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Previous Volume 345:1014-1021 October 4, 2001 Number 14 Next

Abstract PDF Editorial by Rabbani, L. E. Add to Personal Archive Add to Citation Manager Notify a Friend E-mail When Cited PubMed Citation

ABSTRACT

Background Brain (B-type) natriuretic peptide is a neurohormone synthesized predominantly in ventricular myocardium. Although the circulating level of this neurohormone has been shown to provide independent prognostic information in patients with transmural myocardial infarction, few data are available for patients with acute coronary syndromes in the absence of ST-segment elevation.

Methods We measured B-type natriuretic peptide in plasma specimens obtained a mean (±SD) of 40±20 hours after the onset of ischemic symptoms in 2525 patients from the Orbofiban in Patients with Unstable Coronary Syndromes–Thrombolysis in Myocardial Infarction 16 study.

Results The base-line level of B-type natriuretic peptide was correlated with the risk of death, heart failure, and myocardial infarction at 30 days and 10 months. The unadjusted rate of death increased in a stepwise fashion among patients in increasing quartiles of base-line B-type natriuretic peptide levels (P<0.001). This association remained significant in subgroups of patients who had myocardial infarction with ST-segment elevation (P=0.02), patients who had myocardial infarction without ST-segment elevation (P<0.001), and patients who had unstable angina (P<0.001). After adjustment for independent predictors of the long-term risk of death, the odds ratios for death at 10 months in the second, third, and fourth quartiles of B-type natriuretic peptide were 3.8 (95 percent confidence interval, 1.1 to 13.3), 4.0 (95 percent confidence interval, 1.2 to 13.7), and 5.8 (95 percent confidence interval, 1.7 to 19.7). The level of B-type natriuretic peptide was also associated with the risk of new or recurrent myocardial infarction (P=0.01) and new or worsening heart failure (P<0.001) at 10 months.

Conclusions A single measurement of B-type natriuretic peptide, obtained in the first few days after the onset of ischemic symptoms, provides predictive information for use in risk stratification across the spectrum of acute coronary syndromes. Cardiac neurohormonal activation may be a unifying feature among patients at high risk for death after acute coronary syndromes.

Studies evaluating the prognostic implications of B-type natriuretic peptide have been limited to patients with myocardial infarction with ST-segment elevation, and few data are available on patients who have acute coronary syndromes in the absence of ST-segment elevation. Patients with acute coronary syndromes are a heterogeneous group, with differences in pathophysiology, clinical presentation, and the risk of adverse events. We sought to evaluate the prognostic implications of cardiac neurohormonal activation, as reflected by the plasma level of B-type natriuretic peptide, across the entire spectrum of acute coronary syndromes.

Methods

Study Population

The Oral Glycoprotein IIb/IIIa Inhibition with Orbofiban in Patients with Unstable Coronary Syndromes–Thrombolysis in Myocardial Infarction 16 trial was a randomized, multicenter trial comparing an oral platelet glycoprotein IIb/IIIa receptor inhibitor, orbofiban, with placebo in 10,288 patients with acute coronary syndromes. The study protocol was approved by the institutional review board of each participating hospital, and all patients provided written informed consent. Patients were included if they presented within 72 hours after the onset of ischemic discomfort and met one or more of the following criteria: electrocardiographic changes (ST-segment depression or elevation of at least 0.5 mm, T-wave inversion of at least 3 mm in at least three leads, or left bundle-branch block), elevated levels of cardiac markers, a history of coronary disease, or an age of at least 65 years in patients with diabetes or vascular disease.¹⁵ Patients received 150 to 162 mg of aspirin daily and were randomly assigned to receive 50 mg of orbofiban twice daily; 50 mg of orbofiban twice daily for one month, followed by 30 mg of orbofiban twice daily; or placebo. The study was terminated prematurely because of an increase in mortality in the group assigned to receive 50 mg twice daily initially and then 30 mg twice daily.¹⁵ The present substudy included all 2525 patients who were assigned to the group given 50 mg of orbofiban twice daily and who provided a base-line plasma specimen suitable for analysis. The data were collected and retained by the study investigators, who also performed the analyses.

Blood Sampling

At the time of enrollment, blood specimens were collected in citrate-treated tubes and centrifuged for at least 12 minutes. The plasma component was frozen and shipped on dry ice to Children's Hospital (Boston), where samples were stored at –70°C. In 925 patients, C-reactive protein was measured with use of a high-sensitivity assay (N Latex CRP assay, Dade Behring, Newark, Del.) and fibrinogen was measured with use of a commercial assay on a BN II analyzer (Dade Behring). After the trial was completed, all available plasma specimens from the group given 50 mg of orbofiban twice daily were shipped to Biosite Diagnostics (San Diego, Calif.), where they were thawed and analyzed.

Biochemical Analyses

Sequential sandwich immunoassays for the quantification of B-type natriuretic peptide and troponin I were performed in 384-well microtiter plates with use of an automated system (Tecan Genesis robotic sample processor 200/8, Durham, N.C.). The amount of analyte was quantified on the basis of the level of binding of alkaline phosphatase–conjugated antibody. The analytic sensitivity of the B-type natriuretic peptide and troponin I immunoassays were approximately 5 pg per milliliter and 50 pg per milliliter, respectively.

End Points

The end points of death from any cause and nonfatal myocardial infarction were evaluated at 30 days and the end of the follow-up period (10 months). Myocardial infarction was defined according to previously reported criteria,¹⁶ and all cases of suspected infarction were adjudicated by a clinical-events committee. Information on the end point of new or worsening heart failure or cardiogenic shock was collected from the case-record forms.

Statistical Analysis

Patients were divided into quartiles on the basis of their B-type natriuretic peptide level at the time of enrollment. The mean values and proportions of base-line variables were compared among quartiles with the use of linear regression for continuous variables and log-linear analysis for categorical variables. The correlation between B-type natriuretic peptide levels and other continuous base-line variables was assessed with the use of Pearson's product-moment correlation coefficient. B-type natriuretic peptide levels were not adjusted for age.

To evaluate its association with clinical outcomes, B-type natriuretic peptide was considered as both a continuous and a categorical variable. The level of B-type natriuretic peptide was compared between patients who met a study end point and those who did not with use of the Wilcoxon rank-sum test. Cox regression analysis was used to evaluate the association between the quartile of B-type natriuretic peptide and the risk of adverse outcomes for the first 30 days after randomization and at 10 months. Stratified analyses were performed among patients with various troponin I levels, as well as those with and those without a clinical diagnosis of heart failure. Analyses were performed in subgroups defined according to the index diagnosis. The quartile ranges were recalculated for each of these subgroups.

