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J Am Coll Cardiol, 2004; 44:335-339, doi:10.1016/j.jacc.2004.04.033
© 2004 by the American College of Cardiology Foundation
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CLINICAL RESEARCH: PROGNOSTIC MARKERS IN ACUTE MI

B-type natriuretic peptide at presentation and prognosis in patients with ST-segment elevation myocardial infarction

An ENTIRE–TIMI-23 substudy

Jessica L. Mega, MD*, David A. Morrow, MD, MPH, FACC*{dagger},*, James A. de Lemos, MD, FACC{ddagger}, Marc S. Sabatine, MD, MPH*{dagger}, Sabina A. Murphy, MPH*, Nader Rifai, PhD§, C. Michael Gibson, MD, FACC*, Elliott M. Antman, MD, FACC*{dagger} and Eugene Braunwald, MD, FACC*{dagger}

* TIMI Study Group, Boston, Massachusetts 02115, USA
{dagger} Cardiovascular Division, Brigham and Women's Hospital, Boston, Massachusetts, USA
{ddagger} University of Texas Southwestern Medical Center, Dallas, Texas, USA
§ Children's Hospital, Boston, Massachusetts, USA

Manuscript received February 6, 2004; revised manuscript received March 27, 2004, accepted April 6, 2004.

* Reprint requests and correspondence: Dr. David A. Morrow, TIMI Study Group/Cardiovascular Division, Brigham and Women's Hospital, 75 Francis Street, Boston, Massachusetts 02115, USA.
dmorrow{at}partners.org


   Abstract
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 Abstract
Methods
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 Discussion
 References
 
OBJECTIVES: We sought to evaluate B-type natriuretic peptide (BNP), alone and in comparison to cardiac troponin I (cTnI) and high-sensitivity C-reactive protein (hs-CRP), for risk assessment at initial presentation with ST-segment elevation myocardial infarction (STEMI).

BACKGROUND: Elevated levels of BNP drawn two to four days after acute myocardial infarction are associated with higher mortality. Sparse data are available on its use at first presentation with STEMI.

METHODS: We obtained samples from 438 patients presenting within 6 h of STEMI enrolled in the Enoxaparin Tenecteplase-Tissue-Type Plasminogen Activator With or Without Glycoprotein IIb/IIIa Inhibitor as Reperfusion Strategy in ST-Segment Elevation Myocardial Infarction (ENTIRE)–Thrombolysis In Myocardial Infarction (TIMI)-23 trial. Outcomes were assessed through 30 days.

RESULTS: Median BNP was higher in patients who died (89 pg/ml, 25th to 75th percentile: 40 to 192), compared with survivors (15 pg/ml, 25th to 75th percentile: 8.8 to 32, p < 0.0001). Patients with BNP >80 pg/ml were at significantly higher risk of death (17.4% vs. 1.8%, p < 0.0001). Cardiac troponin established a gradient of mortality between the highest and lowest quartile (7.9% vs. 0%, p = 0.007). C-reactive protein was not associated with outcome. After adjustment for cTnI, hs-CRP, and major clinical predictors, including age, heart failure, anterior myocardial infarction location, heart rate, and blood pressure, a BNP level >80 pg/ml was associated with a seven-fold higher mortality risk (odds ratio 7.2, 95% confidence interval 2.1 to 24.5, p = 0.001). Patients with BNP >80 pg/ml were also more likely to have impaired coronary flow (p = 0.049) and incomplete resolution of ST-segment elevation (p = 0.05).

CONCLUSIONS: Increased concentrations of BNP at initial presentation of patients with STEMI are associated with impaired reperfusion after fibrinolysis and higher short-term risk of mortality. These data support the value of combining markers of hemodynamic stress with traditional approaches to risk assessment in acute myocardial infarction.

B-type natriuretic peptide (BNP) is released from the cardiac ventricles in response to increased wall stress (1). It has emerged as an aid to diagnosing congestive heart failure (CHF) (2) and has subsequently been studied in the setting of acute coronary syndromes, where the plasma concentration rises rapidly over 24 h after ST-segment elevation myocardial infarction (STEMI) (3–5). When measured two to seven days after infarction, elevated levels of BNP identify patients with lower survival (6–9). Because of the time-dependent rise in BNP, the value of very early determinations is less clear, and there are sparse data addressing the prognostic implications of BNP drawn at the time of presentation with STEMI (4). Moreover, the prognostic value of BNP relative to other biomarkers has not been assessed in this setting.

