Original Article
Cardiac Troponin and Outcome in Acute Heart Failure
N Engl J Med 2008; 358:2117-2126May 15, 2008
- Abstract
Background
Cardiac troponin provides diagnostic and prognostic information in acute coronary syndromes, but its role in acute decompensated heart failure is unclear. The purpose of our study was to describe the association between elevated cardiac troponin levels and adverse events in hospitalized patients with acute decompensated heart failure.
Methods
We analyzed hospitalizations for acute decompensated heart failure between October 2001 and January 2004 that were recorded in the Acute Decompensated Heart Failure National Registry (ADHERE). Entry criteria included a troponin level that was obtained at the time of hospitalization in patients with a serum creatinine level of less than 2.0 mg per deciliter (177 μmol per liter). A positive troponin test was defined as a cardiac troponin I level of 1.0 μg per liter or higher or a cardiac troponin T level of 0.1 μg per liter or higher.
Results
Troponin was measured at the time of admission in 84,872 of 105,388 patients (80.5%) who were hospitalized for acute decompensated heart failure. Of these patients, 67,924 had a creatinine level of less than 2.0 mg per deciliter. Cardiac troponin I was measured in 61,379 patients, and cardiac troponin T in 7880 patients (both proteins were measured in 1335 patients). Overall, 4240 patients (6.2%) were positive for troponin. Patients who were positive for troponin had lower systolic blood pressure on admission, a lower ejection fraction, and higher in-hospital mortality (8.0% vs. 2.7%, P<0.001) than those who were negative for troponin. The adjusted odds ratio for death in the group of patients with a positive troponin test was 2.55 (95% confidence interval, 2.24 to 2.89; P<0.001 by the Wald test).
Conclusions
In patients with acute decompensated heart failure, a positive cardiac troponin test is associated with higher in-hospital mortality, independently of other predictive variables. (ClinicalTrials.gov number, NCT00366639.)
Media in This Article
Figure 1
Mortality According to Number of Days in the Hospital and Troponin Status at Presentation.Figure 2
In-Hospital Mortality According to Troponin I or Troponin T Quartile.Article Activity
- Article
The United States is in the midst of a heart failure epidemic. More than 1 million hospitalizations in 2007 were for heart failure, and the Centers for Medicaid and Medicare Services currently spends more on the diagnosis and treatment of this condition than on any other medical condition. 1 Most patients with heart failure are admitted to the hospital from the emergency department, where a comprehensive evaluation is required to determine the precipitating cause of the condition. Unfortunately, the definition of a comprehensive evaluation has not been established. Since coronary artery disease is the most common cause of heart failure in the United States, it is appropriate to evaluate patients with heart failure for myocardial ischemia. Initial evaluation of patients who present with heart failure often includes a focused history, physical examination, electrocardiogram, and measurement of biomarkers. Although this approach is well validated for the evaluation of acute coronary syndromes, except for specific laboratory-based investigations, an objective risk-stratification process for the evaluation of acute decompensated heart failure is lacking.
The value of measuring serum cardiac troponin when a patient presents with acute decompensated heart failure remains uncertain. Although several limited analyses suggest that an increase in serum cardiac troponin levels is associated with adverse long-term outcomes,2-5 the short-term implications are less clearly defined. Some small trials involving patients with heart failure have shown that increases in troponin levels, even in the absence of chest pain or an acute coronary syndrome, correlate with a poor prognosis5-7 and that detectable troponin, at any level, is associated with impaired hemodynamics, a progressive decline in left ventricular systolic function, and shortened survival.5-8 We conducted a large study to describe short-term outcomes associated with elevated troponin levels on admission in hospitalized patients with acute decompensated heart failure.
Methods
Registry Data
With the use of data from the Acute Decompensated Heart Failure National Registry (ADHERE), we analyzed outcomes associated with elevated troponin levels in patients with acute decompensated heart failure. The methods and design of ADHERE have been published previously.9 Briefly, ADHERE is an observational registry of individual hospital episodes, from initial presentation through discharge, involving patients with an ultimate discharge diagnosis of acute decompensated heart failure. We examined records from 274 hospitals, from October 2001 through January 2004. Inclusion criteria were hospitalization and documentation of the measurement of cardiac troponin I or cardiac troponin T at the initial evaluation (defined as within 24 hours after admission). Because renal dysfunction may influence cardiac troponin concentrations, patients with a serum creatinine level higher than 2.0 mg per deciliter (176.8 μmol per liter) were excluded from the study. Ischemic heart failure was defined as the cause of the acute decompensated heart failure if the patient reported a history of coronary artery disease or myocardial infarction. Race or ethnic group was self-reported.
Troponin Measurements
We chose to pool cardiac troponin I and cardiac troponin T measurements, first, because an elevated value for either one is consistent with an acute coronary syndrome, and second, because they are used interchangeably in clinical practice and often in a qualitative fashion (as positive or negative for troponin), especially during the initial evaluation (the period examined in this analysis). Since these molecules are treated identically for all other conditions in the clinical setting, we chose to treat them identically in this investigation of acute decompensated heart failure.
ADHERE collected assay data but did not control for the assay platform. Measurement of cardiac troponin T is performed on a uniform platform in the United States, and the cutoff point of 0.1 μg per liter or higher for detection of a myocardial infarction has been defined by the manufacturer and derived from a receiver-operating-characteristic (ROC) curve. Because troponin I has different cutoff points that are dependent on the platform used (more than a dozen different assays), a predefined cutoff point was set at 1.0 μg per liter or higher. This cutoff point was based on expert consensus, approximating values defined from a ROC curve that was optimized for the detection of myocardial infarction. Qualitative tests were considered to be positive if they were recorded as such.
Statistical Analysis
The primary outcome was in-hospital mortality from all causes, and the secondary outcomes included differences in medical management, procedures, and length of stay between the troponin-positive and troponin-negative cohorts. All outcomes were specified before the data were examined. We also examined associations between therapy and mortality, controlling for troponin in patients who received inotropes or vasodilators, but not both.
Analysis of variance, Wilcoxon rank-sum tests, or chi-square tests were used for univariate analyses. All reported P values are two-sided. Because of anticipated differences between troponin-positive and troponin-negative groups with respect to medical history and clinical characteristics at presentation, mortality was adjusted for relevant prognostic factors. Of 80 variables collected in ADHERE, the most important predictors of in-hospital mortality have been previously identified by classification-and-regression-tree (CART) analysis and logistic-regression models.10 For this analysis, mortality according to troponin group was compared by logistic regression adjusted for age, blood urea nitrogen, systolic blood pressure, diastolic blood pressure, serum creatinine, serum sodium, heart rate, and dyspnea at rest. Overall, 1.2% of the records were excluded because of missing values. Since there was little variation in the rate of measurement of troponin by center, hospital type, or region, hierarchical analysis was not performed. Analyses were performed with the use of SAS software, version 8.2 (SAS Institute).