For the end point of death from any cause through the end of follow-up (10 months), we constructed a logistic-regression model using forward stepwise selection. Clinical variables for which data were available from more than 75 percent of patients were entered into the model if they had a univariate P value of less than 0.1; variables were removed if they had a multivariate P value greater than or equal to 0.1. Base-line levels of troponin I and B-type natriuretic peptide were then added to the completed model. The final model included only the 2280 patients for whom data were available for all variables. Finally, we performed analyses using the B-type natriuretic peptide threshold of 80 pg per milliliter that has been established for the diagnosis of congestive heart failure.¹⁷

Results

The study population consisted of 2525 patients: 825 were enrolled after a myocardial infarction with ST-segment elevation, 565 after a myocardial infarction without ST-segment elevation, and 1133 after an episode of unstable angina. In two patients, the index diagnosis was not specified. The B-type natriuretic peptide level ranged from 5 to 1456 pg per milliliter, with a mean (±SD) of 114±126 pg per milliliter, a median of 81 pg per milliliter, and 25th and 75th percentile values of 44 and 138 pg per milliliter, respectively. The mean time from the onset of ischemic symptoms to enrollment was 40±20 hours (median, 40).

Association with Base-Line Clinical Variables

In univariate analyses, higher base-line levels of B-type natriuretic peptide were associated with older age, female sex, white race, and a history of hypertension, heart failure, and vascular disease; the level of B-type natriuretic peptide was inversely associated with a history of hypercholesterolemia and current smoking (Table 1). Patients with higher B-type natriuretic peptide levels were more likely than those with lower levels to present in Killip class II, III, or IV and to have electrocardiographic changes at base line, elevated levels of creatine kinase MB, and renal insufficiency (Table 1). There was no consistent relation between the level of B-type natriuretic peptide and the time from the onset of ischemic symptoms: the median levels were 72, 87, and 81 pg per milliliter for patients presenting less than 24 hours, 24 to 48 hours, and more than 48 hours after the onset of symptoms, respectively.

View this table: [in this window] [in a new window]   Table 1. Base-Line Clinical Characteristics According to the Quartile of B-Type Natriuretic Peptide Level.

 
Although statistically significant, the associations between levels of B-type natriuretic peptide and C-reactive protein levels (r=0.2, P<0.001), fibrinogen levels (r=0.18, P<0.001), peak levels of the MB isoform of creatine kinase (r=0.09, P<0.001), and the ejection fraction (r=0.23, P<0.001) were only moderately strong. Patients with higher B-type natriuretic peptide levels had a greater number of coronary arteries with stenosis of at least 50 percent (P<0.001) and a greater likelihood of a positive stress test (P<0.01) than patients with lower levels (data not shown).

Clinical Outcomes

The base-line level of B-type natriuretic peptide was higher among patients who died than among those who were alive at 30 days (median, 153 vs. 80 pg per milliliter; P<0.001) and at 10 months (median, 143 vs. 79 pg per milliliter; P<0.001). These differences remained significant in subgroups of patients who had myocardial infarction with ST-segment elevation (P=0.002 at 30 days and P=0.008 at 10 months), patients who had myocardial infarction in the absence of ST-segment elevation (P<0.001 at both 30 days and 10 months), and patients who had unstable angina (P=0.002 at 30 days and P<0.001 at 10 months). The level of B-type natriuretic peptide was higher among patients who had new or recurrent myocardial infarction within 30 days (P=0.02) or 10 months (P=0.01) than among patients who were free of infarction. Finally, the level of B-type natriuretic peptide was higher among patients who had new or worsening heart failure within 30 days (P<0.001) or 10 months (P<0.001) than among those in whom heart failure did not develop.

The unadjusted mortality rate increased in a stepwise fashion across increasing quartiles of base-line B-type natriuretic peptide levels (P<0.001) (Figure 1). This association remained significant in subgroups of patients who had myocardial infarction with ST-segment elevation, patients who had myocardial infarction in the absence of ST-segment elevation, and patients who had unstable angina (Figure 2). In addition, the association between the level of B-type natriuretic peptide and the 10-month mortality rate remained graded and significant both among 327 patients with a history of heart failure or a finding of Killip class II, III, or IV at presentation (P=0.007) and among 2165 patients without such findings (P<0.001). When stratification was based on the level of troponin I at the time of enrollment, increasing levels of B-type natriuretic peptide remained associated with a higher 10-month mortality rate, among both 882 patients with a troponin I level of 0.1 ng per milliliter or less (P=0.01) and 1630 patients with a troponin I level of more than 0.1 ng per milliliter (P<0.001). Similar results were obtained when stratification was based on troponin I thresholds of 0.4 and 1.5 ng per milliliter (P<0.001 for each comparison of patients above and patients at or below each threshold). The association between B-type natriuretic peptide and mortality at 10 months was significant for both men (P<0.001) and women (P=0.01).

View larger version (18K): [in this window] [in a new window]   Figure 1. Kaplan–Meier Curves Showing the Cumulative Incidence of Death at 10 Months, According to the Quartile of B-Type Natriuretic Peptide Level at Enrollment. The range of B-type natriuretic peptide levels was as follows: 5.0 to 43.6 pg per milliliter (quartile 1), 43.7 to 81.2 pg per milliliter (quartile 2), 81.3 to 137.8 pg per milliliter (quartile 3), and 137.9 to 1456.6 pg per milliliter (quartile 4). P<0.001 for the trend among the quartiles.

 

View larger version (14K): [in this window] [in a new window]   Figure 2. Association between the B-Type Natriuretic Peptide Level and the Mortality Rate at 10 Months, According to the Index Diagnosis. Quartiles were recalibrated for each of the subgroups. Quartile 1 represents the lowest level of B-type natriuretic peptide, and quartile 4 the highest level. P values are for the trend within each subgroup.

 
In a logistic-regression model in which we adjusted for other independent predictors of the long-term risk of death, including age, troponin I levels, and presence or absence of heart failure, renal insufficiency, and ST-segment deviation, increasing levels of B-type natriuretic peptide remained associated with an increased risk of death at 10 months (Figure 3). The adjusted odds ratios for death at 10 months in the second, third, and fourth quartiles of B-type natriuretic peptide were 3.8 (95 percent confidence interval, 1.1 to 13.3), 4.0 (95 percent confidence interval, 1.2 to 13.7), and 5.8 (95 percent confidence interval, 1.7 to 19.7), respectively (Figure 3). When age was entered into the model as a continuous variable, the results were unchanged.

View larger version (5K): [in this window] [in a new window]   Figure 3. Stepwise Logistic-Regression Model Showing the Association between Selected Base-Line Clinical Variables and the Odds Ratio for Death at 10 Months. The cardiac troponin I level and B-type natriuretic peptide quartiles were forced into the final model. Horizontal lines are 95 percent confidence intervals. In addition to the variables shown in the figure, the final model included presence or absence of a history of hyperlipidemia, peripheral vascular disease, or heart failure; presence or absence of prior therapy with diuretics, angiotensin-converting–enzyme inhibitors, nitrates, or heparin; heart rate; blood pressure; and creatinine clearance. MI denotes myocardial infarction.

