng per milliliter with internal controls.
Serum CK-MB levels were determined in parallel with monoclonal antibodies by the same analyzer. The lower limit of detection in this assay was 0.15 ng per milliliter, and the upper reference (cutoff) level was 5.0 ng per milliliter. The interassay coefficient of variation was 8.4 percent at a level of 8.2 ng per milliliter and 7.2 percent at 14.7 ng per milliliter with internal controls.
Statistical Analysis
To distinguish among patients who derived different degrees of benefit from treatment with abciximab, an exploratory data analysis was chosen.18 Patients with measurable troponin T levels (>0.01 ng per milliliter) were grouped into quartiles of approximately 130 patients each. For each of the four time points, a logistic-regression analysis was performed. The treatment was included in the model equation as a binary variable and was coded as 0 (placebo) or 1 (abciximab). For troponin T values, we used four dichotomous indicator variables to represent the ranges within each quartile (0.02 to 0.04 ng per milliliter, 0.05 to 0.12 ng per milliliter, 0.13 to 0.32 ng per milliliter, and >0.32 ng per milliliter). Patients with troponin T values at or below 0.01 ng per milliliter served as the reference group.
To assess a possible interaction between troponin T levels and the therapeutic benefit of abciximab, terms denoting the interaction between troponin T and treatment were incorporated into the model. The model was fitted with and without the interaction terms. If the introduction of the interaction terms improved the fit of the model, the likelihood-ratio test with four degrees of freedom should have indicated statistical significance. The demonstration of an interaction implied differing degrees of benefit with abciximab at various troponin T levels.
In addition, the troponin T levels (>0.1 vs. ≤0.1 ng per milliliter), CK-MB levels (>5.0 vs. ≤5.0 ng per milliliter), and electrocardiographic findings (presence vs. absence) were coded as dichotomous variables. Reverse stepwise logistic-regression analysis was used to identify variables with independent predictive value for the therapeutic benefit of abciximab.
Continuous variables were expressed as means ±SD, and comparisons between two subgroups were performed with the Mann–Whitney U test (two-sided). P values below 0.05 were considered to indicate statistical significance. Comparisons of categorical variables were performed with Fisher's exact test (two-sided). All calculations were performed with SPSS version 7.5 (SPSS, Chicago) or StatXact 3 (Cytel Software, Cambridge, Mass.) software.
Results
Among 1265 patients enrolled in the CAPTURE trial, 198 patients were excluded from the analysis because they had myocardial infarctions within 14 days before enrollment. Serum troponin T levels may be elevated for up to 14 days after myocardial infarction, and high values therefore do not necessarily reflect minor myocardial damage in these patients.5 The results of the analyses of the serum samples obtained at the time of randomization were available for 890 of the remaining 1067 patients (83 percent).
The base-line characteristics of these 890 patients were similar to those of the total study population with respect to age, sex, cardiovascular-risk profile, and concomitant treatment before and after randomization. During the six months of follow-up, 19 deaths were recorded and 79 patients had nonfatal myocardial infarctions. The degree of reduction in the incidence of cardiac events among the 890 patients in the current analysis was similar to that in the entire CAPTURE study population before PTCA (event rate, 2.4 percent among those receiving placebo vs. 0.9 percent among those receiving abciximab; P=0.12), 72 hours after randomization (8.3 percent vs. 4.3 percent, P=0.02), and 30 days after randomization (9.4 percent vs. 5.4 percent, P=0.012). The absolute difference in event rates in the two treatment groups was fairly consistent during the six-month follow-up; at six months this difference was 4.3 percentage points, although it was no longer significant (12.9 percent vs. 8.6 percent, P=0.14).
Interaction between Serum Troponin T Level and the Therapeutic Benefit of Abciximab
To characterize a possible relation between base-line serum troponin T levels and the benefit of treatment with abciximab, the patients were categorized according to troponin T level (Table 1Table 1
Cumulative Rates of Cardiac Events According to Troponin T Quartile and Time Point.). Troponin T was not detectable in 372 patients (41.8 percent) — 182 receiving placebo and 190 receiving abciximab. In these patients, the event rates did not differ significantly between the placebo and abciximab groups during the 36 hours before PTCA (0 vs. 0.5 percent, P=1.00). Although there was a trend toward reduced events during the period up to 72 hours after randomization for the patients receiving abciximab (4.9 percent vs. 2.1 percent, P=0.17), this difference was not as apparent at 30 days (4.9 percent vs. 2.6 percent, P=0.28) or after 6 months of follow-up (6.6 percent vs. 6.3 percent, P=1.00).Troponin T was detectable in base-line serum samples of 518 patients (58.2 percent). Patients were stratified into quartiles according to the level of troponin T measured: 0.02 to 0.04 ng per milliliter (138 patients), 0.05 to 0.12 ng per milliliter (129 patients), 0.13 to 0.32 ng per milliliter (123 patients), and >0.32 ng per milliliter (128 patients). Table 1 shows that in patients with troponin T levels of 0.12 ng per milliliter or less, event rates were low and did not differ significantly between those receiving abciximab and those receiving placebo at all four time points. In contrast, for patients with troponin T levels above 0.12 ng per milliliter, the risk of a cardiac event was higher in the placebo group than at lower levels, whereas event rates remained essentially unchanged when patients were treated with abciximab. This interaction between the therapeutic benefit of abciximab and the troponin T level was statistically significant at 72 hours, 30 days, and 6 months of follow-up. The therapeutic benefit of abciximab in the CAPTURE trial was evident in the two upper quartiles of patients, with troponin T values higher than 0.12 ng per milliliter (Figure 1Figure 1
Odds Ratios for Cardiac Events Associated with Treatment with Abciximab at the Six-Month Follow-up, According to Quartile of Serum Troponin T.).Stratification According to Serum Troponin T Level
Since the therapeutic cutoff level we identified for serum troponin T is close to the diagnostic cutoff level of 0.1 ng per milliliter, which is widely used in clinical practice, we analyzed the data according to this cutoff level. The base-line characteristics of the 275 patients (30.9 percent) above the cutoff level (those considered to be troponin T–positive) and the 615 patients below this level (those considered to be troponin T–negative) are presented in Table 2Table 2