The study was designed by all the authors; the data were gathered by the 274 hospitals that participated in ADHERE, and the statistical analysis was performed by ADHERE statisticians.
Results
Troponin Levels and Characteristics of the Patients
Troponin levels were measured at the time of admission in 84,872 of 105,388 hospitalized patients (80.5%), with 67,924 patients meeting all inclusion and exclusion criteria. Overall, 4240 patients (6.2%) were positive for troponin on admission. Characteristics of the patients according to whether they were positive or negative for troponin are summarized in Table 1Table 1
Patient Characteristics and Treatment According to Troponin Status.. There were small but significant differences between the two troponin cohorts. On admission, troponin-positive patients had lower systolic blood pressure and lower ejection fractions but were less likely to have atrial fibrillation.Cardiac troponin I was measured in 61,379 patients (90.4%), and cardiac troponin T in 7880 patients (11.6%). The values were positive in 3253 patients (5.3%) and 1035 patients (13.1%), respectively. Both markers were measured in 1335 patients (2.0%); of these, 48 patients were positive for both, 1059 were negative for both, 71 were positive for cardiac troponin I only, and 157 were positive for cardiac troponin T only. For this analysis, if either marker was above the defined cutoff point, the patient was considered to be troponin-positive. Since both cardiac troponin I and cardiac troponin T were measured in only 2% of patients, no comparison between these proteins was made.
In-Hospital Mortality
Overall, troponin-positive patients had a higher rate of in-hospital mortality than troponin-negative patients (8.0% vs. 2.7%, P<0.001). Actuarial analysis showed that within 1 day after admission, in-hospital mortality was higher for troponin-positive than for troponin-negative patients (Figure 1Figure 1
Mortality According to Number of Days in the Hospital and Troponin Status at Presentation.). When the troponin level was examined as a continuous variable, higher values were also associated with higher mortality. The adjusted odds ratio for death among patients with a positive troponin test was 2.55 (95% confidence interval [CI], 2.24 to 2.89; P<0.001). Increased mortality was observed with elevations in either cardiac troponin T or cardiac troponin I.Mortality according to quartiles of cardiac troponin T and cardiac troponin I levels is shown in Figure 2Figure 2
In-Hospital Mortality According to Troponin I or Troponin T Quartile.. For cardiac troponin I, the adjusted odds ratio for death in a comparison of quartile 4 with quartile 1 was 2.33 (95% CI, 1.98 to 2.75; P<0.001). The first two troponin T quartiles were unequal in size because 37% of the records had a value of 0.01 μg per liter. In addition, because qualitative troponin results were not included in the quartile analysis, this cohort was smaller than the total in the study.Ischemic heart failure, which was reported as the cause of the acute decompensated heart failure in 53% and 52% of troponin-positive and troponin-negative patients, respectively, was not a useful discriminator of troponin status, nor was it predictive of mortality. Among troponin-positive patients, mortality was 8.4% for those with ischemic heart failure and 7.4% for those without ischemic heart failure; among troponin-negative patients, mortality was 2.8% and 2.6%, respectively, for these groups.
Treatment, Troponin Status, and Mortality
Although the rate of use of diuretics was similar in the troponin-positive and troponin-negative cohorts (Table 1), troponin-positive patients were more likely to be receiving nitroglycerin, inotropic agents, and vasodilators than were troponin-negative patients. There were also differences in resource utilization and mortality according to treatment (Table 2Table 2
Resource Utilization According to Troponin Status. and Table 3Table 3
In-Hospital Mortality According to Treatment. and Figure 3Figure 3
Mortality According to Type of Treatment and Troponin Status.). However, among troponin-positive patients, mortality, as indicated by the adjusted odds ratio, was independent of treatment. The adjusted odds ratio for the troponin-positive group as compared with the troponin-negative group was 1.84 (95% CI, 1.43 to 2.36) in the subgroup of patients who were treated with inotropic agents and 1.96 (95% CI, 1.37 to 2.81) in the subgroup treated with vasodilators (P<0.001 for both comparisons by the Wald test). Finally, there was no interaction between treatment and troponin status with respect to mortality. The adjusted odds ratio for death among patients receiving inotropic agents as compared with those receiving vasodilators was 4.44 (95% CI, 2.90 to 6.81) for the troponin-positive group and 4.54 (95% CI, 3.75 to 5.49) for the troponin-negative group (P<0.001 for both comparisons by the Wald test).Discussion
In our data set, which included data from 105,388 patients, troponin was measured in 80.5% of the hospitalized patients with acute decompensated heart failure as a part of their routine care. Of these patients, 6.2% were found to be positive for troponin, including those with and those without a history of coronary artery disease or myocardial infarction. Like patients presenting with an acute coronary syndrome, patients presenting with acute decompensated heart failure and a positive troponin status were found to be a high-risk cohort. Patients in this cohort, as compared with those who were negative for troponin, required more cardiac procedures and longer hospitalization and had a higher risk of in-hospital death, even after adjustment for other risk factors. These results suggest that measurement of troponin adds important prognostic information to the initial evaluation of patients with acute decompensated heart failure and should be considered as part of an early assessment of risk.
Since patients who are positive for troponin have a disproportionately high mortality, an association that is independent of other well-validated risk factors for acute decompensated heart failure, the results of troponin tests should be factored into decisions that are made with respect to triage and management. Although we did not study differential management, in our opinion, patients with an increased risk of death should undergo more intensive cardiovascular monitoring; they may require admission to a critical care unit or cardiac telemetry. Our findings add to the existing risk-stratification data for predicting the short-term risk of death among patients with acute decompensated heart failure. Patients with an initial blood urea nitrogen level of more than 43 mg per deciliter (15.4 mmol per liter), systolic blood pressure of less than 115 mm Hg, or a creatinine level of more than 2.75 mg per deciliter (243.1 μmol per liter) have high short-term mortality, exceeding 22% if all three factors are present.10 Since these mortality rates are higher than those that are associated with most episodes of acute myocardial infarction, a more aggressive therapeutic approach is justified. A positive troponin status adds incremental prognostic information to that obtained from vital signs and other laboratory data.
Conversely, we found that a negative troponin status was associated with a short-term mortality rate that was nearly two thirds lower than the rate with a positive troponin level. Although the absence of high-risk predictors does not equate with low risk, the absence of detectable troponin may be helpful in planning treatment. When considered in the context of other predictors of low risk, a negative troponin test may aid in the identification of patients for whom less intense monitoring and therapy are appropriate. Few studies have examined predictors of low risk in patients with acute decompensated heart failure. In a study of patients with acute decompensated heart failure who were in an emergency department observation unit,11 a blood urea nitrogen level of less than 30 mg per deciliter (10.7 mmol per liter) was associated with successful treatment in a short-stay unit. Another analysis showed that an elevated blood pressure (>160 mm Hg) or a negative troponin test was associated with discharge from the hospital within 24 hours and an absence of adverse outcomes within 30 days.12 These analyses suggest that initial blood pressure, renal function, and troponin status are the most useful risk-stratification data in patients presenting with acute decompensated heart failure.