 
Evaluation of a B-Type Natriuretic Peptide Threshold of 80 pg per Milliliter

Patients with a B-type natriuretic peptide level of more than 80 pg per milliliter were significantly more likely to die, have a new or recurrent myocardial infarction, or have new or progressive heart failure than those with a level of 80 pg per milliliter or less (Figure 4). After adjustment for other independent predictors of the long-term risk of death, a B-type natriuretic peptide level of more than 80 pg per milliliter remained significantly associated with an increased 10-month mortality rate (P=0.04).

View larger version (12K): [in this window] [in a new window]   Figure 4. The Incidence of Death, New or Progressive Congestive Heart Failure (CHF), and New or Recurrent Myocardial Infarction (MI) at 30 Days and 10 Months among Patients with B-Type Natriuretic Peptide Levels above or at or below the Prespecified Threshold of 80 pg per Milliliter. P<0.005 for each comparison.

 
Discussion

We have demonstrated in a large, contemporary cohort of patients that a single measurement of B-type natriuretic peptide, obtained a median of 40 hours after the onset of ischemic symptoms, provides powerful information for use in risk stratification across the entire spectrum of acute coronary syndromes. Despite heterogeneity in pathophysiology, clinical presentation, and risk among patients who had myocardial infarction with ST-segment elevation, patients who had myocardial infarction in the absence of ST-segment elevation, and patients who had unstable angina, increasing levels of B-type natriuretic peptide were predictive of an increased risk of death in each of these subgroups. This finding suggests that activation of the cardiac neurohormonal system may be a unifying feature among patients at high risk for death after acute coronary syndromes.

The association between B-type natriuretic peptide and the long-term risk of death was independent of the presence or absence of clinical evidence of heart failure, as well as renal function, the troponin I level, electrocardiographic changes, and other known predictors of the risk of death in patients with acute coronary syndromes. In addition, a high level of B-type natriuretic peptide was associated with an increased risk of nonfatal end points, including new or progressive heart failure and myocardial infarction. Finally, it appears that the previously defined B-type natriuretic peptide threshold of 80 pg per milliliter, indicative of neurohormonal activation in patients with heart failure,¹⁷ is also an appropriate threshold among patients with acute coronary syndromes.

Previous studies have demonstrated that after a myocardial infarction, a higher plasma level of B-type natriuretic peptide is associated with a larger infarct size,^6,18 an increased likelihood of ventricular remodeling,¹⁹ a lower ejection fraction,^11,18 and an increased risk of heart failure and death.^{8,10,11,12,13,14} These studies each included fewer than 150 patients and focused on relatively homogeneous groups of patients who had myocardial infarction with ST-segment elevation. Our study extends these findings to patients with acute coronary syndromes in the absence of ST-segment elevation, including those with unstable angina and no evidence of myocardial necrosis.

Unlike traditional cardiac biomarkers used to predict risk among patients with acute coronary syndromes, B-type natriuretic peptide has a putative role in the counterregulatory response to ischemia. Therefore, it may act as an index of the extent or severity of the ischemic insult, as well as the degree of underlying impairment in left ventricular function. In an animal model of transmural infarction, the level of expression of the B-type natriuretic peptide gene in the left ventricle was tripled within four hours after coronary ligation, and tissue levels of B-type natriuretic peptide were increased in noninfarcted as well as infarcted regions.²⁰ The level of B-type natriuretic peptide increases rapidly and transiently after exercise testing in patients with chronic stable angina, and the degree of elevation is correlated with the size of the ischemic territory as measured with the use of nuclear single-photon-emission computed tomography imaging.²¹ Furthermore, the level increases transiently after uncomplicated percutaneous transluminal coronary angioplasty, even in the absence of changes in pulmonary-capillary wedge pressure.^22,23

Several small cross-sectional studies have shown that the level of B-type natriuretic peptide is higher among patients with unstable angina than among patients with stable angina or among healthy controls.^24,25 In one of these studies, a finding of an elevation in B-type natriuretic peptide correlated with echocardiographic findings of regional wall-motion abnormalities, but not with hemodynamic data obtained at the time of simultaneous cardiac catheterization; furthermore, after medical stabilization, wall-motion abnormalities improved and B-type natriuretic peptide levels fell significantly.²⁵

Taken together, these findings suggest that myocardial ischemia augments the synthesis and release of B-type natriuretic peptide, even in the absence of myocardial necrosis or preexisting left ventricular dysfunction. Reversible ischemia may transiently increase left ventricular wall stress, which may be sufficient to cause an elevation in B-type natriuretic peptide levels. Our findings further suggest that the prognostic implications of neurohormonal activation are distinct from those of myocyte necrosis; even among patients with unstable angina and those without troponin I elevation, the degree of elevation in B-type natriuretic peptide is of prognostic importance.

We measured B-type natriuretic peptide once, approximately two days after the index event. It is not possible from a single measurement to determine whether neurohormonal activation is reflective of the acute (index) event or of preexisting left ventricular dysfunction. However, even after adjustment for variables such as the presence or absence of a history of hypertension, heart failure, and use of diuretics or angiotensin-converting–enzyme inhibitors, the level of B-type natriuretic peptide remained predictive of the long-term risk of death. A study in patients hospitalized with heart failure suggests that serial measurements of B-type natriuretic peptide may provide more prognostic information than a single measurement, since the prognosis was better when levels fell after therapy than when they remained the same.²⁶ Future studies should evaluate the use of serial measurements of B-type natriuretic peptide in patients with acute coronary syndromes.

For a cardiac biomarker to be clinically useful, it must help clinicians select an appropriate therapeutic regimen. For example, patients who have an elevation in troponin T or I levels after acute coronary syndromes appear to derive specific benefit from an early, aggressive strategy that includes potent antiplatelet²⁷ and antithrombotic²⁸ therapy and early revascularization.²⁹ In addition, patients who have elevated C-reactive protein levels after myocardial infarction appear to benefit from statin therapy.³⁰ Patients with elevated levels of B-type natriuretic peptide after an acute coronary syndrome are at high risk for death, a new myocardial infarction, and heart failure and may benefit from intensive antiplatelet and antithrombotic therapies, neurohormonal antagonism with agents such as beta-blockers and angiotensin-converting–enzyme inhibitors, and early revascularization. Equally important, patients who have normal levels of B-type natriuretic peptide after an acute coronary event appear to have a particularly low long-term risk of death and heart failure. In this group of patients, a less intensive management approach may be appropriate, in order to avoid the cost and risk associated with potentially unnecessary therapies. Future studies should directly assess the role of B-type natriuretic peptide in identifying patients who would benefit from various treatment strategies.

The level of B-type natriuretic peptide, measured in the first few days after an acute coronary event, predicts the long-term risk of death and nonfatal cardiac events across the spectrum of acute coronary syndromes. The prognostic usefulness of B-type natriuretic peptide persists after adjustment for the presence or absence of clinical evidence of heart failure, as well as other important predictors of mortality, including clinical characteristics, renal function, electrocardiographic changes, and troponin I levels. These findings suggest that B-type natriuretic peptide should be measured after an acute coronary syndrome in order to identify patients at high and low risk for adverse outcomes and that treatment, including the intensity of surveillance and the use of aggressive pharmacologic and interventional therapy, should be adjusted accordingly.