We thus evaluated the prognostic performance and clinical correlates of BNP, assessed at the time of presentation, along with cardiac troponin I (cTnI) and high-sensitivity C-reactive protein (hs-CRP) among patients with STEMI in the Enoxaparin Tenecteplase-Tissue-Type Plasminogen Activator With or Without Glycoprotein IIb/IIIa Inhibitor as Reperfusion Strategy in ST-Segment Elevation Myocardial Infarction (ENTIRE)–Thrombolysis In Myocardial Infarction (TIMI)-23 trial.


   Methods
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Results
 Discussion
 References
 
Study population.   The ENTIRE–TIMI-23 trial randomized 483 patients with STEMI to either full-dose tenecteplase (TNK)–tissue-type plasminogen activator (tPA) or half-dose TNK-tPA plus abciximab and to either unfractionated heparin or enoxaparin (10). Patients age 21 to 75 years presenting within 6 h were eligible. Exclusion criteria included shock, pulmonary edema requiring intubation, and creatinine clearance ≤30 ml/min. The protocol and biomarker substudy were approved by the institutional review board at each institution, and all patients provided written, informed consent.

Procedures.   Angiography performed 55 to 75 min after reperfusion therapy was interpreted by the TIMI Angiographic Core Laboratory in Boston. Myocardial tissue-level reperfusion was categorized by the TIMI myocardial perfusion grade. ST-segment resolution was assessed using predefined criteria at 180 min after fibrinolysis (11). Blood samples were obtained before fibrinolysis for analysis of cardiac biomarkers. Patients were followed through 30 days (10).

Biomarker testing.   B-type natriuretic peptide was measured in EDTA-anticoagulated plasma using the ADVIA Centaur BNP assay (Bayer, Tarrytown, New York). This assay has a minimal detectable concentration of <2.0 pg/ml and a total imprecision of 4.7% and 2.8% at 29 pg/ml and 410 pg/ml, respectively. The assay is calibrated to have the same cut-point for diagnosis of CHF as an existing method (2). Troponin I was measured using the ACS:180 (Bayer) with a decision limit of 0.1 ng/ml (12). High-sensitivity testing for CRP was performed using an immunonephelometric assay (Dade-Behring, Newark, Delaware). The decision limit (15 mg/l) was prespecified (13).

Statistical analysis.   The plasma levels of BNP were described by the median (interquartile range). The concentration of BNP was also categorized into quartiles and dichotomized using a prespecified decision limit (80 pg/ml) (14,15). An exploratory evaluation of additional cut-points was performed using receiver-operating characteristics (ROC). The baseline characteristics of patients with and without elevated BNP were compared using the Wilcoxon rank-sum test for continuous variables and the chi-square test for categorical variables. The association between each biomarker and clinical outcomes was evaluated using the chi-square or Fisher exact test for dichotomized comparisons and the chi-square test for trend across quartiles. Multivariate analyses of the association between BNP and outcomes were performed using logistic regression to adjust for the other biomarkers and for major clinical predictors of mortality (age, anterior myocardial infarction [MI] location, time from symptom onset, heart rate, blood pressure, and CHF at presentation), as captured by the TIMI risk score for STEMI. All analyses were performed using STATA v7-intercooled (STATA Corp., College Station, Texas).


   Results
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 Methods
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Discussion
 References
 
The BNP results were available for 438 patients (91%). The median concentration of BNP at presentation was 15.6 pg/ml (25th to 75th percentile: 9.1 to 32.6). Patients with elevated levels (>80 pg/ml) were older and more likely to have a history of hypertension, angina, and CHF (Table 1). Consistent with the greater prevalence of angina and CHF, they were also more likely to be receiving beta-blockers and angiotensin-converting enzyme inhibitors at presentation. The proportion of patients with elevated BNP did not differ between men and women. The median time from symptom onset was longer in patients with elevated BNP.