In the current study, patients who were positive for troponin required longer hospitalization and greater use of resources. Since hospitalization and length of stay in an intensive care unit are important determinants of cost, early identification of patients who will require greater resources could allow early implementation of aggressive therapy. The impact of early risk stratification has been supported in other studies of acute decompensated heart failure. In the B-Type Natriuretic Peptide for Acute Shortness of Breath Evaluation (BASEL) trial,13 simply establishing an early, accurate diagnosis of heart failure decreased both length of stay and costs. Early risk stratification may help identify patients who are likely to receive the greatest benefit from early intensive therapy.
In an analysis of subjects in the Enhanced Feedback for Effective Cardiac Treatment (EFFECT) study, You et al. evaluated cardiac troponin I and mortality in 2025 patients who were hospitalized with heart failure.14 They reported that levels of cardiac troponin I higher than 0.5 μg per liter, which were present in 34.5% of the patients, were an independent predictor of short-term death, with a dose–response relationship. However, applying these findings to those from centers that used a different assay platform from that used by EFFECT may be problematic. Furthermore, the rate of elevated troponin levels in the EFFECT study is markedly higher than the rate in the current study and in earlier analyses.15
Smaller studies of patients with heart failure have shown similar implications of elevated troponin levels with respect to short-term morbidity and mortality. In 98 consecutive patients admitted for worsening heart failure, in-hospital death from cardiac causes occurred in 10 of 45 patients (22%) who had cardiac troponin T levels higher than 0.033 μg per liter, as compared with 4 of 53 (8%) who had lower cardiac troponin T levels (P=0.04).3 Cardiac troponin T and brain natriuretic peptide, when considered together, identified patients at low risk (3%), intermediate risk (11%), and high risk (31%) for in-hospital death (P=0.006). A study of 159 patients with acute decompensated heart failure showed that 24 patients (15%) had high levels of troponin.16 Of these patients, 20.8% died during hospitalization or had refractory heart failure, as compared with 3.7% of those with low troponin levels (odds ratio, 6.8; 95% CI, 1.5 to 31.2). Finally, in a subgroup analysis of 133 patients in the Randomized Intravenous TeZosentan 4 (RITZ-4) study, which involved patients with acute decompensated heart failure or an acute coronary syndrome, an elevated cardiac troponin I level before randomization was associated with an increased rate of the composite end point of death, worsening heart failure, recurrent ischemia, or new myocardial infarction within 72 hours (odds ratio, 1.15; 95% CI, 1.01 to 1.32).17
In hospitalized patients with acute decompensated heart failure, but without classic signs of acute myocardial infarction, troponin is correlated with several physiological variables.4,18 In 26 hospitalized patients with heart failure, a significant correlation was found between cardiac troponin T status and the left-ventricular-mass index.4 In a study involving 40 hospitalized patients with heart failure,18 troponin status was correlated with blood pressure and the presence or absence of left ventricular hypertrophy as assessed by electrocardiography. Several hypotheses, including subendocardial ischemia due to a mismatch between myocardial oxygen supply and demand, have been proposed as explanations for these associations, but the mechanisms by which these features cause increases in troponin levels in the absence of an acute coronary syndrome remain uncertain.
An elevation in cardiac troponin can indicate the presence of myocyte injury or death.19 This model recognizes progressive myocyte loss as a prominent pathophysiological mechanism in the evolution of cardiac dysfunction and acute decompensated heart failure.20 The pathophysiological factors that that are thought to be responsible for ongoing myocyte injury or cell death include excessive adrenergic stimulation through renin, angiotensin, aldosterone, or endothelin signaling pathways, abnormalities in calcium handling, inflammatory cytokines, nitric oxide, and oxidative and mechanical stress.6
National guidelines for the evaluation of an acute coronary syndrome recommend that levels of cardiac troponin and brain natriuretic peptide or N-terminal pro–brain natriuretic peptide be used for prognosis and risk stratification. Current guidelines for the evaluation of heart failure do not mention troponin and recommend the measurement of brain natriuretic peptide only in cases in which the diagnosis is uncertain. Our data suggest that the measurement of troponin levels in patients who present with heart failure provides independent prognostic information regarding in-hospital death and other clinical outcomes and can be useful for risk stratification of such patients.
Our study has several limitations. Since we performed a retrospective analysis of registry data, we cannot establish cause and effect. However, the associations are strong and are consistent with prior analyses of troponin in patients with acute decompensated heart failure. Furthermore, the ADHERE registry is a large data set based on a broad sample of patients with heart failure; thus, the data are not confounded as a result of being based on a prespecified subgroup of patients receiving predefined treatments.
A number of factors could have affected the results of the troponin tests. First, we used the results of various cardiac troponin I assays for which we defined cutoff points, rather than core laboratory results. Since many cardiac troponin I platforms are used in clinical practice, each with a unique cutoff point, our prespecified cutoff point may have introduced variability in assay performance.21 However, although a single assay platform could increase the strength of the causality association, the generalizability of our data allows the findings to be considered in actual patient-care scenarios. Second, bias may have been introduced because we were unable to analyze those patients with heart failure in whom troponin was not assessed and are unable to determine why physicians obtained, or did not obtain, troponin measurements. Because troponin was measured only at the time of admission to the hospital, we cannot comment on the number of patients with an acute myocardial infarction, since a typical rise and fall of cardiac biomarkers was not recorded. Finally, the prognostic information that can be gained from an analysis of the interaction of troponin with other biomarkers, such as brain natriuretic peptide, was not explored in this study.
Several limitations of the study are a function of the registry itself. Inclusion in ADHERE required a discharge diagnosis of heart failure, with the determination of a nonischemic cause made at the discretion of the investigator. Because the diagnosis was not objectively ascertained, some patients with both heart failure and an acute coronary syndrome may have been included in our analysis. However, when only data from patients who were categorized as having nonischemic heart failure were analyzed, troponin levels retained their prognostic significance. In addition, ADHERE did not consistently report the cause of death, and noncardiac events may have contributed to the mortality rate. However, we expect that the incidence of noncardiac events would be equally distributed between the troponin-positive and troponin-negative groups. Finally, ADHERE recorded only in-hospital outcomes, not deaths after discharge. Consequently, our findings may underrepresent adverse outcomes, with possible prognostic implications, since others have found that mortality at 30 days may exceed in-hospital mortality.14
In hospitalized patients with acute decompensated heart failure, a positive troponin test is associated with more frequent adverse events, including increased in-hospital mortality, independently of treatment and other prognostic variables. Patients with heart failure who were positive for troponin required greater use of hospital resources, including longer stays in the hospital and in the intensive care unit. We have identified a cohort of patients who have an elevated risk of adverse outcomes. Future research that examines therapies to mitigate these outcomes is needed.