Supported in part by grants from Searle (Skokie, Ill.) and Biosite Diagnostics (San Diego, Calif.).

Drs. de Lemos, Morrow, and Omland have received honorariums from Biosite Diagnostics.

Source Information

From the Thrombolysis in Myocardial Infarction Study Group, Boston (J.A.D., D.A.M., M.S.S., C.H.M., C.P.C., E.B.); the Donald W. Reynolds Cardiovascular Clinical Research Center, University of Texas, Southwestern Medical School, Dallas (J.A.D.); the Cardiovascular Division and Department of Medicine, Brigham and Women's Hospital, Boston (D.A.M., M.S.S., C.H.M., C.P.C., E.B.); the Nottingham Clinical Research Group, Nottingham, United Kingdom (J.H.B.); and the Research Institute for Internal Medicine, National Hospital, University of Oslo, Oslo, Norway (T.O., C.H.).

Address reprint requests to Dr. de Lemos at UT Southwestern Medical Center, 5323 Harry Hines Blvd., Rm. CS7.142, Dallas, TX 75390-9047, or at james.delemos{at}utsouthwestern.edu.

References

1. Wiese S, Breyer T, Dragu A, et al. Gene expression of brain natriuretic peptide in isolated atrial and ventricular human myocardium: influenceof angiotensin II and diastolic fiber length. Circulation 2000;102:3074-3079. [Free Full Text]
2. Yasue H, Yoshimura M, Sumida H, et al. Localization and mechanism of secretion of B-type natriuretic peptide in comparison with those of A-type natriuretic peptide in normal subjects and patients with heart failure. Circulation 1994;90:195-203. [Free Full Text]
3. Yoshimura M, Yasue H, Okumura K, et al. Different secretion patterns of atrial natriuretic peptide and brain natriuretic peptide in patients with congestive heart failure. Circulation 1993;87:464-469. [Free Full Text]
4. Stein BC, Levin RI. Natriuretic peptides: physiology, therapeutic potential, and risk stratification in ischemic heart disease. Am Heart J 1998;135:914-923. [CrossRef][ISI][Medline]
5. Omland T, Aakvaag A, Vik-Mo H. Plasma cardiac natriuretic peptide determination as a screening test for the detection of patients with mild left ventricular impairment. Heart 1996;76:232-237. [Free Full Text]
6. Arakawa N, Nakamura M, Aoki H, Hiramori K. Relationship between plasma level of brain natriuretic peptide and myocardial infarct size. Cardiology 1994;85:334-340. [ISI][Medline]
7. 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][ISI][Medline]
8. 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. [Free Full Text]
9. 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. [Free Full Text]
10. Darbar D, Davidson NC, Gillespie N, et al. Diagnostic value of B-type natriuretic peptide concentrations in patients with acute myocardial infarction. Am J Cardiol 1996;78:284-287. [CrossRef][ISI][Medline]
11. Richards 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. [Free Full Text]
12. 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. [Free Full Text]
13. 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]
14. 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. [Free Full Text]
15. Cannon CP, McCabe CH, Wilcox RG, et al. Oral glycoprotein IIb/IIIa inhibition with orbofiban in patients with unstable coronary syndromes (OPUS-TIMI 16) trial. Circulation 2000;102:149-156. [Free Full Text]
16. Antman EM, McCabe CH, Gurfinkel EP, et al. Enoxaparin prevents death and cardiac ischemic events in unstable angina/non-Q-wave myocardial infarction: results of the Thrombolysis in Myocardial Infarction (TIMI) 11B trial. Circulation 1999;100:1593-1601. [Free Full Text]
17. Dao Q, Krishnaswamy P, Kazanegra R, et al. Utility of B-type natriuretic peptide in the diagnosis of congestive heart failure in an urgent-care setting. J Am Coll Cardiol 2001;37:379-385. [Free Full Text]
18. Horio T, Shimada K, Kohno M, et al. Serial changes in atrial and brain natriuretic peptides in patients with acute myocardial infarction treated with early coronary angioplasty. Am Heart J 1993;126:293-299. [CrossRef][ISI][Medline]
19. Nagaya N, Nishikimi T, Goto Y, et al. Plasma brain natriuretic peptide is a biochemical marker for the prediction of progressive ventricular remodeling after acute myocardial infarction. Am Heart J 1998;135:21-28. [CrossRef][ISI][Medline]
20. Hama N, Itoh H, Shirakami G, et al. Rapid ventricular induction of brain natriuretic peptide gene expression in experimental acute myocardial infarction. Circulation 1995;92:1558-1564. [Free Full Text]
21. Marumoto K, Hamada M, Hiwada K. Increased secretion of atrial and brain natriuretic peptides during acute myocardial ischaemia induced by dynamic exercise in patients with angina pectoris. Clin Sci (Colch) 1995;88:551-556. [Medline]
22. Tateishi J, Masutani M, Ohyanagi M, Iwasaki T. Transient increase in plasma brain (B-type) natriuretic peptide after percutaneous transluminal coronary angioplasty. Clin Cardiol 2000;23:776-780. [ISI][Medline]
23. Kyriakides ZS, Markianos M, Michalis L, Antoniadis A, Nikolaou NI, Kremastinos DT. Brain natriuretic peptide increases acutely and much more prominently than atrial natriuretic peptide during coronary angioplasty. Clin Cardiol 2000;23:285-288. [ISI][Medline]
24. Talwar S, Squire IB, Downie PF, Davies JE, Ng LL. Plasma N terminal pro-brain natriuretic peptide and cardiotrophin 1 are raised in unstable angina. Heart 2000;84:421-424. [Free Full Text]
25. Kikuta K, Yasue H, Yoshimura M, et al. Increased plasma levels of B-type natriuretic peptide in patients with unstable angina. Am Heart J 1996;132:101-107. [CrossRef][ISI][Medline]
26. Cheng V, Kazanagra R, Garcia A, et al. A rapid bedside test for B-type peptide predicts treatment outcomes in patients admitted for decompensated heart failure: a pilot study. J Am Coll Cardiol 2001;37:386-391. [Free Full Text]
27. Hamm CW, Heeschen C, Goldmann B, et al. Benefit of abciximab in patients with refractory unstable angina in relation to serum troponin T levels. N Engl J Med 1999;340:1623-1629. [Free Full Text]
28. Morrow DA, Antman EM, Tanasijevic M, et al. Cardiac troponin I for stratification of early outcomes and the efficacy of enoxaparin in unstable angina: a TIMI 11B substudy. J Am Coll Cardiol 2000;36:1812-1817. [Free Full Text]
29. Cannon CP, Weintraub WS, Demopoulos LA, et al. Comparison of early invasive and conservative strategies in patients with unstable coronary syndromes treated with the glycoprotein IIb/IIIa inhibitor tirofiban. N Engl J Med 2001;344:1879-1887. [Free Full Text]
30. Ridker PM, Rifai N, Pfeffer MA, et al. Inflammation, pravastatin, and the risk of coronary events after myocardial infarction in patients with average cholesterol levels. Circulation 1998;98:839-844. [Free Full Text]