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  		Table 1 Univariate Associations With Elevated Levels of BNP

 
Prognosis and BNP.   The baseline concentration of BNP was significantly higher in the 15 patients who died by 30 days (89 pg/ml, 25th to 75th percentile: 40 to 192), compared with the 423 survivors (15 pg/ml, 25th to 75th percentile: 8.8 to 32, p < 0.0001). The relationships between the baseline concentration of BNP (quartiles) and clinical outcomes are detailed in Table 2. Patients with BNP in the highest quartile had an 11-fold higher risk of death compared to quartiles 1 to 3 (p < 0.0001). When treated dichotomously, BNP >80 pg/ml was associated with a significantly higher risk of death through 30 days (p < 0.0001) (Figs. 1 and 2). A trend toward more frequent new or worsening CHF was also apparent among those with BNP >80 pg/ml (8.7% vs. 3.3%, p = 0.09), with a consequently increased risk of death or CHF (23.9% vs. 5.1, p < 0.0001).


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  		Table 2 Association Between Biomarkers and Clinical Outcomes

 


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  		Figure 1 Relationship between elevated biomarkers and mortality at 30 days. Positive results (solid bars) were defined as B-type natriuretic peptide (BNP) >80 pg/ml, cardiac troponin ≥0.1 ng/ml, and high sensitivity C-reactive protein (CRP) ≥15 mg/l (negative results = open bars).

 


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  		Figure 2 Probability of death through 30 days stratified by B-type natriuretic peptide (BNP).

 
In addition to evaluating the prespecified decision limit, we performed an exploratory analysis of alternative cut-points. The ROC analysis indicated an optimal cut-point in this data set of <80 pg/ml (Fig. 3). Using a decision limit of 40 pg/ml, an elevated BNP was associated with a >10-fold higher risk of death (13.5% vs. 0.86%, p < 0.0001) and a nearly five-fold higher risk of death/CHF (19.1% vs. 4.0%, p < 0.0001). Notably, as a single predictor for mortality, BNP performed very well (c statistic = 0.81).



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  		Figure 3 The receiver-operator characteristic curve for B-type natriuretic peptide at 10-pg/ml intervals for predicting death at 30 days.

 
Clinical predictors and BNP and other biomarkers
Compared with cTnI and hs-CRP, BNP was a substantially more robust marker of 30-day mortality (Fig. 1). C-reactive protein was not associated with mortality or recurrent MI in this study. Patients with cTnI in the highest quartile were at increased risk of death (Table 2). However, cTnI did not offer prognostic information independent of BNP (p = 0.9, adjusted for BNP). In contrast, BNP maintained an independent contribution to risk assessment. Among patients with positive cTnI results, those with BNP >80 pg/ml were at significantly higher risk of death at 30 days (p < 0.0001) (Fig. 4). In addition, although few patients with negative initial cTnI results had elevated BNP, a trend toward higher mortality was also evident among this group (p = 0.081).



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  		Figure 4 Association of B-type natriuretic peptide (BNP), in conjunction with cardiac troponin and high sensitivity C-reactive protein (CRP), with mortality at 30 days. Positive results (solid bars) were defined as BNP >80 pg/ml, cardiac troponin ≥0.1 ng/ml, and high sensitivity CRP ≥15 mg/l (negative results = open bars).

 
Moreover, assessed using logistic regression, BNP remained independently associated with mortality (odds ratio [OR] 7.2, 95% confidence interval [CI] 2.1 to 24.5, p = 0.001) after adjustment for cTnI and hs-CRP (evaluated as dichotomous and continuous variables), as well as major clinical predictors of mortality (age, anterior MI location, time from symptom onset to fibrinolysis, heart rate, blood pressure, and CHF at presentation). This independent risk relationship with BNP was unaltered (OR 8.2, 95% CI 2.3 to 28.4, p = 0.001) when the population was restricted to those with no history of CHF. The prognostic association between BNP and mortality was even stronger using a cut-point of 40 pg/ml (OR 15.9, 95% CI 3.1 to 81, p = 0.001; likelihood ratio test vs. 80 pg/ml, p = 0.02).