Supported by Scios.
Dr. Peacock reports serving as a consultant to Abbott, Beckman Coulter, Biosite, Ortho Clinical Diagnostics, and Response Biomedical; receiving honoraria from Abbott, Beckman Coulter, Biosite, Ortho-Biotech, and Scios; and receiving grant support from Abbott, Biosite, and Scios. Dr. Fonarow reports serving as a consultant to Scios; receiving honoraria from Scios and Biosite; and receiving grant support from the National Heart, Lung, and Blood Institute. Dr. Diercks reports receiving honoraria from Scios and grant support from Dade Behring. Ms. Wynne reports having been an employee of Johnson & Johnson. Dr. Apple reports serving as a consultant to Abbott, Ortho Clinical Diagnostics, and Biosite; receiving honoraria from Abbott and bioMérieux; and receiving grant support from Ortho Clinical Diagnostics, bioMérieux, Abbott, Dade Behring, DPC, Bayer, Response Biomedical, Mitsubishi Kagaku, and Roche. No other potential conflict of interest relevant to this article was reported.
Source Information
From the Department of Emergency Medicine, Cleveland Clinic Foundation, Cleveland (W.F.P.); the Division of Cardiology (T.D.M.) and the Department of Laboratory Medicine (A.H.B.W.), University of California at San Francisco, San Francisco; Ahmanson–UCLA Cardiomyopathy Center, UCLA, Los Angeles (G.C.F.); the Department of Emergency Medicine, University of California, Davis, Sacramento (D.D.); the Department of Statistics, Scios, Mountain View, CA (J.W.); and the Department of Laboratory Medicine and Pathology, Hennepin County Medical Center and University of Minnesota School of Medicine, Minneapolis (F.S.A.).
Address reprint requests to Dr. Peacock at the Department of Emergency Medicine E19, Cleveland Clinic Foundation, 9500 Euclid Ave., Cleveland OH 44195, or at peacocw@ccf.org.
- References
References
1
Rosamond W ,Flegal K ,Friday G , et al. Heart disease and stroke statistics -- 2007 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation 2007;115:e69-e171
CrossRef | Web of Science | Medline2
Goto T ,Takase H ,Toriyama T , et al. Circulating concentrations of cardiac proteins indicate the severity of congestive heart failure. Heart 2003;89:1303-1307
CrossRef | Web of Science | Medline3
Ishii J ,Nomura M ,Nakamura Y , et al. Risk stratification using a combination of cardiac troponin T and brain natriuretic peptide in patients hospitalized for worsening chronic heart failure. Am J Cardiol 2002;89:691-695
CrossRef | Web of Science | Medline4
Lowbeer C ,Gustafsson SA ,Seeberger A ,Bouvier F ,Hulting J . Serum cardiac troponin T in patients hospitalized with heart failure is associated with left ventricular hypertrophy and systolic dysfunction. Scand J Clin Lab Invest 2004;64:667-676
CrossRef | Web of Science | Medline5
Horwich TB ,Patel J ,MacLellan WR ,Fonarow GC . Cardiac troponin I is associated with impaired hemodynamics, progressive left ventricular dysfunction, and increased mortality rates in advanced heart failure. Circulation 2003;108:833-838
CrossRef | Web of Science | Medline6
Fonarow GC ,Horwich TB . Combining natriuretic peptides and necrosis markers in determining prognosis in heart failure. Rev Cardiovasc Med 2003;4:Suppl 4:S20-S28
Medline7
Del Carlo CH ,O'Connor CM . Cardiac troponins in congestive heart failure. Am Heart J 1999;138:646-653
CrossRef | Web of Science | Medline8
Xue C ,Yu H ,Li R , et al. Clinical significance of serum cardiac troponin T in patients with congestive heart failure. Chin Med J (Engl) 2003;116:469-471
Web of Science | Medline9
Adams KF Jr ,Fonarow GC ,Emerman CL , et al. Characteristics and outcomes of patients hospitalized for heart failure in the United States: rationale, design, and preliminary observations from the Acute Decompensated Heart Failure National Registry (ADHERE). Am Heart J 2005;149:209-216
CrossRef | Web of Science | Medline10
Fonarow GC ,Adams KF Jr ,Abraham WT , et al. Risk stratification for in-hospital mortality in acutely decompensated heart failure: classification and regression tree analysis. JAMA 2005;293:572-580
CrossRef | Web of Science | Medline11
Burkhardt J ,Peacock WF ,Emerman CL . Predictors of emergency department observation unit outcomes. Acad Emerg Med 2005;12:869-874
CrossRef | Web of Science | Medline12
Diercks DB ,Peacock WF ,Kirk JD Weber JE . ED patients with heart failure: identification of an observational unit-appropriate cohort. Am J Emerg Med 2006;24:319-324
CrossRef | Web of Science | Medline13
Mueller C ,Scholer A ,Laule-Kilian K , et al. Use of B-type natriuretic peptide in the evaluation and management of acute dyspnea. N Engl J Med 2004;350:647-654
Full Text | Web of Science | Medline14
You JJ ,Austin PC ,Alter DA ,Ko DT ,Tu JV . Relation between cardiac troponin I and mortality in acute decompensated heart failure. Am Heart J 2007;153:462-470
CrossRef | Web of Science | Medline15
Peacock WF ,Emerman CL ,Doleh M ,Civic K ,Butt S . Retrospective review: the incidence of non-ST segment elevation MI in emergency department patients presenting with decompensated heart failure. Congest Heart Fail 2003;9:303-308
CrossRef | Medline16
Perna ER ,Macin SM ,Cimbaro Canella JP , et al. High levels of troponin T are associated with ventricular remodeling and adverse in-hospital outcome in heart failure. Med Sci Monit 2004;10:CR90-5
Web of Science | Medline17
Gattis WA ,O'Connor CM ,Hasselblad V ,Adams KF Jr ,Kobron I ,Gheorghiade M . Usefulness of an elevated troponin-I in predicting clinical events in patients admitted with acute heart failure and acute coronary syndrome (from the RITZ-4 trial). Am J Cardiol 2004;93:1436-1437
CrossRef | Web of Science | Medline18