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• Bonaca, M. P., Morrow, D. A. (2008). Defining a Role for Novel Biomarkers in Acute Coronary Syndromes. Clin. Chem. 54: 1424-1431 [Abstract] [Full Text]  
• Daniels, L. B., Laughlin, G. A., Clopton, P., Maisel, A. S., Barrett-Connor, E. (2008). Minimally Elevated Cardiac Troponin T and Elevated N-Terminal Pro-B-Type Natriuretic Peptide Predict Mortality in Older Adults: Results From the Rancho Bernardo Study. J Am Coll Cardiol 52: 450-459 [Abstract] [Full Text]  
• Fox, A. A., Shernan, S. K., Collard, C. D., Liu, K.-Y., Aranki, S. F., DeSantis, S. M., Jarolim, P., Body, S. C. (2008). Preoperative B-type natriuretic peptide is as independent predictor of ventricular dysfunction and mortality after primary coronary artery bypass grafting.. J. Thorac. Cardiovasc. Surg. 136: 452-461 [Abstract] [Full Text]  
• Ferrante, G., Cosentino, N., Barlis, P., Niccoli, G. (2008). Association of adiponectin with adverse outcome in coronary artery disease patients: results from the AtheroGene study. Eur Heart J 29: 1922-1923 [Full Text]  
• Zeller, M., Steg, P. G., Ravisy, J., Lorgis, L., Laurent, Y., Sicard, P., Janin-Manificat, L., Beer, J.-C., Makki, H., Lagrost, A.-C., Rochette, L., Cottin, Y., for the RICO Survey Working Group, (2008). Relation Between Body Mass Index, Waist Circumference, and Death After Acute Myocardial Infarction. Circulation 118: 482-490 [Abstract] [Full Text]  
• Mega, J. L., Morrow, D. A., de Lemos, J. A., Mohanavelu, S., Cannon, C. P., Sabatine, M. S. (2008). Thrombus precursor protein and clinical outcomes in patients with acute coronary syndromes.. J Am Coll Cardiol 51: 2422-2429 [Abstract] [Full Text]  
• Goetze, J. P. (2008). Markers of activated coagulation in acute coronary syndromes.. J Am Coll Cardiol 51: 2430-2431 [Full Text]  
• Waldo, S. W., Beede, J., Isakson, S., Villard-Saussine, S., Fareh, J., Clopton, P., Fitzgerald, R. L., Maisel, A. S. (2008). Pro-B-Type Natriuretic Peptide Levels in Acute Decompensated Heart Failure. J Am Coll Cardiol 51: 1874-1882 [Abstract] [Full Text]  
• Yip, G. W (2008). B-type natriuretic peptide: a treatment, not a diagnostic marker. Heart 94: 542-544 [Full Text]  
• Sabatine, M. S., Morrow, D. A., Higgins, L. J., MacGillivray, C., Guo, W., Bode, C., Rifai, N., Cannon, C. P., Gerszten, R. E., Lee, R. T. (2008). Complementary Roles for Biomarkers of Biomechanical Strain ST2 and N-Terminal Prohormone B-Type Natriuretic Peptide in Patients With ST-Elevation Myocardial Infarction. Circulation 117: 1936-1944 [Abstract] [Full Text]  
• Schnabel, R., Messow, C. M., Lubos, E., Espinola-Klein, C., Rupprecht, H. J., Bickel, C., Sinning, C., Tzikas, S., Keller, T., Genth-Zotz, S., Lackner, K. J., Munzel, T. F., Blankenberg, S. (2008). Association of adiponectin with adverse outcome in coronary artery disease patients: results from the AtheroGene study. Eur Heart J 29: 649-657 [Abstract] [Full Text]  
• Kandil, E., Burack, J., Sawas, A., Bibawy, H., Schwartzman, A., Zenilman, M. E., Bluth, M. H. (2008). B-Type Natriuretic Peptide: A Biomarker for the Diagnosis and Risk Stratification of Patients With Septic Shock. Arch Surg 143: 242-246 [Abstract] [Full Text]  
• Paniagua, R., Amato, D., Mujais, S., Vonesh, E., Ramos, A., Correa-Rotter, R., Horl, W. H. (2008). Predictive Value of Brain Natriuretic Peptides in Patients on Peritoneal Dialysis: Results from the ADEMEX Trial. CJASN 3: 407-415 [Abstract] [Full Text]  
• Sanchis, J, Bosch, X, Bodi, V, Bellera, N, Nunez, J, Benito, B, Ordonez, J, Consuegra, L, Heras, M, Llecer, A (2008). Combination of clinical risk profile, early exercise testing and circulating biomarkers for evaluation of patients with acute chest pain without ST-segment deviation or troponin elevation. Heart 94: 311-315 [Abstract] [Full Text]  
• Ekelund, U, Forberg, J L (2008). New methods for improved evaluation of patients with suspected acute coronary syndrome in the emergency department. Postgrad. Med. J. 84: 83-86 [Abstract] [Full Text]  
• Strand, A., Kjeldsen, S.E., Gudmundsdottir, H., Os, I., Smith, G., Bjornerheim, R. (2008). Tissue Doppler imaging describes diastolic function in men prone to develop hypertension over twenty years. Eur J Echocardiogr 9: 34-39 [Abstract] [Full Text]  
• Daniels, L. B., Maisel, A. S. (2007). Natriuretic Peptides. J Am Coll Cardiol 50: 2357-2368 [Abstract] [Full Text]  
• Brown, A., George, J., Murphy, M.J., Struthers, A. (2007). Could BNP screening of acute chest pain cases lead to safe earlier discharge of patients with non-cardiac causes? A pilot study. QJM 100: 755-761 [Abstract] [Full Text]  
• Ekelund, U, Forberg, J L (2007). New methods for improved evaluation of patients with suspected acute coronary syndrome in the emergency department. Emerg. Med. J. 24: 811-814 [Abstract] [Full Text]  
• de Lemos, J. A., Morrow, D. A., Blazing, M. A., Jarolim, P., Wiviott, S. D., Sabatine, M. S., Califf, R. M., Braunwald, E. (2007). Serial Measurement of Monocyte Chemoattractant Protein-1 After Acute Coronary Syndromes: Results From the A to Z Trial. J Am Coll Cardiol 50: 2117-2124 [Abstract] [Full Text]  
• Lajer, M., Tarnow, L., Jorsal, A., Parving, H.-H. (2007). Polymorphisms in the B-type natriuretic peptide (BNP) gene are associated with NT-proBNP levels but not with diabetic nephropathy or mortality in type 1 diabetic patients. Nephrol Dial Transplant 22: 3235-3239 [Abstract] [Full Text]  
• Wang, T. J. (2007). Significance of Circulating Troponins in Heart Failure: If These Walls Could Talk. Circulation 116: 1217-1220 [Full Text]  