Base-Line Characteristics of the Patients According to Serum Troponin T Level.. There were no significant differences between these groups.Cardiac events (death or nonfatal myocardial infarction) are shown according to troponin T level and the randomly assigned treatment group in Figure 2AFigure 2
Rates of Cardiac Events in the Initial 72 Hours after Randomization (Panel A) and during the 6 Months of Follow-up (Panel B) among Patients with Serum Troponin T Levels above and Those with Levels below the Diagnostic Cutoff Point. and Figure 2B. Among the troponin T–negative patients who were receiving placebo, events during the 36 hours before PTCA were infrequent (0.7 percent), whereas events occurred in association with the procedure (within 72 hours after randomization) in 3.5 percent of patients. Only a few additional events were recorded in the subsequent six months of follow-up, resulting in a total event rate of 7.5 percent (odds ratio, 1.26; 95 percent confidence interval, 0.74 to 2.31; P=0.47). There were no significant differences in event rates between the placebo and abciximab groups at any of the four time points (Table 3Table 3
Cumulative Rates of Cardiac Events According to Time Point.).In contrast, the event rates for troponin T–positive patients who were receiving placebo were high — both before PTCA (6.6 percent) and in association with PTCA (10.8 percent), as well as during the subsequent period after discharge, resulting in a total event rate of 23.9 percent at six months (P<0.001 for comparison with troponin T–negative patients). The rates of events occurring before and in association with PTCA were reduced by treatment with abciximab — to 0.7 percent before PTCA (odds ratio, 0.45; 95 percent confidence interval, 0.21 to 0.95; P=0.02) and to 2.9 percent in the 72 hours after randomization (cumulative event rate, 3.6 percent; odds ratio, 0.29; 95 percent confidence interval, 0.11 to 0.54; P=0.007). This initial benefit — an absolute risk reduction of 13.8 percentage points at 30 days — was preserved during the six months of follow-up (cumulative event rates, 9.5 percent for the abciximab group vs. 23.9 percent for the placebo group; odds ratio, 0.32; 95 percent confidence interval, 0.14 to 0.62; P=0.002).
The risk of cardiac events among the troponin T–positive patients treated with abciximab was similar to that observed among the troponin T–negative patients (Table 3). The lower event rates were attributable to a reduction in the rate of myocardial infarction (odds ratio, 0.23; 95 percent confidence interval, 0.12 to 0.49; P<0.001). Total mortality in the CAPTURE trial was low, 0.8 percent at 30 days and 2.1 percent at 6 months. Among the troponin T–positive patients, mortality in the placebo group was 3.6 percent and did not differ significantly from that in the abciximab group (2.9 percent, P=0.74).
Serum CK-MB Level
At the time of study entry, the CK-MB value was above the cutoff level of 5.0 ng per milliliter in 116 patients (13.0 percent; 63 receiving placebo and 53 receiving abciximab). The mean value was 8.7±6.2 ng per milliliter (range, 5.0 to 36.5).
The presence of an elevated CK-MB level was a significant predictor of an increased risk of cardiac events at all time points. However, a regression analysis that included a term for interaction indicated no significant relation between the CK-MB level and the benefit of treatment with abciximab. This lack of relation was consistent regardless of CK-MB level or time point. At the six-month follow-up, there was no significant benefit of abciximab treatment, either among the patients with CK-MB levels above 5.0 ng per milliliter (odds ratio, 0.63; 95 percent confidence interval, 0.28 to 1.24; P=0.11) or among those with normal CK-MB values (odds ratio, 0.75; 95 percent confidence interval, 0.48 to 1.14; P=0.16).
Comparison of Predictive Values
At six months, only troponin T levels above the diagnostic cutoff level were significant predictive factors (Figure 3Figure 3
Odds Ratios for Cardiac Events Associated with Treatment with Abciximab at the Six-Month Follow-up, in Subgroups of Patients Defined According to Serum Troponin T (TnT) Level, Serum Creatine Kinase MB Fraction (CK-MB), ST-Segment Depression, and T-Wave Inversion.). In a stepwise logistic-regression model, the inclusion of the CK-MB level and electrocardiographic findings indicating unstable angina (ST-segment depression and T-wave inversion) did not have independent predictive value when troponin T was forced into the model first.Discussion
Previous studies of patients with unstable angina or evolving myocardial infarction without ST-segment elevation have shown that serum troponin T and troponin I levels are potent, independent predictors of the short-term and long-term risk of myocardial infarction and death.6-15 Our findings indicate that patients with refractory unstable angina and elevated troponin T levels may be treated effectively with glycoprotein IIb/IIIa–receptor blockers.
The CAPTURE trial enrolled patients with refractory unstable angina who were scheduled to undergo PTCA for a single culprit lesion. Treatment with the glycoprotein IIb/IIIa–receptor blocker abciximab effectively reduced the risk of myocardial infarction both before and during PTCA. This post hoc analysis of the serum samples collected on study entry revealed that 30.9 percent of the patients had elevated levels of circulating troponin T (>0.1 ng per milliliter), in concordance with other studies.6-15 As in previous studies, the level of troponin T correlated with the event rates.9,11 The six-month event rate in the placebo group was 23.9 percent when troponin T was elevated, as compared with 7.5 percent when levels were normal (P<0.001). Abciximab reduced this risk to approximately that of patients with troponin T levels below the diagnostic cutoff value. The risk reduction brought about by abciximab was mainly apparent as a reduction in the rate of myocardial infarction before as well as during PTCA and was maintained over a period of six months (odds ratio, 0.32; P=0.002). The CK-MB level was not predictive of the therapeutic benefit of abciximab.
These findings may serve as the basis for a new therapeutic approach to the treatment of high-risk patients with unstable angina pectoris. High serum levels of troponin T or troponin I in such patients reflect an active thrombotic process, with distal embolization of platelet thrombi originating from the culprit lesion.2,3 Antithrombotic therapy with high doses of glycoprotein IIb/IIIa–receptor blockers will reduce the incidence of thrombus formation at the culprit lesion and may facilitate the resolution of distal microthrombi. Thus, glycoprotein IIb/IIIa–receptor blockers provide protection from further myocardial damage. Our data indicate that this mechanism applies to both thrombotic complications arising from spontaneous plaque disruption (as shown by the reduction of events before PTCA) and thrombotic complications associated with the rupture of plaque induced by PTCA.