Angheloiu GO ,Dickerson RP ,Ravakhah K . Etiology of troponin I elevation in patients with congestive heart failure and low clinical suspicion of myocardial infarction. Resuscitation 2004;63:195-201
CrossRef | Web of Science | Medline19
Wu AH ,Ford L . Release of cardiac troponin in acute coronary syndromes: ischemia or necrosis? Clin Chim Acta 1999;284:161-174
CrossRef | Web of Science | Medline20
Mann DL . Mechanisms and models in heart failure: a combinatorial approach. Circulation 1999;100:999-1008
Web of Science | Medline21
Apple FS ,Wu AHB ,Jaffe AS . European Society of Cardiology and American College of Cardiology guidelines for redefinition of myocardial infarction: how to use existing assays clinically and for clinical trials. Am Heart J 2002;144:981-986
CrossRef | Web of Science | Medline
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Citing Articles
1
M. Usman Khan, Yaser Cheema, Atta U. Shahbaz, Robert A. Ahokas, Yao Sun, Ivan C. Gerling, Syamal K. Bhattacharya, Karl T. Weber. (2012) Mitochondria play a central role in nonischemic cardiomyocyte necrosis: common to acute and chronic stressor states. Pflügers Archiv - European Journal of Physiology
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Sean P. Collins, Christopher J. Lindsell, Alan B. Storrow, Gregory J. Fermann, Phillip D. Levy, Peter S. Pang, Neal Weintraub, W. Frank Peacock, Douglas B. Sawyer, Mihai Gheorghiade. (2011) Early changes in clinical characteristics after emergency department therapy for acute heart failure syndromes: identifying patients who do not respond to standard therapy. Heart Failure Reviews
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CrossRef6
N. Arenja, T. Reichlin, B. Drexler, S. Oshima, K. Denhaerynck, P. Haaf, M. Potocki, T. Breidthardt, M. Noveanu, C. Stelzig, C. Heinisch, R. Twerenbold, M. Reiter, T. Socrates, C. Mueller. (2011) Sensitive cardiac troponin in the diagnosis and risk stratification of acute heart failure. Journal of Internal Medicineno-no
CrossRef7
Sameer Ather, Ravi S. Hira, Maithili Shenoy, Omid Fatemi, Anita Deswal, David Aguilar, Kumudha Ramasubbu, Mariana Bolos, Wenyaw Chan, Biykem Bozkurt. (2011) Recurrent low-level Troponin I elevation is a worse prognostic indicator than occasional injury pattern in patients hospitalized with heart failure. International Journal of Cardiology
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Yukihito Sato, Erika Yamamoto, Takuma Sawa, Keizo Toda, Tomoko Hara, Toshiaki Iwasaki, Hisayoshi Fujiwara, Yoshiki Takatsu. (2011) High-sensitivity cardiac troponin T in essential hypertension. Journal of Cardiology 58:3, 226-231
CrossRef9
G. Michael Felker. (2011) Biomarkers as Surrogate End Points in Heart Failure Trials. Heart Failure Clinics 7:4, 501-507
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Chiho Kawahara, Takayoshi Tsutamoto, Hiroshi Sakai, Keizo Nishiyama, Masayuki Yamaji, Masanori Fujii, Takashi Yamamoto, Minoru Horie. (2011) Prognostic value of serial measurements of highly sensitive cardiac troponin I in stable outpatients with nonischemic chronic heart failure. American Heart Journal 162:4, 639-645
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M. Calderón Moreno, A.I. Castuera Gil, F.J. de Castro Martínez, E. Gargallo García. (2011) Insuficiencia cardiaca aguda. Medicine - Programa de Formación Médica Continuada Acreditado 10:88, 5932-5939
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Alan Maisel. (2011) Biomonitoring and Biomarker-Guided Therapy. Journal of the American College of Cardiology 58:18, 1890-1892
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Brian C Hiestand. (2011) Research in acute decompensated heart failure: challenges and opportunities. Clinical Investigation 1:10, 1361-1373
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CrossRef15
Kai M. Eggers, Magnus Nygren, Per Venge, Tomas Jernberg, Bernt G. Wikström. (2011) High-sensitive troponin T and I are related to invasive hemodynamic data and mortality in patients with left-ventricular dysfunction and precapillary pulmonary hypertension. Clinica Chimica Acta 412:17-18, 1582-1588
CrossRef16
Antwon D. Robinson, Kodangudi B. Ramanathan, Jesse E. McGee, Kevin P. Newman, Karl T. Weber. (2011) Oxidative Stress and Cardiomyocyte Necrosis With Elevated Serum Troponins: Pathophysiologic Mechanisms. The American Journal of the Medical Sciences 342:2, 129-134
CrossRef17
B. J. Borkowski, Y. Cheema, A. U. Shahbaz, S. K. Bhattacharya, K. T. Weber. (2011) Cation dyshomeostasis and cardiomyocyte necrosis: the Fleckenstein hypothesis revisited. European Heart Journal 32:15, 1846-1853
CrossRef18
Yaser Cheema, Jonathan N Sherrod, Wenyuan Zhao, Tieqiang Zhao, Robert A Ahokas, Yao Sun, Ivan C Gerling, Syamal K Bhattacharya, Karl T Weber. (2011) Mitochondriocentric Pathway to Cardiomyocyte Necrosis in Aldosteronism: Cardioprotective Responses to Carvedilol and Nebivolol. Journal of Cardiovascular Pharmacology 58:1, 80-86
CrossRef19
Vijaiganesh Nagarajan, W. H. Wilson Tang. (2011) Biomarkers in Advanced Heart Failure: Diagnostic and Therapeutic Insights. Congestive Heart Failure 17:4, 169-174
CrossRef20
D. A. Pascual-Figal, S. Manzano-Fernandez, M. Boronat, T. Casas, I. P. Garrido, J. C. Bonaque, F. Pastor-Perez, M. Valdes, J. L. Januzzi. (2011) Soluble ST2, high-sensitivity troponin T- and N-terminal pro-B-type natriuretic peptide: complementary role for risk stratification in acutely decompensated heart failure. European Journal of Heart Failure 13:7, 718-725
CrossRef21
Gabriel Greenberg, Eytan Cohen, Moshe Garty, Zaza Iakobishvili, Amir Sandach, Solomon Behar, Avraham Shotan, Shmuel Gottlieb, Aviv Mager, Alexander Battler, David Hasdai. (2011) Outcomes of acute heart failure associated with acute coronary syndrome versus other causes. Acute Cardiac Care 13:2, 87-92