• Pascual-Figal, D. A, Antolinos, M. J, Bayes-Genis, A., Casas, T., Nicolas, F., Valdes, M. (2007). B-type natriuretic peptide release in the coronary effluent after acute transient ischaemia in humans. Heart 93: 1077-1080 [Abstract] [Full Text]  
• Karabinos, I., Karvouni, E., Chiotinis, N., Papadopoulos, A., Simeonidis, P., Tsolas, O., Katritsis, D. (2007). Acute changes in N-terminal pro-brain natriuretic peptide induced by dobutamine stress echocardiography. Eur J Echocardiogr 8: 265-274 [Abstract] [Full Text]  
• Cuthbertson, B. H., Amiri, A. R., Croal, B. L., Rajagopalan, S., Alozairi, O., Brittenden, J., Hillis, G. S. (2007). Utility of B-type natriuretic peptide in predicting perioperative cardiac events in patients undergoing major non-cardiac surgery. Br J Anaesth 99: 170-176 [Abstract] [Full Text]  
• Winkler, K., Hoffmann, M. M., Winkelmann, B. R., Friedrich, I., Schafer, G., Seelhorst, U., Wellnitz, B., Wieland, H., Boehm, B. O., Marz, W. (2007). Lipoprotein-Associated Phospholipase A2 Predicts 5-Year Cardiac Mortality Independently of Established Risk Factors and Adds Prognostic Information in Patients with Low and Medium High-Sensitivity C-Reactive Protein (The Ludwigshafen Risk and Cardiovascular Health Study). Clin. Chem. 53: 1440-1447 [Abstract] [Full Text]  
• Mueller, C. (2007). The Use of B-Type Natriuretic Peptides in Coronary Artery Disease: Utile or Futile?. J Am Coll Cardiol 50: 215-216 [Full Text]  
• Omland, T., Sabatine, M. S., Jablonski, K. A., Rice, M. M., Hsia, J., Wergeland, R., Landaas, S., Rouleau, J. L., Domanski, M. J., Hall, C., Pfeffer, M. A., Braunwald, E., for the PEACE Investigators, (2007). Prognostic Value of B-Type Natriuretic Peptides in Patients With Stable Coronary Artery Disease: The PEACE Trial. J Am Coll Cardiol 50: 205-214 [Abstract] [Full Text]  
• Struthers, A., Lang, C. (2007). The potential to improve primary prevention in the future by using BNP/N-BNP as an indicator of silent 'pancardiac' target organ damage: BNP/N-BNP could become for the heart what microalbuminuria is for the kidney. Eur Heart J 28: 1678-1682 [Abstract] [Full Text]  
• Authors/Task Force Members, , Bassand, J.-P., Hamm, C. W., Ardissino, D., Boersma, E., Budaj, A., Fernandez-Aviles, F., Fox, K. A.A., Hasdai, D., Ohman, E. M., Wallentin, L., Wijns, W., ESC Committee for Practice Guidelines (CPG), , Vahanian, A., Camm, J., De Caterina, R., Dean, V., Dickstein, K., Filippatos, G., Kristensen, S. D., Widimsky, P., McGregor, K., Sechtem, U., Tendera, M., Hellemans, I., Gomez, J. L. Z., Silber, S., Funck-Brentano, C., Document Reviewers, , Kristensen, S. D., Andreotti, F., Benzer, W., Bertrand, M., Betriu, A., De Caterina, R., DeSutter, J., Falk, V., Ortiz, A. F., Gitt, A., Hasin, Y., Huber, K., Kornowski, R., Lopez-Sendon, J., Morais, J., Nordrehaug, J. E., Silber, S., Steg, P. G., Thygesen, K., Tubaro, M., Turpie, A. G.G., Verheugt, F., Windecker, S. (2007). Guidelines for the diagnosis and treatment of non-ST-segment elevation acute coronary syndromes: The Task Force for the Diagnosis and Treatment of Non-ST-Segment Elevation Acute Coronary Syndromes of the European Society of Cardiology. Eur Heart J 28: 1598-1660 [Full Text]  
• McClure, S. J., Gall, S., Schechter, C. B., Kearney, M., Zaman, A. G. (2007). Percutaneous Coronary Revascularization Reduces Plasma N-Terminal Pro-B-Type Natriuretic Peptide Concentration in Stable Coronary Artery Disease. J Am Coll Cardiol 49: 2394-2397 [Abstract] [Full Text]  
• Shadman, R., Allison, M. A., Criqui, M. H. (2007). Glomerular Filtration Rate and N-Terminal Pro-Brain Natriuretic Peptide as Predictors of Cardiovascular Mortality in Vascular Patients. J Am Coll Cardiol 49: 2172-2181 [Abstract] [Full Text]  
• Ahmed, W., Zafar, S., Alam, A. Y., Ahktar, N., Shah, M. A., Alpert, M. A. (2007). Plasma Levels of B-Type Natriuretic Peptide in Patients With Unstable Angina Pectoris or Acute Myocardial Infarction: Prognostic Significance and Therapeutic Implications. ANGIOLOGY 58: 269-274 [Abstract]  
• Marz, W., Tiran, B., Seelhorst, U., Wellnitz, B., Bauersachs, J., Winkelmann, B. R., Boehm, B. O. (2007). N-Terminal Pro-B-Type Natriuretic Peptide Predicts Total and Cardiovascular Mortality in Individuals with or without Stable Coronary Artery Disease: The Ludwigshafen Risk and Cardiovascular Health Study. Clin. Chem. 53: 1075-1083 [Abstract] [Full Text]  
• Fonarow, G. C., Peacock, W. F., Phillips, C. O., Givertz, M. M., Lopatin, M., for the ADHERE Scientific Advisory Committee and I, (2007). Admission B-Type Natriuretic Peptide Levels and In-Hospital Mortality in Acute Decompensated Heart Failure. J Am Coll Cardiol 49: 1943-1950 [Abstract] [Full Text]  
• NACB WRITING GROUP MEMBERS, , Morrow, D. A., Cannon, C. P., Jesse, R. L., Newby, L. K., Ravkilde, J., Storrow, A. B., Wu, A. H.B., Christenson, R. H. (2007). National Academy of Clinical Biochemistry Laboratory Medicine Practice Guidelines: Clinical Characteristics and Utilization of Biochemical Markers in Acute Coronary Syndromes. Circulation 115: e356-e375 [Full Text]  
• Lorgis, L., Zeller, M., Dentan, G., Sicard, P., Jolak, M., L'Huillier, I., Vincent-Martin, M., Beer, J.C., Makki, H., Gambert, P., Cottin, Y., on behalf of the RICO survey working group, (2007). High levels of N-terminal pro B-type natriuretic peptide are associated with ST resolution failure after reperfusion for acute myocardial infarction. QJM 100: 211-216 [Abstract] [Full Text]  
