JACC
HOME SUBSCRIPTIONS CURRENT ISSUE PAST ISSUES CARDIOSOURCE SEARCH HELP FEEDBACK
QUICK SEARCH:   [advanced]


     

J Am Coll Cardiol, 2007; 49:1733-1739, doi:10.1016/j.jacc.2006.10.081 (Published online 30 March 2007).
© 2007 by the American College of Cardiology Foundation
This Article
Right arrow Abstract Freely available
Right arrow Figures Only
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
j.jacc.2006.10.081v1
49/16/1733    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (44)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Jourdain, P.
Right arrow Articles by Juillière, Y.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Jourdain, P.
Right arrow Articles by Juillière, Y.

EXPEDITED REVIEW

Plasma Brain Natriuretic Peptide-Guided Therapy to Improve Outcome in Heart Failure

The STARS-BNP Multicenter Study

Patrick Jourdain, MD*,{dagger},{ddagger},*, Guillaume Jondeau, MD, PhD§, François Funck, MD{ddagger}, Pascal Gueffet, MD||, Alain Le Helloco, MD, Erwan Donal, MD, Jean F. Aupetit, MD#, Marie C. Aumont, MD§, Michel Galinier, MD, PhD**, Jean C. Eicher, MD{dagger}{dagger}, Alain Cohen-Solal, MD, PhD{ddagger}{ddagger} and Yves Juillière, MD, PhD§§

* René Descartes University, Paris, France
{dagger} Georges Pompidou Hospital, Paris, France
§ Department of Cardiology, Bichat University Hospital, Paris, France
{ddagger}{ddagger} Department of Cardiology, Centre Hospitalier Universitaire de Lariboisière, Paris, France
{ddagger} Hospitalier de Rene Dubos, Pontoise, France
|| Centre Hospitalier Universitaire de Nantes, Nantes, France
Centre Hospitalier Universitaire de Rennes, Rennes, France
# Hopital Saint Luc Lyon, Lyon, France
** Department of Cardiology, Centre Hospitalier Universitaire de Toulouse, Toulouse, France
{dagger}{dagger} Centre Hospitalier Universitaire de Dijon, Dijon, France
§§ Department of Cardiology, Centre Hospitalier Universitaire de Vandoeuvre Les Nancy, Vandoeuvre Les Nancy, France.

Manuscript received September 12, 2006; revised manuscript received October 10, 2006, accepted October 22, 2006.

* Reprint requests and correspondence: Dr. Patrick Jourdain, Hopital de Pontoise, CH Rene Dubos, Heart Failure Department, 6 Avenue de France, Pontoise, 95301 France. (Email: patrick.jourdain{at}ch-pontoise.fr).


   Abstract
Top
 Abstract
Methods
 Results
 Discussion
 Conclusions
 References
 
Objectives: The aim of this multicenter study was to evaluate the prognostic impact of a therapeutic strategy using plasma brain natriuretic peptide (BNP) levels.

Background: The prognosis of chronic heart failure (CHF) remains poor, even among patients treated in specialized departments.

Methods: A total of 220 New York Heart Association functional class II to III patients considered optimally treated with angiotensin-converting enzyme inhibitors (ACEIs), beta-blockers, and diuretics by CHF specialists were randomized to medical treatment according to either current guidelines (clinical group) or a goal of decreasing BNP plasma levels <100 pg/ml (BNP group). Outpatient visits were scheduled every month for 3 months, then every 3 months. The primary combined end point was CHF-related death or hospital stay for CHF.

Results: Both groups were similar for baseline clinical and biological characteristics. Left ventricular ejection fraction was slightly lower in the BNP group than in the clinical group (29.9 ± 7.7% vs. 31.8 ± 8.4%, p = 0.05). At the end of the first 3 months, all types of drugs were changed more frequently in the BNP group. Mean dosages of ACEIs and beta-blockers were significantly higher in the BNP group (p < 0.05), whereas the mean increase in furosemide dosage was similar in both groups. During follow-up (median 15 months), significantly fewer patients reached the combined end point in the BNP group (24% vs. 52%, p < 0.001).

Conclusions: In optimally treated CHF patients, a BNP-guided strategy reduced the risk of CHF-related death or hospital stay for CHF. The result was mainly obtained through an increase in ACEI and beta-blocker dosages.