CrossRef22
Edward E. Payne, Brian K. Roberts, Nick Schroeder, Ronald L. Burk, Thomas Schermerhorn. (2011) Assessment of a point-of-care cardiac troponin I test to differentiate cardiac from noncardiac causes of respiratory distress in dogs. Journal of Veterinary Emergency and Critical Care 21:3, 217-225
CrossRef23
Maria Rosa Costanzo, Mariell Jessup. (2011) Treatment of congestion in heart failure with diuretics and extracorporeal therapies: effects on symptoms, renal function, and prognosis. Heart Failure Reviews
CrossRef24
Andrew Ambrosy, Jane Wilcox, Savina Nodari, Mihai Gheorghiade. (2011) Acute heart failure syndromes: assessment and reconstructing the heart. Journal of Cardiovascular Medicine1
CrossRef25
S. Agewall, E. Giannitsis, T. Jernberg, H. Katus. (2011) Troponin elevation in coronary vs. non-coronary disease. European Heart Journal 32:4, 404-411
CrossRef26
Michael R. Bennett, Prasad Devarajan. (2011) Proteomic analysis of acute kidney injury: Biomarkers to mechanisms. PROTEOMICS - Clinical Applications 5:1-2, 67-77
CrossRef27
Malay S. Gandhi, German Kamalov, Atta U. Shahbaz, Syamal K. Bhattacharya, Robert A. Ahokas, Yao Sun, Ivan C. Gerling, Karl T. Weber. (2011) Cellular and molecular pathways to myocardial necrosis and replacement fibrosis. Heart Failure Reviews 16:1, 23-34
CrossRef28
Olga Milo-Cotter, Beth Cotter-Davison, Carlo Lombardi, Hengrui Sun, Luca Bettari, Silvia Bugatti, Michele Rund, Marco Metra, Edo Kaluski, Isaac Kobrin, Aline Frey, Maurizio Rainisio, John J.V. McMurray, John R. Teerlink, Gad Cotter-Davison. (2011) Neurohormonal Activation in Acute Heart Failure: Results from VERITAS. Cardiology 119:2, 96-105
CrossRef29
Marcella Canton, Sara Menazza, Freya L. Sheeran, Patrizia Polverino de Laureto, Fabio Di Lisa, Salvatore Pepe. (2011) Oxidation of Myofibrillar Proteins in Human Heart Failure. Journal of the American College of Cardiology 57:3, 300-309
CrossRef30
Carl V. Leier. (2011) Coronary Microcirculation Remodelling in Dilated Cardiomyopathy: Another Brick in the Wall. Cardiology 119:4, 206-207
CrossRef31
Gerd Heusch, Rainer Schulz. (2011) A Radical View on the Contractile Machinery in Human Heart Failure
Editorials published in the Journal of the American College of Cardiology reflect the views of the authors and do not necessarily represent the views of JACC or the American College of Cardiology.. Journal of the American College of Cardiology 57:3, 310-312
CrossRef32
Husam M. Abdel-Qadir, Shaan Chugh, Douglas S. Lee. (2011) Improving Prognosis Estimation in Patients with Heart Failure and the Cardiorenal Syndrome. International Journal of Nephrology 2011, 1-11
CrossRef33
Y. Xue, P. Clopton, W. F. Peacock, A. S. Maisel. (2011) Serial changes in high-sensitive troponin I predict outcome in patients with decompensated heart failure. European Journal of Heart Failure 13:1, 37-42
CrossRef34
Andrew Binder, Ignacio M. Seropian, Michael C. Kontos, Benjamin W. Van Tassell, Giuseppe G.L. Biondi-Zoccai, Antonio Abbate. (2010) Limited value of brain natriuretic peptide as a prognostic marker in acute heart failure — A meta-analysis. International Journal of Cardiology 145:3, 540-541
CrossRef35
Kirkwood F. Adams, Mandeep R. Mehra, Ron M. Oren, Christopher M. O'Connor, Jun R. Chiong, Jalal K. Ghali, Daniel J. Lenihan, Stephanie H. Dunlap, J. Herbert Patterson, Todd A. Schwartz, G. Michael Felker. (2010) Prospective evaluation of the association between cardiac troponin T and markers of disturbed erythropoiesis in patients with heart failure. American Heart Journal 160:6, 1142-1148
CrossRef36
Takahiro Ohara, William C Little. (2010) Evolving focus on diastolic dysfunction in patients with coronary artery disease. Current Opinion in Cardiology 25:6, 613-621
CrossRef37
Leo Slavin, Thomas K. Ro, Alan S. Maisel. 2010. Biomarkers in Heart Failure. , 27-43.
CrossRef38
John R. Teerlink. 2010. Treatment of Acutely Decompensated Heart Failure. , 327-356.
CrossRef39
Marco Metra, G. Michael Felker, Valerio Zacà, Silvia Bugatti, Carlo Lombardi, Luca Bettari, Adrian A. Voors, Mihai Gheorghiade, Livio Dei Cas. (2010) Acute heart failure: Multiple clinical profiles and mechanisms require tailored therapy. International Journal of Cardiology 144:2, 175-179
CrossRef40
Ing-Kit Lee, Wen-Huei Lee, Jien-Wei Liu, Kuender D. Yang. (2010) Acute myocarditis in dengue hemorrhagic fever: a case report and review of cardiac complications in dengue-affected patients. International Journal of Infectious Diseases 14:10, e919-e922
CrossRef41
Gregory J. Fermann, Sean P. Collins. (2010) Observation Units in the Management of Acute Heart Failure Syndromes. Current Heart Failure Reports 7:3, 125-133
CrossRef42
Robb D. Kociol, Peter S. Pang, Mihai Gheorghiade, Gregg C. Fonarow, Christopher M. O'Connor, G. Michael Felker. (2010) Troponin Elevation in Heart Failure. Journal of the American College of Cardiology 56:14, 1071-1078
CrossRef43
German Kamalov, Syamal K Bhattacharya, Karl T Weber. (2010) Congestive Heart Failure: Where Homeostasis Begets Dyshomeostasis. Journal of Cardiovascular Pharmacology 56:3, 320-328
CrossRef44
R. V. Shah, A. A. Chen-Tournoux, M. H. Picard, R. R. J. van Kimmenade, J. L. Januzzi. (2010) Galectin-3, cardiac structure and function, and long-term mortality in patients with acutely decompensated heart failure. European Journal of Heart Failure 12:8, 826-832
CrossRef45
J. Nunez, J. Sanchis, V. Bodi, G. C. Fonarow, E. Nunez, V. Bertomeu-Gonzalez, G. Minana, L. Consuegra, M. J. Bosch, A. Carratala, F. J. Chorro, A. Llacer. (2010) Improvement in risk stratification with the combination of the tumour marker antigen carbohydrate 125 and brain natriuretic peptide in patients with acute heart failure. European Heart Journal 31:14, 1752-1763