• NACB WRITING GROUP MEMBERS, , Morrow, D. A., Cannon, C. P., Jesse, R. L., Newby, L. K., Ravkilde, J., Storrow, A. B., Wu, A. H.B., Christenson, R. H., NACB COMMITTEE MEMBERS, , Christenson, R. H., Apple, F. S., Cannon, C. P., Francis, G., Jesse, R. L., Morrow, D. A., Newby, L. K., Ravkilde, J., Storrow, A. B., Tang, W., Wu, A. H.B. (2007). National Academy of Clinical Biochemistry Laboratory Medicine Practice Guidelines: Clinical Characteristics and Utilization of Biochemical Markers in Acute Coronary Syndromes. Clin. Chem. 53: 552-574 [Full Text]  
• Kwan, G., Isakson, S. R., Beede, J., Clopton, P., Maisel, A. S., Fitzgerald, R. L. (2007). Short-Term Serial Sampling of Natriuretic Peptides in Patients Presenting With Chest Pain. J Am Coll Cardiol 49: 1186-1192 [Abstract] [Full Text]  
• Liang, F., O'Rear, J., Schellenberger, U., Tai, L., Lasecki, M., Schreiner, G. F., Apple, F. S., Maisel, A. S., Pollitt, N. S., Protter, A. A. (2007). Evidence for Functional Heterogeneity of Circulating B-Type Natriuretic Peptide. J Am Coll Cardiol 49: 1071-1078 [Abstract] [Full Text]  
• Naegeli, B., Kurz, D. J., Koller, D., Straumann, E., Furrer, M., Maurer, D., Minder, E., Bertel, O. (2007). Single-chamber ventricular pacing increases markers of left ventricular dysfunction compared with dual-chamber pacing. Europace 9: 194-199 [Abstract] [Full Text]  
• Wollert, K. C., Kempf, T., Peter, T., Olofsson, S., James, S., Johnston, N., Lindahl, B., Horn-Wichmann, R., Brabant, G., Simoons, M. L., Armstrong, P. W., Califf, R. M., Drexler, H., Wallentin, L. (2007). Prognostic Value of Growth-Differentiation Factor-15 in Patients With Non-ST-Elevation Acute Coronary Syndrome. Circulation 115: 962-971 [Abstract] [Full Text]  
• Bibbins-Domingo, K., Gupta, R., Na, B., Wu, A. H. B., Schiller, N. B., Whooley, M. A. (2007). N-Terminal Fragment of the Prohormone Brain-Type Natriuretic Peptide (NT-proBNP), Cardiovascular Events, and Mortality in Patients With Stable Coronary Heart Disease. JAMA 297: 169-176 [Abstract] [Full Text]  
• Konstam, M. A. (2007). Natriuretic Peptides and Cardiovascular Events: More Than a Stretch. JAMA 297: 212-214 [Full Text]  
• Chang, A. Y., Abdullah, S. M., Jain, T., Stanek, H. G., Das, S. R., McGuire, D. K., Auchus, R. J., de Lemos, J. A. (2007). Associations Among Androgens, Estrogens, and Natriuretic Peptides in Young Women: Observations From the Dallas Heart Study. J Am Coll Cardiol 49: 109-116 [Abstract] [Full Text]  
• Ben-Dor, I., Haim, M., Rechavia, E., Murninkas, D., Harell, D., Porter, A., Iakobishvili, Z., Battler, A., Hasdai, D. (2007). Serum NT-proBNP Concentrations in the Early Phase Do Not Predict the Severity of Systolic or Diastolic Left Ventricular Dysfunction Among Patients With ST-Elevation Acute Myocardial Infarction. ANGIOLOGY 57: 686-693 [Abstract]  
• de Lemos, J. A. (2006). The Latest and Greatest New Biomarkers: Which Ones Should We Measure for Risk Prediction in Our Practice?. Arch Intern Med 166: 2428-2430 [Full Text]  
• Rothenbacher, D., Koenig, W., Brenner, H. (2006). Comparison of N-Terminal Pro-B-Natriuretic Peptide, C-Reactive Protein, and Creatinine Clearance for Prognosis in Patients With Known Coronary Heart Disease. Arch Intern Med 166: 2455-2460 [Abstract] [Full Text]  
• Whalley, G A, Gamble, G D, Doughty, R N (2006). Restrictive diastolic filling predicts death after acute myocardial infarction: systematic review and meta-analysis of prospective studies. Heart 92: 1588-1594 [Abstract] [Full Text]  
• James, S. K., Lindback, J., Tilly, J., Siegbahn, A., Venge, P., Armstrong, P., Califf, R., Simoons, M. L., Wallentin, L., Lindahl, B. (2006). Troponin-T and N-Terminal Pro-B-Type Natriuretic Peptide Predict Mortality Benefit From Coronary Revascularization in Acute Coronary Syndromes: A GUSTO-IV Substudy. J Am Coll Cardiol 48: 1146-1154 [Abstract] [Full Text]  
• Westerhout, C. M., Fu, Y., Lauer, M. S., James, S., Armstrong, P. W., Al-Hattab, E., Califf, R. M., Simoons, M. L., Wallentin, L., Boersma, E., on behalf of the GUSTO-IV ACS Trial Investigators, (2006). Short- and Long-Term Risk Stratification in Acute Coronary Syndromes: The Added Value of Quantitative ST-Segment Depression and Multiple Biomarkers. J Am Coll Cardiol 48: 939-947 [Abstract] [Full Text]  
• O'Donoghue, M., de Lemos, J. A., Morrow, D. A., Murphy, S. A., Buros, J. L., Cannon, C. P., Sabatine, M. S. (2006). Prognostic Utility of Heart-Type Fatty Acid Binding Protein in Patients With Acute Coronary Syndromes. Circulation 114: 550-557 [Abstract] [Full Text]  
• Adesanya, A. O., de Lemos, J. A., Greilich, N. B., Whitten, C. W. (2006). Management of perioperative myocardial infarction in noncardiac surgical patients.. Chest 130: 584-596 [Abstract] [Full Text]  
• Giugliano, R. P., Braunwald, E. (2006). The Year in Non-ST-Segment Elevation Acute Coronary Syndromes. J Am Coll Cardiol 48: 386-395 [Full Text]  
• Kistorp, C. (2006). Risk Stratification in Secondary Prevention: Advances in Multimarker Profiles, or Back to Basics?. Circulation 114: 184-186 [Full Text]  
• Blankenberg, S., McQueen, M. J., Smieja, M., Pogue, J., Balion, C., Lonn, E., Rupprecht, H. J., Bickel, C., Tiret, L., Cambien, F., Gerstein, H., Munzel, T., Yusuf, S., for the HOPE Study Investigators, (2006). Comparative Impact of Multiple Biomarkers and N-Terminal Pro-Brain Natriuretic Peptide in the Context of Conventional Risk Factors for the Prediction of Recurrent Cardiovascular Events in the Heart Outcomes Prevention Evaluation (HOPE) Study. Circulation 114: 201-208 [Abstract] [Full Text]  