The event rate before PTCA and that associated with PTCA were low among the patients with refractory unstable angina who did not have elevated troponin T levels and who were receiving placebo. In contrast, those with troponin T levels above 0.1 ng per milliliter had high rates of events before PTCA as well as after the procedure; these rates were effectively reduced by treatment with abciximab. Treatment of 100 patients with elevated troponin T levels with abciximab, rather than standard treatment, would prevent 15 cardiac events. Similarly, in the Fragmin during Instability in Coronary Artery Disease trial, the benefit of prolonged treatment with low-molecular-weight heparin was apparent only in patients with elevated troponin T levels, and only over a period of 42 days.19 However, the rates of cardiac events and coronary interventions in that trial were lower than in the CAPTURE trial.
There are a few limitations to using troponin T measurements in therapeutic decision making. The timing of sampling is crucial for accurate interpretation of troponin T findings. Measuring troponin T a mean of 8.7 hours after the qualifying episode of chest pain, as was done in this study, appears adequate, whereas a single measurement obtained on arrival at the hospital was shown to be inappropriate for determining risk.10 The absence of detectable troponin T does not rule out the presence of coronary heart disease, but it does identify a patient at lower risk for cardiac events. Positive tests for troponin T can also indicate other serious conditions, such as acute pulmonary embolism or myocarditis,10 but false positive tests are rare.20
In conclusion, troponin T may serve as a surrogate marker of active thrombus formation. An elevated troponin T value (>0.1 ng per milliliter) identifies some patients with unstable angina who are at high risk for cardiac events both before and after PTCA and who will benefit the most from treatment with abciximab. Accordingly, this study demonstrates how a new diagnostic test (for detecting troponin T) and a therapeutic advance (abciximab) can be combined for the benefit of patients with acute coronary syndromes.
Presented in part at the 47th Annual Scientific Session of the American College of Cardiology, Atlanta, March 29–April 1, 1998.
We are indebted to Sabine Wohlrath and Ariane Deu for their expert technical assistance.
Source Information
From the Department of Cardiology (C.W.H., C.H., B.G.) and the Institute of Mathematics and Computer Science in Medicine (J.B.), University Hospital Eppendorf, Hamburg, Germany; the Service de Cardiologie, Hôpital Tenon, Paris (A.V.); the Cardiac Department of the Royal Victoria Hospital, Belfast, Northern Ireland (J.A.); Unidad de Hemodinamica, Hospital Universitario San Carlos, Madrid (C.M.M.); the Department of Cardiology, Charité University Hospital, Berlin, Germany (W.R.); and Cardialysis and Erasmus University, Rotterdam, the Netherlands (J.K., M.L.S.).
Address reprint requests to Dr. Hamm at Kerckhoff Heart Center, Benekestrasse 2-8, D-61231 Bad Nauheim, Germany, or at christian. hamm@kerckhoff.med.uni-giessen.de.
Other participants in the trial are listed in the Appendix.
Appendix
In addition to the authors, the following persons participated in the CAPTURE trial: the Netherlands — M. de Boer, H. Suryapranata, A. Liem, and G. Velsink, Zwolle; G. Laarman, R. van der Wieken, J. Ezechiels, and S. Zonneveld, Amsterdam; M. van den Brand, C. van der Zwaan, and P. Kint, Rotterdam; R. Michels, J. Bonnier, I. van de Kerkhof, and C. Hanekamp, Eindhoven; J. Peels, L. Drok, and P. den Heijer, Groningen; T. Plokker, E. Mast, and K. Marquez, Nieuwegein; A. Van den Bos and U. Chin, Breda; V. Umans, J. Cornel, and A. Arnold, Alkmaar; France — E. Gabarz, O. Nallet, and B. Farrah, Paris; D. Carrie, J. Puel, and M. Jean, Toulouse; B. Charbonnier, G. Pacouret, and R. Raynaud, Tours; B. Bertrand and G. Vanzetto, Grenoble; G. Grollier and B. Valette, Caen; C. Thery and J. Lablanche, Lille; F. Duclos and P. Coste, Pessac; P. Beaufils and E. Eiferman, Paris; C. Daubert and C. Leclercq, Rennes; J. Juliard and P. Steg, Paris; J. Bassand and N. Meneveau, Besançon; J. Guermonprez, Paris; Belgium — M. Vrolix, J. Van Lierde, and S. Jacobs, Genk; J. Boland, G. Saat, and P. Baumans, Liege; G. Heyndricks, F. Staelens, and B. De Bruyne, Aalst; Y. Taeymans and P. Gheeraert, Ghent; J. Col and K. al-Schwafi, Brussels; P. van den Heuvel and R. Rogiers, Antwerp; M. Castadot and E. de Wit, Brussels; Germany — D. Gulba, R. Dechend, and S. Christow, Berlin-Buch; R. Simon and N. Al Mokthari, Kiel; J. vom Dahl and U. Janssens, Aachen; M. Haude and D. Baumgart, Essen; K. Karsch and R. Maier, Tübingen; C. Brunckhorst, Berlin; N. Reifart and M. Krajcar, Frankfurt; H. Rupprecht and M. Cobaugh, Mainz; Spain — R. Hernandez-Antolin, J. Segovia, and P. Garcia, Madrid; A. Cequir, E. Esplugas, J. Gomez-Hospital, and J. Mauri, Bellvitge; J. Angel and R. Ballester, Barcelona; C. Morris de la Tassa and F. Barriales, Oviedo; J. Auge and J. Garcia, Barcelona; R. Melgares, Granada; United Kingdom — M. Khan, P. Johnston, and Y. McKay, Belfast; M. Been and A. Kahn, Coventry; C. Ilsley and A. Ewan, Harefield; D. Reid and A. McDermott, Newcastle; D. Ward, London; N. Buller, London; R. Balcon, London; Italy — C. Vassanello, P. Zardini, and I. Loschiavo, Verona; A. Casari, A. Piti, and A. Costalunga, Bergamo; S. Repetto and S. Carella, Varese; M. Marzilli and S. Fedele, Pisa; R. Chioiin and B. Reimers, Padua; A. Mazzari, Gemelli; G. Specchia, Pavia; M. Chiariello, Naples; Israel — H. Miller and D. Shepps, Tel Aviv; S. Sclarovski and B. Gal, Tel Aviv; A. Caspi and O. Ayzenberg, Rehovot; T. Sharir and H. Hod, Tel Aviv; Switzerland — P. Buser, M. Pfisterer, and R. Ritz, Basel; O. Bertel and F. Rohner, Zurich; Canada — J. Ducas and U. Shick, Winnipeg, Man.; P. Cheung, Winnipeg, Man; R. Chisholm, Toronto; A. Adelman, Toronto; E. Cohen, Toronto; Portugal — R. Seabra Gomez and J. Ferreira, Lisbon; Austria — V. Mühlberger, Innsbruck.