CrossRef46
Pam R. Taub, Paulette Gabbai-Saldate, Alan Maisel. (2010) Biomarkers of Heart Failure. Congestive Heart Failure 16, S19-S24
CrossRef47
Kimberly D Tran, Niraj V Parekh, Alan S Maisel. (2010) Natriuretic peptides in heart failure. Therapy 7:4, 355-365
CrossRef48
W. Frank Peacock, Eugene Braunwald, William Abraham, Nancy Albert, John Burnett, Rob Christenson, Sean Collins, Deborah Diercks, Greg Fonarow, Judd Hollander, Art Kellerman, Mihai Gheorghiade, Doug Kirk, Phil Levy, Alan Maisel, Barry M. Massie, Christopher O'Connor, Peter Pang, Monica Shah, George Sopko, Lynne Stevenson, Alan Storrow, John Teerlink. (2010) National Heart, Lung, and Blood Institute Working Group on Emergency Department Management of Acute Heart Failure. Journal of the American College of Cardiology 56:5, 343-351
CrossRef49
Wilbert S. Aronow. (2010) Prognostic Value of Cardiac Troponins and Natriuretic Peptides in Hospitalized Nursing Home Residents. Journal of the American Medical Directors Association 11:6, 386-388
CrossRef50
Kirkwood F. Adams, G. Michael Felker, Ghassan Fraij, J. Herbert Patterson, Christopher M. O’Connor. (2010) Biomarker guided therapy for heart failure: focus on natriuretic peptides. Heart Failure Reviews 15:4, 351-370
CrossRef51
Almasa Bass, J. Herbert Patterson, Kirkwood F. Adams. (2010) Perspective on the clinical application of troponin in heart failure and states of cardiac injury. Heart Failure Reviews 15:4, 305-317
CrossRef52
Michael N. Zairis, George Z. Tsiaousis, Anastassios Theodossis Georgilas, Stamatis S. Makrygiannis, Evdokia N. Adamopoulou, Stelios M. Handanis, Pelagia C. Batika, Athanasios A. Prekates, Dimitris Velissaris, Nikolaos T. Kouris, Demetrios Z. Mytas, Demetrios K. Babalis, Kostas S. Karidis, Stefanos G. Foussas. (2010) Multimarker strategy for the prediction of 31 days cardiac death in patients with acutely decompensated chronic heart failure. International Journal of Cardiology 141:3, 284-290
CrossRef53
Tetsuji Miura, Masaya Tanno. (2010) Mitochondria and GSK-3β in Cardioprotection Against Ischemia/Reperfusion Injury. Cardiovascular Drugs and Therapy 24:3, 255-263
CrossRef54
Sam L. Teichman, Elaine Unemori, John R. Teerlink, Gad Cotter, Marco Metra. (2010) Relaxin: Review of Biology and Potential Role in Treating Heart Failure. Current Heart Failure Reports 7:2, 75-82
CrossRef55
Kimi Koide, Tsutomu Yoshikawa, Yuji Nagatomo, Shun Kohsaka, Toshihisa Anzai, Tomomi Meguro, Satoshi Ogawa. (2010) Elevated troponin T on discharge predicts poor outcome of decompensated heart failure. Heart and Vessels 25:3, 217-222
CrossRef56
Alan Maisel, Christian Mueller, Richard Nowak, W. Frank Peacock, Judd W. Landsberg, Piotr Ponikowski, Martin Mockel, Christopher Hogan, Alan H.B. Wu, Mark Richards, Paul Clopton, Gerasimos S. Filippatos, Salvatore Di Somma, Inder Anand, Leong Ng, Lori B. Daniels, Sean-Xavier Neath, Robert Christenson, Mihael Potocki, James McCord, Garret Terracciano, Dimitrios Kremastinos, Oliver Hartmann, Stephan von Haehling, Andreas Bergmann, Nils G. Morgenthaler, Stefan D. Anker. (2010) Mid-Region Pro-Hormone Markers for Diagnosis and Prognosis in Acute Dyspnea. Journal of the American College of Cardiology 55:19, 2062-2076
CrossRef57
P. S. Pang, M. Komajda, M. Gheorghiade. (2010) The current and future management of acute heart failure syndromes. European Heart Journal 31:7, 784-793
CrossRef58
Alberto Morales Salinas, Antonio Coca. (2010) Obesidad, actividad física y riesgo cardiovascular: clasificación ergoantropométrica, variables farmacológicas, biomarcadores y «paradoja del obeso». Medicina Clínica 134:11, 492-498
CrossRef59
Prasad Devarajan. (2010) Neutrophil gelatinase-associated lipocalin: a promising biomarker for human acute kidney injury. Biomarkers in Medicine 4:2, 265-280
CrossRef60
Britta Goldmann, Thomas Meinertz. (2010) Benefits of biomarkers in heart failure. Clinical Research in Cardiology Supplements 5:S1, 21-26
CrossRef61
German Kamalov, Robert A Ahokas, Wenyuan Zhao, Tieqiang Zhao, Atta U Shahbaz, Patti L Johnson, Syamal K Bhattacharya, Yao Sun, Ivan C Gerling, Karl T Weber. (2010) Uncoupling the Coupled Calcium and Zinc Dyshomeostasis in Cardiac Myocytes and Mitochondria Seen in Aldosteronism. Journal of Cardiovascular Pharmacology 55:3, 248-254
CrossRef62
Steven R. Goldsmith, Filippo Brandimarte, Mihai Gheorghiade. (2010) Congestion as a Therapeutic Target in Acute Heart Failure Syndromes. Progress in Cardiovascular Diseases 52:5, 383-392
CrossRef63
Peter E. Hickman, Julia M. Potter, Con Aroney, Gus Koerbin, Emma Southcott, Alan H.B. Wu, Michael S. Roberts. (2010) Cardiac troponin may be released by ischemia alone, without necrosis. Clinica Chimica Acta 411:5-6, 318-323
CrossRef64
Serge Masson, Roberto Latini, Inder S. Anand. (2010) An Update on Cardiac Troponins as Circulating Biomarkers in Heart Failure. Current Heart Failure Reports 7:1, 15-21
CrossRef65
T. Breidthardt, M. Noveanu, M. Potocki, T. Reichlin, P. Egli, S. Hartwiger, T. Socrates, E. Gayat, M. Christ, A. Mebazaa, C. Mueller. (2010) Impact of a high-dose nitrate strategy on cardiac stress in acute heart failure: a pilot study. Journal of Internal Medicine 267:3, 322-330
CrossRef66
Yoshitaka Iwanaga, Shunichi Miyazaki. (2010) Heart Failure, Chronic Kidney Disease, and Biomarkers. Circulation Journal 74:7, 1274-1282
CrossRef67
Mitja Lainscak, Markus S. Anker, Stephan Haehling, Stefan D. Anker. (2009) Biomarkers for Chronic Heart Failure. Herz 34:8, 589-593
CrossRef68
Bernhard C. Danner, Vassilios N. Didilis, Tomislav Stojanovic, Aron Popov, Marius Grossmann, Ralf Seipelt, Friedrich A. Schöndube. (2009) A Three-Group Model to Predict Mortality in Emergent Coronary Artery Bypass Graft Surgery. The Annals of Thoracic Surgery 88:5, 1433-1439