• Rana, B S, Davies, J I, Band, M M, Pringle, S D, Morris, A, Struthers, A D (2006). B-type natriuretic peptide can detect silent myocardial ischaemia in asymptomatic type 2 diabetes. Heart 92: 916-920 [Abstract] [Full Text]  
• Koenig, W., Twardella, D., Brenner, H., Rothenbacher, D. (2006). Lipoprotein-Associated Phospholipase A2 Predicts Future Cardiovascular Events in Patients With Coronary Heart Disease Independently of Traditional Risk Factors, Markers of Inflammation, Renal Function, and Hemodynamic Stress. Arterioscler. Thromb. Vasc. Bio. 26: 1586-1593 [Abstract] [Full Text]  
• Hammerer-Lercher, A., Geiger, R., Mair, J., Url, C., Tulzer, G., Lechner, E., Puschendorf, B., Sommer, R. (2006). Utility of N-Terminal Pro-B-Type Natriuretic Peptide to Differentiate Cardiac Diseases from Noncardiac Diseases in Young Pediatric Patients. Clin. Chem. 52: 1415-1419 [Abstract] [Full Text]  
• Scirica, B. M., Morrow, D. A., Cannon, C. P., Ray, K. K., Sabatine, M. S., Jarolim, P., Shui, A., McCabe, C. H., Braunwald, E., for the PROVE IT-TIMI 22 Investigators, (2006). Intensive Statin Therapy and the Risk of Hospitalization for Heart Failure After an Acute Coronary Syndrome in the PROVE IT-TIMI 22 Study. J Am Coll Cardiol 47: 2326-2331 [Abstract] [Full Text]  
• Vasan, R. S. (2006). Biomarkers of Cardiovascular Disease: Molecular Basis and Practical Considerations. Circulation 113: 2335-2362 [Full Text]  
• Laukkanen, J. A., Kurl, S., Ala-Kopsala, M., Vuolteenaho, O., Ruskoaho, H., Nyyssonen, K., Salonen, J. T. (2006). Plasma N-terminal fragments of natriuretic propeptides predict the risk of cardiovascular events and mortality in middle-aged men. Eur Heart J 27: 1230-1237 [Abstract] [Full Text]  
• Body, R., Roberts, C. (2006). Brain natriuretic peptide as a potential marker of acute coronary syndromes. Emerg. Med. J. 23: 403-407 [Abstract] [Full Text]  
• McKie, P. M., Rodeheffer, R. J., Cataliotti, A., Martin, F. L., Urban, L. H., Mahoney, D. W., Jacobsen, S. J., Redfield, M. M., Burnett, J. C. Jr (2006). Amino-Terminal Pro-B-Type Natriuretic Peptide and B-Type Natriuretic Peptide: Biomarkers for Mortality in a Large Community-Based Cohort Free of Heart Failure. Hypertension 47: 874-880 [Abstract] [Full Text]  
• Morrow, D. A. (2006). Prognostic Value of B-Type Natriuretic Peptide in Unstable Coronary Artery Disease--Reply. JAMA 295: 1895-1896 [Full Text]  
• Chen, A. A., Wood, M. J., Krauser, D. G., Baggish, A. L., Tung, R., Anwaruddin, S., Picard, M. H., Januzzi, J. L. (2006). NT-proBNP levels, echocardiographic findings, and outcomes in breathless patients: results from the ProBNP Investigation of Dyspnoea in the Emergency Department (PRIDE) echocardiographic substudy. Eur Heart J 27: 839-845 [Abstract] [Full Text]  
• Suleiman, M., Khatib, R., Agmon, Y., Mahamid, R., Boulos, M., Kapeliovich, M., Levy, Y., Beyar, R., Markiewicz, W., Hammerman, H., Aronson, D. (2006). Early Inflammation and Risk of Long-Term Development of Heart Failure and Mortality in Survivors of Acute Myocardial Infarction: Predictive Role of C-Reactive Protein. J Am Coll Cardiol 47: 962-968 [Abstract] [Full Text]  
• Iwanaga, Y., Nishi, I., Furuichi, S., Noguchi, T., Sase, K., Kihara, Y., Goto, Y., Nonogi, H. (2006). B-Type Natriuretic Peptide Strongly Reflects Diastolic Wall Stress in Patients With Chronic Heart Failure: Comparison Between Systolic and Diastolic Heart Failure. J Am Coll Cardiol 47: 742-748 [Abstract] [Full Text]  
• Davis, M. E., Richards, A. M., Nicholls, M. G., Yandle, T. G., Frampton, C. M., Troughton, R. W. (2006). Introduction of Metoprolol Increases Plasma B-Type Cardiac Natriuretic Peptides in Mild, Stable Heart Failure. Circulation 113: 977-985 [Abstract] [Full Text]  
• Schnabel, R., Lubos, E., Rupprecht, H. J., Espinola-Klein, C., Bickel, C., Lackner, K. J., Cambien, F., Tiret, L., Munzel, T., Blankenberg, S. (2006). B-Type Natriuretic Peptide and the Risk of Cardiovascular Events and Death in Patients With Stable Angina: Results From the AtheroGene Study. J Am Coll Cardiol 47: 552-558 [Abstract] [Full Text]  
• Richards, M., Nicholls, M. G., Espiner, E. A., Lainchbury, J. G., Troughton, R. W., Elliott, J., Frampton, C. M., Crozier, I. G., Yandle, T. G., Doughty, R., MacMahon, S., Sharpe, N., for the Christchurch Cardioendocrine Research Grou, , and the Australia-New Zealand Heart Failure Group, (2006). Comparison of B-Type Natriuretic Peptides for Assessment of Cardiac Function and Prognosis in Stable Ischemic Heart Disease. J Am Coll Cardiol 47: 52-60 [Abstract] [Full Text]  
• Talens-Visconti, R., Rivera Otero, M., Sancho-Tello, M. J., de Burgos, F. G., Martinez-Dolz, L., Sevilla, B., Climent, V., Cortes, R., Salvador, A., Sogorb, F., Miro, V., Valero, R., Perez-Bosca, J. L., Bertomeu, V., Portoles, M., Paya, R. (2006). Left ventricular cavity area reflects N-terminal pro-brain natriuretic peptide plasma levels in heart failure. Eur J Echocardiogr 7: 45-52 [Abstract] [Full Text]  
• Morrow, D. A., de Lemos, J. A., Blazing, M. A., Sabatine, M. S., Murphy, S. A., Jarolim, P., White, H. D., Fox, K. A. A., Califf, R. M., Braunwald, E., for the A to Z Investigators, (2005). Prognostic Value of Serial B-Type Natriuretic Peptide Testing During Follow-up of Patients With Unstable Coronary Artery Disease. JAMA 294: 2866-2871 [Abstract] [Full Text]  
• De Sutter, J., De Bacquer, D., Cuypers, S., Delanghe, J., De Buyzere, M., Kornitzer, M., De Backer, G. (2005). Plasma N-terminal pro-brain natriuretic peptide concentration predicts coronary events in men at work: a report from the BELSTRESS study. Eur Heart J 26: 2644-2649 [Abstract] [Full Text]