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Citing Articles
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Glenn N. Levine, Eric R. Bates, James C. Blankenship, Steven R. Bailey, John A. Bittl, Bojan Cercek, Charles E. Chambers, Stephen G. Ellis, Robert A. Guyton, Steven M. Hollenberg, Umesh N. Khot, Richard A. Lange, Laura Mauri, Roxana Mehran, Issam D. Moussa, Debabrata Mukherjee, Brahmajee K. Nallamothu, Henry H. Ting, Alice K. Jacobs, Jeffrey L. Anderson, Nancy Albert, Mark A. Creager, Steven M. Ettinger, Robert A. Guyton, Jonathan L. Halperin, Judith S. Hochman, Frederick G. Kushner, E. Magnus Ohman, William Stevenson, Clyde W. Yancy. (2012) 2011 ACCF/AHA/SCAI guideline for percutaneous coronary intervention: Executive Summary. Catheterization and Cardiovascular Interventions 79:3, 453-495
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R. Twerenbold, A. Jaffe, T. Reichlin, M. Reiter, C. Mueller. (2012) High-sensitive troponin T measurements: what do we gain and what are the challenges?. European Heart Journal
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Glenn N. Levine, Eric R. Bates, James C. Blankenship, Steven R. Bailey, John A. Bittl, Bojan Cercek, Charles E. Chambers, Stephen G. Ellis, Robert A. Guyton, Steven M. Hollenberg, Umesh N. Khot, Richard A. Lange, Laura Mauri, Roxana Mehran, Issam D. Moussa, Debabrata Mukherjee, Brahmajee K. Nallamothu, Henry H. Ting. (2011) 2011 ACCF/AHA/SCAI Guideline for Percutaneous Coronary Intervention: Executive Summary. Journal of the American College of Cardiology
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Glenn N. Levine, Eric R. Bates, James C. Blankenship, Steven R. Bailey, John A. Bittl, Bojan Cercek, Charles E. Chambers, Stephen G. Ellis, Robert A. Guyton, Steven M. Hollenberg, Umesh N. Khot, Richard A. Lange, Laura Mauri, Roxana Mehran, Issam D. Moussa, Debabrata Mukherjee, Brahmajee K. Nallamothu, Henry H. Ting. (2011) 2011 ACCF/AHA/SCAI Guideline for Percutaneous Coronary Intervention. Journal of the American College of Cardiology
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Inder M. Singh, David R. Holmes. (2011) Myocardial Revascularization by Percutaneous Coronary Intervention: Past, Present, and the Future. Current Problems in Cardiology 36:10, 375-401
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Dina Melki, Suzanne Lind, Stefan Agewall, Tomas Jernberg. (2011) Diagnostic value of high sensitive troponin T in chest pain patients with no persistent ST-elevations. Scandinavian Cardiovascular Journal 45:4, 198-204
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Beau M Hawkins, Jorge F Saucedo, Sunil V Rao. (2011) The rationale and evidence for triple antiplatelet therapy in acute coronary syndromes. Clinical Investigation 1:8, 1155-1165
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Michael Weber, Oscar Bazzino, Jose Luis Navarro Estrada, Raul de Miguel, Simon Salzberg, Juan J. Fuselli, Christoph Liebetrau, Mariella Woelken, Helge Moellmann, Holger Nef, Christian Hamm. (2011) Improved diagnostic and prognostic performance of a new high-sensitive troponin T assay in patients with acute coronary syndrome. American Heart Journal 162:1, 81-88
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R. Scott Wright, Jeffrey L. Anderson, Cynthia D. Adams, Charles R. Bridges, Donald E. Casey, Steven M. Ettinger, Francis M. Fesmire, Theodore G. Ganiats, Hani Jneid, A. Michael Lincoff, Eric D. Peterson, George J. Philippides, Pierre Theroux, Nanette K. Wenger, James Patrick Zidar. (2011) 2011 ACCF/AHA Focused Update of the Guidelines for the Management of Patients With Unstable Angina/Non–ST-Elevation Myocardial Infarction (Updating the 2007 Guideline). Journal of the American College of Cardiology 57:19, 1920-1959
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R. Scott Wright, Jeffrey L. Anderson, Cynthia D. Adams, Charles R. Bridges, Donald E. Casey, Steven M. Ettinger, Francis M. Fesmire, Theodore G. Ganiats, Hani Jneid, A. Michael Lincoff, Eric D. Peterson, George J. Philippides, Pierre Theroux, Nanette K. Wenger, James Patrick Zidar. (2011) 2011 ACCF/AHA Focused Update Incorporated Into the ACC/AHA 2007 Guidelines for the Management of Patients With Unstable Angina/Non–ST-Elevation Myocardial Infarction. Journal of the American College of Cardiology 57:19, e215-e367
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Eric Heller, George D. Dangas. 2011. Heparin, LMWH, GIIb/IIIa, and Direct Thrombin Inhibitors. , 110-143.