Angiographic and electrocardiographic observations
Elevated BNP at presentation was associated with evidence of subsequent impaired epicardial and myocardial reperfusion. Specifically, patients with BNP >80 pg/ml were more likely to have incomplete reperfusion of the infarct-related artery (Table 3). In addition, elevated BNP was associated with incomplete (<70%) resolution of ST-segment elevation, an indicator of impaired myocardial tissue-level reperfusion (95.8% vs. 79.2%, p = 0.05) (Table 3) (11). The baseline concentration of BNP was not a surrogate for extent of necrosis (Spearman's rho = –0.065 for creatine kinase-MB fraction, p = 0.19).


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  		Table 3 Association Between Biomarkers, Coronary Flow, and Electrocardiographic Abnormalities

 

   Discussion
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 Abstract
 Methods
 Results
 Discussion
References
 
In this study of concurrent assessment of BNP, cTnI, and hs-CRP at the time of presentation with STEMI, we found that BNP was a robust and independent indicator of mortality risk, with risk assessment performance superior to cTnI or hs-CRP. Even when assessed early after symptom onset, BNP maintained the strong prognostic relationship evident in previous studies with later sample acquisition (1).

Clinical application of biomarkers in STEMI.   Cardiac biomarkers provide prognostic information that is incremental to clinical predictors in patients with STEMI. Patients with elevated cTnT at the time of presentation have two- to three-fold higher mortality risk at 30 days, independent of the time from symptom onset (16). Sparse data exist on the prognostic importance of hs-CRP in STEMI. In one study, patients with elevated CRP were more likely to suffer complications of acute MI (myocardial rupture, ventricular aneurysm, and death by one year) (17). The contrasting absence of a relationship between hs-CRP and outcome in the ENTIRE–TIMI-23 trial may relate both to the very early sample acquisition and the assessment of short- rather than long-term outcomes.

Including our present analysis, BNP has been evaluated in at least seven studies of patients with STEMI (1,3,4,6–8). Together, these studies provide consistent evidence for the additive prognostic value of BNP. Although BNP levels are correlated with age, gender, intracardiac pressures, ejection fraction, and renal function, BNP provides prognostic information that is independent of these variables. Moreover, whether measured at presentation, as in the present report, or later during recovery, BNP is one of the most robust indicators of mortality risk. This strong prognostic association in STEMI parallels that among patients with non–ST-segment elevation acute coronary syndromes (15). An important and, as yet, unanswered question is whether biomarkers, such as BNP, evaluated in STEMI should be used to select specific therapies.

Mechanistic information provided in this and other studies (18) points toward hypotheses regarding interventions that may ameliorate this risk. We have shown that an elevated BNP level before fibrinolysis is associated with a lower likelihood of successful epicardial and myocardial reperfusion. Although not directly addressed in this study, we may speculate that underlying left ventricular hypertrophy, unrecognized left ventricular dysfunction, and/or a large territory of infarct/ischemia may be contributing to the increased concentration of BNP and are associated with impaired reperfusion and increased mortality. Therefore, patients with elevated BNP may be particularly appropriate candidates for primary angioplasty and for transfer when presenting to hospitals without available catheterization facilities. Others have shown that when measured subacutely after MI, elevated BNP identifies patients at risk of adverse left ventricular remodeling, chronic left ventricular dysfunction, and CHF (1). In this setting, routine treatment, even among patients without evident left ventricular dysfunction or CHF, with afterload-reducing agents or novel agents that may improve infarct healing or ventricular remodeling after MI, may be particularly beneficial.

Study limitations
Limitations to this analysis should be considered. First, given the relatively low mortality rate in this study, it is possible that an association between hs-CRP and short-term mortality could not be detected. However, the observations regarding the relative strength of the risk relationships for BNP compared with cTnI and hs-CRP are unlikely to be altered in a larger population. Second, although this study provides interesting data on the association of BNP with impaired reperfusion, it does not provide direct insight into the underlying pathobiology. Third, the prevalence of pre-existing CHF among patients presenting with STEMI in the community is higher than that observed in this trial. It is possible that the prognostic implications of elevated BNP in patients with chronic CHF presenting with STEMI differ from those of patients without chronic CHF. Also, the lower cut-point (40 pg/ml) may not be optimal in populations with a greater proportion of women and elderly. For these reasons, additional community-based studies with STEMI will be valuable.