Abbreviations and Acronyms
  ACEI = angiotensin-converting enzyme inhibitor
  ARB = angiotensin II-receptor blockers
  BNP = brain natriuretic peptide
  CHF = chronic heart failure
  LVEF = left ventricular ejection fraction
  NYHA = New York Heart Association

Optimal treatment of heart failure includes angiotensin-converting enzyme inhibitors (ACEIs), beta-blockers, spironolactone, and diuretics, as recommended by the international guidelines (1,2). Treatment optimization is currently based on physician experience and patient tolerance. Chronic heart failure (CHF) remains the main reason for hospital stay among patients >65 years of age and is associated with high mortality (3,4). However, implementation of guidelines remains imperfect (5).

Brain natriuretic peptide (BNP) is a 32-amino acid protein secreted by cardiac ventricles (6–9). The diagnostic and prognostic value of BNP plasma levels in CHF is supported by many studies (10–15). Most drugs used to treat heart failure significantly reduce BNP levels (16–18). In the Val-HeFT (Valsartan Heart Failure Trial), only patients receiving valsartan in addition to conventional therapy presented with a significant reduction in plasma BNP levels compared with the placebo group (19). Recent data from RALES (Randomized Aldactone Evaluation Study) showed that spironolactone can also markedly reduce BNP levels in patients with severe heart failure (20). The effect of beta-blockers on BNP remains controversial. In randomized trials, patients with the most marked neurohormonal activation and the highest BNP levels at enrollment seemed to benefit most from beta-blocker therapy (21–23). More recent data showed a significant N-terminal pro-BNP reduction in patients receiving carvedilol or metoprolol (24).

Plasma BNP level monitoring has been proposed for treatment optimization in patients with heart failure (25–27). However, these studies included few patients, most of whom did not receive beta-blocker therapy. Thus, the aim of this French multicenter randomized study was to evaluate the benefit of BNP-guided therapy on outcome in CHF patients in clinical practice.


   Methods
Top
 Abstract
 Methods
Results
 Discussion
 Conclusions
 References
 
Study population.   The patients were included by CHF specialists from 17 university hospitals. All investigators had expertise in CHF management and were members of the Working Group on Heart Failure (WGHF) of the French Society of Cardiology.

The inclusion criteria were as follows: patients older than 18 years with symptomatic (New York Heart Association [NYHA] functional class II to III) systolic heart failure defined by left ventricular ejection fraction (LVEF) <45% assessed by echocardiography using the American Society of Echocardiography guidelines, in stable condition (no hospital stay in the previous month), and treated by optimal medical therapy according to the European guidelines at the time of the study (1); dosages of medications were to be stable for at least 1 month before inclusion. Patients had to receive diuretics, ACEIs, or angiotensin II-receptor blockers (ARB) at the maximal tolerated dosage unless documented intolerance and beta-blockers approved for CHF (carvedilol, bisoprolol, and metoprolol XR-CL), at the maximal tolerated dosage unless documented intolerance or specific contra-indication. All patients signed informed consent.

The exclusion criteria were as follows: acute coronary syndrome within 3 months, chronic renal failure (plasma creatininemia >250 µmol/l), documented hepatic cirrhosis, asthma, or chronic obstructive pulmonary disease.

Study design.   Patients were randomized into 2 groups:

• BNP group: medical therapy was increased with the aim of lowering plasma BNP levels (target <100 pg/ml) (1,10); each class of therapy could be modified according to the judgment of the investigator.
• Clinical group: medical therapy was adjusted according to the opinion of the investigator, on the basis of the physical examination and usual paraclinical and biological parameters. The investigators were not allowed to measure plasma BNP level.
Outpatient visits were scheduled every month for the first 3 months and every 3 months thereafter. During the titration phase (3 months), each visit included physical examination, electrocardiogram recording, and blood sample measurements. Plasma sodium levels, renal function, and hemoglobin were measured in both groups, whereas plasma BNP level was measured only in patients belonging to BNP group. During the follow-up phase, each visit included a clinical examination. The BNP was systematically measured only in the BNP group.

The protocol of the study was written by the WGHF of the French Society of Cardiology and approved by the CCPPRB (French legal ethics committee). Each patient gave written informed consent.

Plasma BNP level measurement.   Venous blood sample was taken after 20 min of rest in the supine position and collected on an EDTA tube. The BNP was immediately measured with the immunofluorometric triage method (28) (Biosite Inc., San Diego, California). The BNP triage assay variability was 10% for a threshold of 800 pg/ml and 15% for a threshold of 100 pg/ml.