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Glenn N. Levine, Eric R. Bates, James C. Blankenship, Steven R. Bailey, John A. Bittl, Bojan Cercek, Charles E. Chambers, Stephen G. Ellis, Robert A. Guyton, Steven M. Hollenberg, Umesh N. Khot, Richard A. Lange, Laura Mauri, Roxana Mehran, Issam D. Moussa, Debabrata Mukherjee, Brahmajee K. Nallamothu, Henry H. Ting, Alice K. Jacobs, Jeffrey L. Anderson, Nancy Albert, Mark A. Creager, Steven M. Ettinger, Robert A. Guyton, Jonathan L. Halperin, Judith S. Hochman, Frederick G. Kushner, E. Magnus Ohman, William Stevenson, Clyde W. Yancy. (2011) 2011 ACCF/AHA/SCAI Guideline for Percutaneous Coronary Intervention. Catheterization and Cardiovascular Interventionsn/a-n/a
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, Helge Røsjø, Marjut Varpula, Tor-Arne Hagve, Sari Karlsson, Esko Ruokonen, Ville Pettilä, Torbjørn Omland. (2011) Circulating high sensitivity troponin T in severe sepsis and septic shock: distribution, associated factors, and relation to outcome. Intensive Care Medicine 37:1, 77-85
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M. J. S. Zaman, K. Vrotsou, G. S. Chu, H. M. May, P. K. Myint. (2011) A high incidental rise in cardiac troponin I carries a higher mortality risk in older patients than in those with a diagnosed acute coronary syndrome. Age and Ageing 40:1, 122-125
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Elias B. Hanna, Sunil V. Rao, Steven V. Manoukian, Jorge F. Saucedo. (2010) The Evolving Role of Glycoprotein IIb/IIIa Inhibitors in the Setting of Percutaneous Coronary Intervention. JACC: Cardiovascular Interventions 3:12, 1209-1219
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Jonas Hallén, Dan Atar. (2010) A window into your heart: taking cardiac troponin to the next level. Biomarkers in Medicine 4:6, 889-894
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Xavier Bosch, Jaume Marrugat, Juan Sanchis, Xavier Bosch. 2010. Platelet glycoprotein IIb/IIIa blockers during percutaneous coronary intervention and as the initial medical treatment of non-ST segment elevation acute coronary syndromes. .
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C. M. Gibson. (2010) Introduction. European Heart Journal Supplements 12:Suppl D, D1-D3
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N. Uren. (2010) Acute coronary syndromes: assessing risk and choosing optimal pharmacological regimens for a superior outcome. European Heart Journal Supplements 12:Suppl D, D4-D13
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T. Omland. (2010) New features of troponin testing in different clinical settings. Journal of Internal Medicine 268:3, 207-217
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Nicolas Danchin, Nadia Aïssaoui. (2010) Pharmacologic Therapy for Non ST-segment Elevation Acute Coronary Syndromes: Focus on Antithrombotic Therapy. Cardiovascular Drugs and Therapy 24:4, 325-330
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Michael Koutouzis, Lars Grip. (2010) Glycoprotein IIb/IIIa inhibitors during percutaneous coronary interventions. Interventional Cardiology 2:3, 301-318
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JA Shand, IB Menown, DJ McEneaney. (2010) A timely diagnosis of myocardial infarction. Biomarkers in Medicine 4:3, 385-393
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Gina Biasillo, Milena Leo, Roberta Della Bona, Luigi Marzio Biasucci. (2010) Inflammatory biomarkers and coronary heart disease: from bench to bedside and back. Internal and Emergency Medicine 5:3, 225-233
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Raphael Twerenbold, Tobias Reichlin, Christian Mueller. (2010) Clinical application of sensitive cardiac troponin assays: potential and limitations. Biomarkers in Medicine 4:3, 395-401
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Michel R Hoenig, Constantine N Aroney, Ian A Scott, Michel R Hoenig. 2010. Early invasive versus conservative strategies for unstable angina and non-ST elevation myocardial infarction in the stent era. .
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William M. Stone, Sailendra G. Naidu, Alyssa Chapital, Samuel R. Money. (2010) Antiplatelet Medications: Old and Emerging Therapies. Annals of Vascular Surgery 24:1, 140-148
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Pawan D Patel, Rohit R Arora. (2010) Practical Implications of ACC/AHA 2007 Guidelines for the Management of Unstable Angina/Non-ST Elevation Myocardial Infarction. American Journal of Therapeutics 17:1, e24-e40
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Asim A. Mohammed, James L. Januzzi. (2010) Clinical Applications of Highly Sensitive Troponin Assays. Cardiology in Review 18:1, 12-19
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M. Roser, K. Graf. (2009) EARLY-ACS-Studie – GP-IIb/IIIa-Antagonisten: „Upstream“ oder „Downstream“?. Der Kardiologe 3:5, 425-428
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A. Kumar, C. P. Cannon. (2009) Acute Coronary Syndromes: Diagnosis and Management, Part I. Mayo Clinic Proceedings 84:10, 917-938
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Reichlin, Tobias, Hochholzer, Willibald, Bassetti, Stefano, Steuer, Stephan, Stelzig, Claudia, Hartwiger, Sabine, Biedert, Stefan, Schaub, Nora, Buerge, Christine, Potocki, Mihael, Noveanu, Markus, Breidthardt, Tobias, Twerenbold, Raphael, Winkler, Katrin, Bingisser, Roland, Mueller, Christian, . (2009) Early Diagnosis of Myocardial Infarction with Sensitive Cardiac Troponin Assays. New England Journal of Medicine 361:9, 858-867
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Suhas Lele, Sudhir Shah, Peter McCullough, Mohan Rajapurkar. (2009) Serum catalytic iron as a novel biomarker of vascular injury in acute coronary syndromes. EuroIntervention 5:3, 336-342
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Jason N. Katz and, Robert A. Harrington. 2009. Intravenous Glycoprotein IIb/IIIa Antagonists. , 429-456.