Conclusions
In patients with STEMI, elevated levels of BNP at initial presentation are associated with impaired reperfusion after fibrinolysis and increased risk of short-term mortality. These data support the value of combining markers of hemodynamic stress, such as BNP, with established biomarkers of necrosis, for risk assessment at the time of presentation with acute MI.


   Footnotes
 
Aventis supported ENTIRE-TIMI 23. Bayer supported reagents and analysis costs. Drs. Mega and Morrow contributed equally to the drafting/editing of this manuscript.

Abbreviations: BNP, B-type natriuretic peptide; CHF, congestive heart failure; cTnI, cardiac troponin I; ENTIRE–TIMI-23, Enoxaparin Tenecteplase-Tissue-Type Plasminogen Activator With or Without Glycoprotein IIb/IIIa Inhibitor as Reperfusion Strategy in ST-Segment Elevation Myocardial Infarction (ENTIRE)–Thrombolysis In Myocardial Infarction (TIMI)-23 trial; hs-CRP, high-sensitivity C-reactive protein; MI, myocardial infarction; ROC, receiver-operating characteristics; STEMI, ST-segment elevation myocardial infarction; TNK-tPA, tenecteplase–tissue-type plasminogen activator.


   References
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 Abstract
 Methods
 Results
 Discussion
 References
 

  1. de Lemos JA, McGuire DK, Drazner MH. B-type natriuretic peptide in cardiovascular disease. Lancet. 2003;362:316–322[CrossRef][Medline]
  2. Maisel AS, Krishnaswamy P, Nowak RM, et al. Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure. N Engl J Med. 2002;347:161–167[Abstract/Free Full Text]
  3. Talwar S, Squire IB, Downie PF, et al. Profile of plasma N-terminal proBNP following acute myocardial infarction: Correlation with left ventricular systolic dysfunction. Eur Heart J. 2000;21:1514–1521[Abstract/Free Full Text]
  4. Morita E, Yasue H, Yoshimura M, et al. Increased plasma levels of brain natriuretic peptide in patients with acute myocardial infarction. Circulation. 1993;88:82–91[Abstract/Free Full Text]
  5. Motwani JG, McAlpine H, Kennedy N, Struthers AD. Plasma brain natriuretic peptide as an indicator for angiotensin-converting enzyme inhibition after myocardial infarction. Lancet. 1993;341:1109–1113[CrossRef][Medline]
  6. Omland T, Aakvaag A, Bonarjee VV, et al. Plasma brain natriuretic peptide as an indicator of left ventricular systolic function and long-term survival after acute myocardial infarction: Comparison with plasma atrial natriuretic peptide and N-terminal proatrial natriuretic peptide. Circulation. 1996;93:1963–1969[Abstract/Free Full Text]
  7. Arakawa N, Nakamura M, Aoki H, Hiramori K. Plasma brain natriuretic peptide concentrations predict survival after acute myocardial infarction. J Am Coll Cardiol. 1996;27:1656–1661[Abstract]
  8. Richards AM, Nicholls MG, Yandle TG, et al. Plasma N-terminal pro-brain natriuretic peptide and adrenomedullin: New neurohormonal predictors of left ventricular function and prognosis after myocardial infarction. Circulation. 1998;97:1921–1929[Abstract/Free Full Text]
  9. the Christchurch Cardioendocrine Research GroupRichards AM, Nicholls MG, Yandle TG, et al. Neuroendocrine prediction of left ventricular function and heart failure after acute myocardial infarction. Heart. 1999;81:114–120[Abstract/Free Full Text]
  10. Antman EM, Louwerenburg HW, Baars HF, et al. Enoxaparin as adjunctive antithrombin therapy for ST-elevation myocardial infarction: Results of the ENTIRE-(TIMI) 23 trial. Circulation. 2002;105:1642–1649[Abstract/Free Full Text]
  11. de Lemos JA, Braunwald E. ST segment resolution as a tool for assessing the efficacy of reperfusion therapy. J Am Coll Cardiol. 2001;38:1283–1294[Abstract/Free Full Text]
  12. Morrow DA, Rifai N, Tanasijevic MJ, Wybenga DR, de Lemos JA, Antman EM. Clinical efficacy of three assays for cardiac troponin I for risk stratification in acute coronary syndromes: A TIMI 11B substudy. Clin Chem. 2000;46:453–460[Abstract/Free Full Text]
  13. Morrow DA, Rifai N, Antman EM, et al. C-reactive protein is a potent predictor of mortality independently of and in combination with troponin T in acute coronary syndromes: A TIMI 11A substudy. J Am Coll Cardiol. 1998;31:1460–1465[Abstract/Free Full Text]
  14. de Lemos JA, Morrow DA, Bentley JH, et al. The prognostic value of B-type natriuretic peptide in patients with acute coronary syndromes. N Engl J Med. 2001;345:1014–1021[Abstract/Free Full Text]
  15. Morrow DA, de Lemos JA, Sabatine MS, et al. Evaluation of B-type natriuretic peptide for risk assessment in unstable angina/non–ST-elevation myocardial infarction: B-type natriuretic peptide and prognosis in TACTICS-TIMI 18. J Am Coll Cardiol. 2003;41:1264–1272[Abstract/Free Full Text]
  16. the GUSTO III InvestigatorsOhman EM, Armstrong PW, White HD, et al. Risk stratification with a point-of-care cardiac troponin T test in acute myocardial infarction. Am J Cardiol. 1999;84:1281–1286[CrossRef][Medline]
  17. Anzai T, Yoshikawa T, Shiraki H, et al. C-reactive protein as a predictor of infarct expansion and cardiac rupture after a first Q-wave acute myocardial infarction. Circulation. 1997;96:778–784[Abstract/Free Full Text]
  18. Richards AM, Nicholls MG, Espiner EA, et al. B-type natriuretic peptides and ejection fraction for prognosis after myocardial infarction. Circulation. 2003;107:2786–2792[Abstract/Free Full Text]