Primary and secondary end points.   The primary composite end point was defined as unplanned hospital stays for heart failure or death related to heart failure. Hospital stays were decided by the physician in the emergency room, not involved in the study, and unaware of plasma BNP levels. The BNP plasma levels were kept in a specific patient chart and accessible only to investigator. Patients also were blinded for BNP results. The secondary end points were all-cause death, death related to heart failure, all-cause hospital stay, and hospital stay for heart failure.

Statistical analysis.   Intent-to-treat principles were used. Continuous variables are presented as mean ± SD. Comparisons between continuous variables were made with Student parametric unpaired t test for between group comparison and paired t test for 6-month versus baseline comparison. Proportions were compared with the chi-square test. A statistical difference was considered significant if p < 0.05. Survival was evaluated with the Kaplan-Meier method. Differences in survival between the 2 groups were compared with log-rank analysis. Statistical analyses were performed with the SPSS version 11.0 software (SPSS Inc., Chicago, Illinois).


   Results
Top
 Abstract
 Methods
 Results
Discussion
 Conclusions
 References
 
Baseline.   Each group included 110 patients. Mean age of the patients was 65 ± 5 years; 73% were male. Complete baseline patient characteristics are reported in Table 1. Patients had severe heart failure with a mean LVEF of 30 ± 8% and a mean left ventricular end-diastolic diameter of 67 ± 12 mm.


View this table:
[in this window]
[in a new window]

  		Table 1 Population Characteristics at Baseline According to the Group Allocation
 
The 2 groups were comparable in terms of left ventricular end-diastolic diameter, NYHA functional class, hemodynamic parameters, QRS duration, and biological parameters. However, percentage of active smokers (p = 0.03) and mean LVEF (p = 0.05) were lower in the BNP group than in the clinical group. Both groups were also similar for background medical therapies. At baseline, medical treatment was optimized in the population: 99% of patients received an ACEI or an ARB at 94% of the recommended dosage (Table 1). Similarly, 94% of patients received a beta-blocker at 58% of the recommended dosage. All the patients received furosemide. Therefore, the background therapy was truly optimized before entry into the study.

Titration phase: treatment adjustment during the first 3 months.   Changes in treatment occurred more frequently in the BNP group compared with the clinical group, 134 versus 66 occasions (p < 0.05). In the BNP group, the treatment was adjusted according to the plasma BNP level in 79% of the cases (106 of 134 treatment changes) (Fig. 1).


Figure 1
View larger version (20K):
[in this window]
[in a new window]
[Download PPT slide]
  		Figure 1 Number of Changes in Medical Therapy During the First 3 Months

Changes were related to high brain natriuretic peptide (BNP) value according to protocol or clinical reasons.

 
The most frequently changed pharmacological drugs were diuretics (41% of the changes in the BNP group vs. 39% of the changes in the clinical group, p = NS) (Fig. 2). The mean increase in furosemide dosage was 9 ± 20 mg and was similar in both groups. However, all types of drugs were changed more frequently in the BNP group (furosemide: 55% vs. 26% of the patients; spironolactone: 17% vs. 7% of the patients; ACEI or ARB: 21% vs. 9% of the patients; beta-blockers: 36% vs. 20% of the patients).


Figure 2
View larger version (35K):
[in this window]
[in a new window]
[Download PPT slide]
  		Figure 2 Changes in Medical Therapy During the Titration Phase in BNP Group and Clinical Group

Therapeutic modifications during titration phase. ACEI = angiotensin-converting enzyme inhibitor; BNP = brain natriuretic peptide.

 
During the first 3 months, the mean daily dosage of ACEI increased in the 2 groups (from 94% to 98% of the recommended dosage in the clinical group, p = NS, and from 94% to 106% of the recommended dosage in the BNP group, p < 0.05) as well as the mean daily dosage of beta-blockers (from 57% to 67% of the recommended dosage in the clinical group, p < 0.05, and from 58% to 77% of the recommended dosage in the BNP group, p < 0.05). However, at the end of the first 3 months, the mean dosages of ACEIs and beta-blockers, expressed as percentage of recommended dosage, were significantly higher in the BNP group than in the clinical group (p < 0.05).

Titration phase: clinical and biological variations.   During the first 3 months, NYHA functional class improved in both groups. There was no difference for mean NYHA class for the 2 groups at the end of the titration phase (2.1 ± 0.5 vs. 2.0 ± 0.4, p = NS). Blood pressure, heart rate, and weight decreased in a comparable way in the 2 groups (Fig. 3). Similar clinical adverse events rates occurred in the 2 groups.