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Richard Body. (2008) Emergent diagnosis of acute coronary syndromes: Today's challenges and tomorrow's possibilities. Resuscitation 78:1, 13-20
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Charles V. Pollack, Eugene Braunwald. (2008) 2007 Update to the ACC/AHA Guidelines for the Management of Patients With Unstable Angina and Non–ST-Segment Elevation Myocardial Infarction: Implications for Emergency Department Practice. Annals of Emergency Medicine 51:5, 591-606
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A. Skyschally, R. Schulz, G. Heusch. (2008) Myokardiale Mikroinfarkte. Der Kardiologe 2:2, 85-92
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Raisuke Iijima, Gjin Ndrepepa, Julinda Mehilli, Franz-Josef Neumann, Stefanie Schulz, Jurriën Berg, Olga Bruskina, Franz Dotzer, Josef Dirschinger, Peter B. Berger, Albert Schömig, Adnan Kastrati. (2008) Troponin level and efficacy of abciximab in patients with acute coronary syndromes undergoing early intervention after clopidogrel pretreatment. Clinical Research in Cardiology 97:3, 160-168
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Michael Weber, Oscar Bazzino, Jose L. Navarro Estrada, Juan J. Fuselli, Fernando Botto, Diego Perez de Arenaza, Helge Möllmann, Holger N. Nef, Albrecht Elsässer, Christian W. Hamm. (2008) N-Terminal B-Type Natriuretic Peptide Assessment Provides Incremental Prognostic Information in Patients With Acute Coronary Syndromes and Normal Troponin T Values Upon Admission. Journal of the American College of Cardiology 51:12, 1188-1195
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Pierluigi Tricoci, L Kristin Newby. (2008) GP IIb???IIIa Inhibitors Administered Upstream. Cardiology in Review 16:2, 89-94
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Jae-Youn Moon, Weon Kim, Ju Han Kim, Youngkeun Ahn, Myung Ho Jeong, Young-Hak Kim, Myeong-Ki Hong, Seong-Wook Park, Seung-Jung Park, Sungha Park, Young-Guk Ko, Donghoon Choi, Yangsoo Jang. (2008) A Multicenter, Randomized, Open-Label, Therapeutic, and Exploratory Trial to Evaluate the Tolerability and Efficacy of Platelet Glycoprotein IIb/IIIa Receptor Blocker (Clotinab?? in High-Risk Patients with Percutaneous Coronary Intervention. Yonsei Medical Journal 49:3, 389
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Maarten L Simoons. (2007) Does early abciximab improve angiographic outcome and left ventricular function in patients with acute MI?. Nature Clinical Practice Cardiovascular Medicine 4:10, 536-537
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(2007) Guía de Práctica Clínica para el diagnóstico y tratamiento del síndrome coronario agudo sin elevación del segmento ST. Revista Española de Cardiología 60:10, 1070.e1-1070.e80
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Sachin Gupta, James A. de Lemos. (2007) Use and Misuse of Cardiac Troponins in Clinical Practice. Progress in Cardiovascular Diseases 50:2, 151-165
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Rajeev Garg, Barry F. Uretsky, Eli I. Lev. (2007) Anti-platelet and anti-thrombotic approaches in patients undergoing percutaneous coronary intervention. Catheterization and Cardiovascular Interventions 70:3, 388-406
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Mustafa Yazici, Sabri Demircan, Kenan Durna. (2007) Association between nitric oxide levels on myocardial injury in non-ST elevation acute coronary syndromes. Journal of Thrombosis and Thrombolysis 24:2, 145-151
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Jeffrey L. Anderson, Cynthia D. Adams, Elliott M. Antman, Charles R. Bridges, Robert M. Califf, Donald E. Casey, William E. Chavey, Francis M. Fesmire, Judith S. Hochman, Thomas N. Levin, A. Michael Lincoff, Eric D. Peterson, Pierre Theroux, Nanette Kass Wenger, R. Scott Wright, Sidney C. Smith, Alice K. Jacobs, Cynthia D. Adams, Jeffrey L. Anderson, Elliott M. Antman, Jonathan L. Halperin, Sharon A. Hunt, Harlan M. Krumholz, Frederick G. Kushner, Bruce W. Lytle, Rick Nishimura, Joseph P. Ornato, Richard L. Page, Barbara Riegel. (2007) ACC/AHA 2007 Guidelines for the Management of Patients With Unstable Angina/Non–ST-Elevation Myocardial Infarction. Journal of the American College of Cardiology 50:7, e1-e157
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Jeffrey L. Anderson, Cynthia D. Adams, Elliott M. Antman, Charles R. Bridges, Robert M. Califf, Donald E. Casey, William E. Chavey, Francis M. Fesmire, Judith S. Hochman, Thomas N. Levin, A. Michael Lincoff, Eric D. Peterson, Pierre Theroux, Nanette Kass Wenger, R. Scott Wright, Sidney C. Smith, Alice K. Jacobs, Cynthia D. Adams, Jeffrey L. Anderson, Elliot M. Antman, Jonathan L. Halperin, Sharon A. Hunt, Harlan M. Krumholz, Frederick G. Kushner, Bruce W. Lytle, Rick Nishimura, Joseph P. Ornato, Richard L. Page, Barbara Riegel. (2007) ACC/AHA 2007 Guidelines for the Management of Patients With Unstable Angina/Non–ST-Elevation Myocardial Infarction—Executive Summary. Journal of the American College of Cardiology 50:7, 652-726
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Eric Durand, Christian Hamm, Carlos Macaya, Jean-Louis Georges, Pierre Coste, Jean Wolf, Michel Slama, Steen Husted, Morris Mosseri, Antoine Lafont. (2007) A randomised controlled trial of upstream administration of eptifibatide in patients presenting non-ST segment elevation acute coronary syndrome treated with an invasive strategy. EuroIntervention 3:2, 228-234
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Amy K. Saenger, Allan S. Jaffe. (2007) The Use of Biomarkers for the Evaluation and Treatment of Patients with Acute Coronary Syndromes. Medical Clinics of North America 91:4, 657-681
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Gustavo B.F. Oliveira, Alvaro Avezum, Frederick A. Anderson, Andrzej Budaj, Omar H. Dabbous, Shaun G. Goodman, Philippe Gabriel Steg, Robert J. Goldberg, David Brieger, Keith A.A. Fox, Joel M. Gore, Christopher B. Granger. (2007) Use of proven therapies in non–ST-elevation acute coronary syndromes according to evidence-based risk stratification. American Heart Journal 153:4, 493-499
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Scott J. Cameron, Lori J. Sokoll, Omar F. Laterza, Sanket Shah, Gary B. Green. (2007) A multi-marker approach for the prediction of adverse events in patients with acute coronary syndromes. Clinica Chimica Acta 376:1-2, 168-173
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Evangelos Giannitsis, Kerstin Kurz, Hugo A Katus. (2007) Multimarker strategy in acute coronary syndrome—pro‐multimarker. Acute Cardiac Care 9:1, 6-9
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E. T. H. YEH, B. V. KHAN. (2006) The potential role of antiplatelet agents in modulating inflammatory markers in atherothrombosis. Journal of Thrombosis and Haemostasis 4:11, 2308-2316
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James T. Willerson, Paul W Armstrong. 2006. Acute Myocardial Infarction. , 611-646.
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H Mesquita Gabriel, Eduardo Infante Oliveira. (2006) Role of abciximab in the treatment of coronary artery disease. Expert Opinion on Biological Therapy 6:9, 935-942
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Matthew A. Roberts, David L. Hare, Sujiva Ratnaike, Francesco L. Ierino. (2006) Cardiovascular Biomarkers in CKD: Pathophysiology and Implications for Clinical Management of Cardiac Disease. American Journal of Kidney Diseases 48:3, 341-360
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Michel R Hoenig, Jenny Doust, Constantine N Aroney, Ian A Scott, Michel R Hoenig. 2006. Early invasive versus conservative strategies for unstable angina & non-ST-elevation myocardial infarction in the stent era. .