CrossRef69
Bill P.C. Hsieh, Adam M. Rogers, Beeya Na, Alan H.B. Wu, Nelson B. Schiller, Mary A. Whooley. (2009) Prevalence and prognostic significance of incidental cardiac troponin T elevation in ambulatory patients with stable coronary artery disease: Data from The Heart and Soul Study. American Heart Journal 158:4, 673-679
CrossRef70
Colette E Jackson, Jonathan R Dalzell, Roy S Gardner. (2009) Prognostic utility of cardiac troponin in heart failure: a novel role for an established biomarker. Biomarkers in Medicine 3:5, 483-493
CrossRef71
WH Wilson Tang. (2009) Biomarkers of risk stratification in congestive heart failure: North American view. Biomarkers in Medicine 3:5, 443-452
CrossRef72
Roberto Latini, Serge Masson. (2009) Biomarkers of Myocyte Injury in Heart Failure. Heart Failure Clinics 5:4, 529-536
CrossRef73
R. V. Shah, A. A. Chen-Tournoux, M. H. Picard, J. L. Januzzi. (2009) Association between troponin T and impaired left ventricular relaxation in patients with acute decompensated heart failure with preserved systolic function. European Journal of Echocardiography 10:6, 765-768
CrossRef74
Johan Sundström. (2009) Troponin and heart failure: an early warning system worth listening to?. Future Cardiology 5:4, 321-324
CrossRef75
Maliha Zahid, Chester B. Good, Ish Singla, Ali F. Sonel. (2009) Clinical Significance of Borderline Elevated Troponin I Levels Across Different Assays in Patients With Suspected Acute Coronary Syndrome. The American Journal of Cardiology 104:2, 164-168
CrossRef76
T. Tsutamoto, C. Kawahara, M. Yamaji, K. Nishiyama, M. Fujii, T. Yamamoto, M. Horie. (2009) Relationship between renal function and serum cardiac troponin T in patients with chronic heart failure. European Journal of Heart Failure 11:7, 653-658
CrossRef77
MOHAMAD A. ALAITI, ANJLI MAROO, THOMAS B. EDEL. (2009) Troponin Levels after Cardiac Electrophysiology Procedures: Review of the Literature. Pacing and Clinical Electrophysiology 32:6, 800-810
CrossRef78
Christopher A. Paciullo, Steven P. Dunn, Tracy E. Macaulay, Kelly M. Smith. (2009) Heart Failure Management Strategies in a Surgical Population. Orthopedics 32:6, 421-426
CrossRef79
Mitja Lainscak, Stephan von Haehling, Stefan D. Anker. (2009) Natriuretic peptides and other biomarkers in chronic heart failure: From BNP, NT-proBNP, and MR-proANP to routine biochemical markers. International Journal of Cardiology 132:3, 303-311
CrossRef80
Alan H.B. Wu. (2009) Interpretation of high sensitivity cardiac troponin I results: Reference to biological variability in patients who present to the emergency room with chest pain: Case report series. Clinica Chimica Acta 401:1-2, 170-174
CrossRef81
David C. Sane, Nathan P. Streer, John Owen. (2009) Myocardial necrosis in patients with thrombotic thrombocytopenic purpura: pathophysiology and rationale for specific therapy. European Journal of Haematology 82:2, 83-92
CrossRef82
Justin A. Ezekowitz, Adrian F. Hernandez, Randall C. Starling, Clyde W. Yancy, Barry Massie, James A. Hill, Henry Krum, Rafael Diaz, Piotr Ponikowski, Marco Metra, Jonathon G. Howlett, Daniel Gennevois, Christopher M. O'Connor, Robert M. Califf, Gregg C. Fonarow. (2009) Standardizing care for acute decompensated heart failure in a large megatrial: The approach for the Acute Studies of Clinical Effectiveness of Nesiritide in Subjects with Decompensated Heart Failure (ASCEND-HF). American Heart Journal 157:2, 219-228
CrossRef83
Mihai Gheorghiade, Peter S. Pang. (2009) Acute Heart Failure Syndromes. Journal of the American College of Cardiology 53:7, 557-573
CrossRef84
W. Frank Peacock, Karina M. Soto-Ruiz. (2009) Risk stratification for suspected acute coronary syndromes and heart failure in the emergency department. Acute Cardiac Care 11:3, 138-145
CrossRef85
Josep Comín Colet, Roberto Muñoz Aguilera, José J. Cuenca Castillo, Juan F. Delgado Jiménez. (2009) Temas de actualidad en insuficiencia cardiaca. Revista Española de Cardiología 62, 92-100
CrossRef86
James D. Flaherty, Jeroen J. Bax, Leonardo De Luca, Joseph S. Rossi, Charles J. Davidson, Gerasimos Filippatos, Peter P. Liu, Marvin A. Konstam, Barry Greenberg, Mandeep R. Mehra, Günter Breithardt, Peter S. Pang, James B. Young, Gregg C. Fonarow, Robert O. Bonow, Mihai Gheorghiade. (2009) Acute Heart Failure Syndromes in Patients With Coronary Artery Disease. Journal of the American College of Cardiology 53:3, 254-263
CrossRef87
J. Sundstrom, E. Ingelsson, L. Berglund, B. Zethelius, L. Lind, P. Venge, J. Arnlov. (2008) Cardiac troponin-I and risk of heart failure: a community-based cohort study. European Heart Journal 30:7, 773-781
CrossRef88
Mariell Jessup, Iván J. Núñez-Gil. (2008) Insuficiencia cardiaca y asistencias ventriculares: nuevas respuestas para antiguas preguntas. Revista Española de Cardiología 61:12, 1231-1235
CrossRef89
Christian Mueller. (2008) Risk stratification in acute decompensated heart failure: the role of cardiac troponin. Nature Clinical Practice Cardiovascular Medicine 5:11, 680-681
CrossRef90
L. J. Hickson, F. G. Cosio, Z. M. El-Zoghby, J. M. Gloor, W. K. Kremers, M. D. Stegall, M. D. Griffin, A. S. Jaffe. (2008) Survival of Patients on the Kidney Transplant Wait List: Relationship to Cardiac Troponin T. American Journal of Transplantation 8:11, 2352-2359
CrossRef91
P. Devarajan. (2008) Neutrophil gelatinase-associated lipocalin--an emerging troponin for kidney injury. Nephrology Dialysis Transplantation 23:12, 3737-3743
CrossRef92
Braunwald, Eugene, . (2008) Biomarkers in Heart Failure. New England Journal of Medicine 358:20, 2148-2159
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