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C. J. Terkelsen, B. L. Norgaard, J. F. Lassen, S. H. Poulsen, J. C. Gerdes, E. Sloth, L. B.-H. Gotzsche, F. K. Romer, L. Thuesen, T. T. Nielsen, et al.
Potential significance of spontaneous and interventional ST-changes in patients transferred for primary percutaneous coronary intervention: observations from the ST-MONitoring in Acute Myocardial Infarction study (The MONAMI study)
Eur. Heart J., February 1, 2006; 27(3): 267 - 275.
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 JAMAHome page
D. A. Morrow, J. A. de Lemos, M. A. Blazing, M. S. Sabatine, S. A. Murphy, P. Jarolim, H. D. White, K. A. A. Fox, R. M. Califf, E. Braunwald, et al.
Prognostic Value of Serial B-Type Natriuretic Peptide Testing During Follow-up of Patients With Unstable Coronary Artery Disease
JAMA, December 14, 2005; 294(22): 2866 - 2871.
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 CirculationHome page
G. Ndrepepa, S. Braun, K. Niemoller, J. Mehilli, N. von Beckerath, O. von Beckerath, W. Vogt, A. Schomig, and A. Kastrati
Prognostic Value of N-Terminal Pro-Brain Natriuretic Peptide in Patients With Chronic Stable Angina
Circulation, October 4, 2005; 112(14): 2102 - 2107.
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 CirculationHome page
D. Detaint, D. Messika-Zeitoun, J.-F. Avierinos, C. Scott, H. Chen, J. C. Burnett Jr, and M. Enriquez-Sarano
B-Type Natriuretic Peptide in Organic Mitral Regurgitation: Determinants and Impact on Outcome
Circulation, May 10, 2005; 111(18): 2391 - 2397.
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S. Namiuchi, Y. Kagaya, J. Ohta, N. Shiba, M. Sugi, M. Oikawa, H. Kunii, H. Yamao, N. Komatsu, M. Yui, et al.
High Serum Erythropoietin Level Is Associated With Smaller Infarct Size in Patients With Acute Myocardial Infarction Who Undergo Successful Primary Percutaneous Coronary Intervention
J. Am. Coll. Cardiol., May 3, 2005; 45(9): 1406 - 1412.
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R. M. Mills
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J. Am. Coll. Cardiol., February 15, 2005; 45(4): 542 - 543.
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