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A. Dolci, M. Panteghini. (2006) The exciting story of cardiac biomarkers: From retrospective detection to gold diagnostic standard for acute myocardial infarction and more. Clinica Chimica Acta 369:2, 179-187
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S. Pruvot, G. Galidie, J.-F. Bergmann, I. Mahé. (2006) La troponine et les autres marqueurs de souffrance myocardique, quelle signification en médecine interne ?. La Revue de Médecine Interne 27:3, 215-226
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Ori Ben-Yehuda. (2006) Upstream/Downstream. Journal of the American College of Cardiology 47:3, 538-540
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Benjamin M. Scirica, David A. Morrow. (2006) Appropriate invasive and conservative treatment approaches for patients with non-ST-elevation MI. Current Treatment Options in Cardiovascular Medicine 8:1, 13-21
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Sidney C. Smith, Ted E. Feldman, John W. Hirshfeld, Alice K. Jacobs, Morton J. Kern, Spencer B. King, Douglass A. Morrison, William W. O’Neill, Hartzell V. Schaff, Patrick L. Whitlow, David O. Williams, Elliott M. Antman, Sidney C. Smith, Cynthia D. Adams, Jeffrey L. Anderson, David P. Faxon, Valentin Fuster, Jonathan L. Halperin, Loren F. Hiratzka, Sharon Ann Hunt, Alice K. Jacobs, Rick Nishimura, Joseph P. Ornato, Richard L. Page, Barbara Riegel. (2006) ACC/AHA/SCAI 2005 Guideline Update for Percutaneous Coronary Intervention. Journal of the American College of Cardiology 47:1, e1-e121
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L. Kristin Newby, Matthew T. Roe, Anita Y. Chen, E. Magnus Ohman, Robert H. Christenson, Charles V. Pollack, James W. Hoekstra, W. Frank Peacock, Robert A. Harrington, Robert L. Jesse, W. Brian Gibler, Eric D. Peterson. (2006) Frequency and Clinical Implications of Discordant Creatine Kinase-MB and Troponin Measurements in Acute Coronary Syndromes. Journal of the American College of Cardiology 47:2, 312-318
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Timo Lenderink, Christopher Heeschen, Stephan Fichtlscherer, Stefanie Dimmeler, Christian W. Hamm, Andreas M. Zeiher, Maarten L. Simoons, Eric Boersma. (2006) Elevated Placental Growth Factor Levels Are Associated With Adverse Outcomes at Four-Year Follow-Up in Patients With Acute Coronary Syndromes. Journal of the American College of Cardiology 47:2, 307-311
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Geoffrey S. Ginsburg, Mark P. Donahue, L. Kristin Newby. (2005) Prospects for Personalized Cardiovascular Medicine. Journal of the American College of Cardiology 46:9, 1615-1627
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Deanne J Crosbie. (2005) Use of glycoprotein IIb/IIIa inhibitors in unstable angina and non-ST-elevation myocardial infarction. Emergency Medicine Australasia 17:5-6, 500-510
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Francesco Prati, Piotr Kwiatkowski, Constantino Caroselli, Fabrizio Imola, Alessandro Manzoli, Tamer Fouad, Pierfrancesco Corvo, Vito Ramazzotti. (2005) Use of abciximab prevents microcirculatory impairment in patients treated with coronary angioplasty for unstable angina: Results of a prospective randomized study. Catheterization and Cardiovascular Interventions 66:2, 165-169
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Huseyin Yilmaz, Ibrahim Başarici. (2005) Troponin Levels and Acute Coronary Syndrome. Journal of the American College of Cardiology 46:4, 741
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James K McCord. (2005) Cardiac markers in acute coronary syndrome. Future Cardiology 1:4, 489-494
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(2005) Guías de Práctica Clínica sobre intervencionismo coronario percutáneo. Revista Española de Cardiología 58:6, 679-728
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M. Kelm, B. E. Strauer. (2005) Das akute Koronarsyndrom. Der Internist 46:3, 265-274
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Brendan Duffy, Deepak L Bhatt. (2005) Antiplatelet Agents in Patients Undergoing Percutaneous Coronary Intervention. American Journal of Cardiovascular Drugs 5:5, 307-318
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Brett D Atwater, Matthew T Roe, Kenneth W Mahaffey. (2005) Platelet Glycoprotein IIb/IIIa Receptor Antagonists in Non-ST Segment Elevation Acute Coronary Syndromes. Drugs 65:3, 313-324
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Mustafa Yazici, Sabri Demircan, Kenan Durna, Erdogan Yasar, Mahmut Sahin. (2005) Relationship Between Myocardial Injury and Soluble P-Selectin in Non-ST Elevation Acute Coronary Syndromes. Circulation Journal 69:5, 530-535
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David Gaze, Paul O. Collinson, Markus Haass, Ulla Derhaschnig, Michael M. Hirschl, Hugo A. Katus, Frank Chwallek, Margit Mueller-Bardorff, John Kellett, Jordi Ord????ez-Llanos, Miquel Santal??-Bel, Javier Merc??-Munta??ola, Christer Sylv??n, Ilse Schulz, Rainer Zerback. (2004) The Use of a Quantitative Point-of-Care System Greatly Reduces the Turnaround Time of Cardiac Marker Determination. Point of Care: The Journal of Near-Patient Testing & Technology 3:4, 156-158
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J.A. Páramo Fernández, J. Feliú Sánchez, M.P. Sánchez Antón, E. Rocha Hernando. (2004) Nuevas estrategias antitrombóticas en la trombosis arterial. Medicine - Programa de Formación Médica Continuada Acreditado 9:22, 1414-1422
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Patricia E. Casey. (2004) Markers of Myocardial Injury and Dysfunction. AACN Clinical Issues: Advanced Practice in Acute and Critical Care 15:4, 547-557
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James Kevin McCord. (2004) The Future of Cardiac Markers in the Emergency Department. Critical Pathways in Cardiology: A Journal of Evidence-Based Medicine 3:3, 107-109
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Asvin Latsch, Tim Suselbeck, Nathalie Muth, Tudor Poerner, Andreas Baumbach, Stefan Pfleger, Martin Borggrefe, Karl K Haase. (2004) Utilization of eptifibatide for treatment of severe dissections as a bail-out procedure. International Journal of Cardiology 96:2, 229-233
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Stephen D Wiviott, James A de Lemos, David A Morrow. (2004) Pathophysiology, prognostic significance and clinical utility of B-type natriuretic peptide in acute coronary syndromes. Clinica Chimica Acta 346:2, 119-128
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B. Charles Solymoss, Martial G. Bourassa, Peter Cernacek, Annik Fortier, Pierre Théroux. (2004) Classification and risk stratification of patients with acute chest pain using a low discriminatory level of cardiac troponin T. Clinical Cardiology 27:3, 130-136
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Michael C Kontos, Rakesh Shah, Lucie M Fritz, F.Philip Anderson, James L Tatum, Joseph P Ornato, Robert L Jesse. (2004) Implication of different cardiac troponin I levels for clinical outcomes and prognosis of acute chest pain patients. Journal of the American College of Cardiology 43:6, 958-965
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Marco Zimarino, Raffaele De Caterina. (2004) Glycoprotein IIb-IIIa Antagonists in Non-ST Elevation Acute Coronary Syndromes and Percutaneous Interventions: from Pharmacology to Individual Patient's Therapy. Journal of Cardiovascular Pharmacology 43:3, 325-332
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David Kovar, Christopher P. Cannon, Jane H. Bentley, Andrew Charlesworth, William J. Rogers. (2004) Does initial and delayed heart rate predict mortality in patients with acute coronary syndromes?. Clinical Cardiology 27:2, 80-86
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Ramesh M Gowda, Ijaz A Khan, Balendu C Vasavada, Terrence J Sacchi. (2004) Therapeutics of Platelet Glycoprotein IIb/IIIa Receptor Antagonism. American Journal of Therapeutics 11:4, 302-307
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Sherwin K B Sy, Aaron L Levenstadt. (2004) A Perspective on the Toxicological Mechanisms Possibly Contributing to the Failure of Oral Glycoprotein IIb/IIIa Antagonists in the Clinic. American Journal of Cardiovascular Drugs 4:1, 1-10
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Stefan James. (2004) Coagulation, inflammation and myocardial dysfunction in unstable coronary artery disease and the influence of glycoprotein IIb/IIIa inhibition and low molecular weight heparin. Upsala Journal of Medical Sciences 109:2, 71-122
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R Choussat, J.P Collet, F Beygui, M Borentain, G Montalescot. (2003) Intérêt de la prise en charge précoce des syndromes coronaires aigus par les anti-GPIIb/IIIa. Annales de Cardiologie et d'Angéiologie 52, S1-S9
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Allan S. Jaffe. (2003) A small step for man, a leap forward for postoperative management. Journal of the American College of Cardiology 42:9, 1555-1557
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D VIJAY ANAND, A LAHIRI. (2003) Myocardial perfusion imaging versus biochemical markers in acute coronary syndromes. Nuclear Medicine Communications 24:10, 1049-1054
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Christopher P. Cannon. (2003) Oral platelet glycoprotein IIb/IIIa receptor inhibitors-part II. Clinical Cardiology 26:9, 401-406
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G. Hafner, D. Peetz, F. Dati. (2003) Patientennahe Bestimmung der Troponine zur Diagnostik akuter Koronarsyndrome/Near-Patient Testing of Troponins for the Diagnosis of Acute Coronary Syndromes. LaboratoriumsMedizin 27:7-8, 279-287
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(2003) Soluble CD40 Ligand in Acute Coronary Syndromes. New England Journal of Medicine 348:25, 2575-2577
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Hendrik Zimmet. (2003) The Twilight Zone of Troponins. Heart Lung <html_ent glyph="@amp;" ascii="&"/> Circulation 12:s2, S90-S94
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G Shi, T.L Lloyd, S.K.B Sy, Q Jiao, A Wernicki, A Mutlib, T.A Emm, S.E Unger, H.J Pieniaszek. (2003) Simultaneous quantification of seven active metabolites of roxifiban in human plasma by LC/MS/MS in the presence of an interfering displacer at millimolar concentrations. Journal of Pharmaceutical and Biomedical Analysis 31:5, 937-951
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Heeschen, Christopher, Dimmeler, Stefanie, Hamm, Christian W., van den Brand, Marcel J., Boersma, Eric, Zeiher, Andreas M., Simoons, Maarten L., . (2003) Soluble CD40 Ligand in Acute Coronary Syndromes. New England Journal of Medicine 348:12, 1104-1111
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Andra L. Blomkalns, Christopher J. Lindsell, Abhinav Chandra, Mary E. Osterlund, W. Brian Gibler, Charles V. Pollack, Brian R. Tiffany, Judd E. Hollander, James W. Hoekstra. (2003) Can Electrocardiographic Criteria Predict Adverse Cardiac Events and Positive Cardiac Markers?. Academic Emergency Medicine 10:3, 205-210
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Graham S. Hillis, Pamela Taggart, Delana Wardlaw, Lorraine Hillis, Ning Zhao, William C. Dalsey, Antoinette Mangione. (2003) The relative utility of cardiac troponin i, creatine kinase-mb mass , and myosin light chain-1 in the long-term risk stratification of patients with chest pain. Clinical Cardiology 26:3, 147-152
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Padma Kaul, L.Kristin Newby, Yuling Fu, Vic Hasselblad, Kenneth W Mahaffey, Robert H Christenson, Robert A Harrington, E.Magnus Ohman, Eric J Topol, Robert M Califf, Frans Van de Werf, Paul W Armstrong. (2003) Troponin T and quantitative ST-segment depression offer complementary prognostic information in the risk stratification of acute coronary syndrome patients. Journal of the American College of Cardiology 41:3, 371-380
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L.Kristin Newby, Britta U Goldmann, E.Magnus Ohman. (2003) Troponin: an important prognostic marker and risk-stratification tool in non–ST-segment elevation acute coronary syndromes. Journal of the American College of Cardiology 41:4, S31-S36
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Christopher P Cannon. (2003) Small molecule glycoprotein IIb/IIIa receptor inhibitors as upstream therapy in acute coronary syndromes. Journal of the American College of Cardiology 41:4, S43-S48
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