Figure 3
View larger version (18K):
[in this window]
[in a new window]
[Download PPT slide]
  		Figure 3 Evolution of Systolic Blood Pressure, Heart Rate, Weight, and Creatininemia During the First 3 Months

Hemodynamic and biological variations during titration phase. BNP = brain natriuretic peptide; M = month.

 
Creatininemia (Fig. 3) and azotemia tended to increase during the titration phase in the 2 groups (p = NS). Increase in creatininemia by more than 30% was observed in 9% of the control group and in 7% of the BNP group (p = NS). There was no significant variation in potassium or sodium levels.

Follow-up.   No patient was lost to follow-up (Fig. 4). During follow-up (minimum 6 months, median 15 months), the primary composite end point (unplanned hospital stays for heart failure or death related to heart failure) was observed in 83 occasions in the 220 patients (38%) (25 of 110 [24%] in the BNP group vs. 57 of 110 [52%] in the clinical group, p < 0.001). By log-rank analysis, event-free survival was also significantly better in the BNP group (84%) than in the clinical group (73%) (p < 0.01) (Fig. 4).


Figure 4
View larger version (12K):
[in this window]
[in a new window]
[Download PPT slide]
  		Figure 4 Event-Free (Hospital Stay for Heart Failure or Death Related to Heart Failure) Survival in the 2 Groups

Event-free survival. BNP = brain natriuretic peptide.

 
All-cause death was not significantly different between the groups (7 in the BNP group vs. 11 in the clinical group, p = NS). Death related to heart failure was observed in 3 patients in the BNP group versus 9 patients in the clinical group. Six patients died from non–CHF-related causes (2 of cancer, 3 of pulmonary embolism, 1 of endocarditis).

All-cause hospital stays were not significantly different between the 2 groups: 60 patients in the clinical group versus 52 in the BNP group (p = NS).

Hospital stays for heart failure were observed in 22 patients in the BNP group versus 48 patients in the clinical group (p < 0.0001). Two patients in the BNP group versus 10 patients in the clinical group were hospitalized twice or more for acute heart failure decompensation (p < 0.02).

In the BNP group, mean plasma BNP levels significantly decreased during follow-up from 352 ± 260 pg/ml at baseline to 284 ± 180 pg/ml at 3-month follow-up (p = 0.03). Accordingly, the target (<100 pg/ml) was reached in 16% of patients at baseline to 33% at 3-month follow-up (p = 0.04) (Fig. 5).


Figure 5
View larger version (41K):
[in this window]
[in a new window]
[Download PPT slide]
  		Figure 5 Plasma BNP Level in BNP Group During Titration Phase and % of Patients Reaching Target BNP Value

BNP = brain natriuretic peptide; M = month.

 

   Discussion
Top
 Abstract
 Methods
 Results
 Discussion
Conclusions
 References
 
This study has shown that CHF treatment optimization based on plasma BNP levels is associated with a lower risk of death related to heart failure or hospital stay related to heart failure than the usual strategy based on clinical expertise. The benefit was observed despite optimization of therapy in both groups by cardiologists specialized in congestive heart failure before entry into the study (more than 95% of the patients received a recommended triple therapy: ACEI or ARB + beta-blocker + furosemide).

Suboptimal dosages of beta-blockers were reported in the EuroHeart Failure Survey (29), much lower than that prescribed at baseline in our study. However, in our study, dosage at baseline remained below those reached during recent multicenter beta-blocker trials (30,31), and inclusion into the study led to significant increase in diuretics, ACEIs, and beta-blockers in both groups. Optimization is actually a long-term aim, and a patient’s condition varies from time to time. Beta-blocker and ACEI increases were well tolerated.

Previous studies have examined BNP variations and their prognostic implications during medical therapy. In the first landmark study, Throughton et al. (26) observed a significant reduction in all-cause mortality and in heart failure-related hospital stay with BNP-guided medical therapy. However, the sample size was limited (69 patients), and medical therapy mainly consisted of ACEI and diuretics without beta-blockers.

Brain natriuretic peptide is a noninvasive marker of ventricular myocyte stretch and correlates with left end-diastolic pressure (9,32). High BNP values can identify patients with high left end-diastolic pressures who would benefit from medical optimization (32). Interestingly, in our study, diuretic dosages and weight variations were similar in both groups, whereas plasma BNP level is dependent on blood volume.

It had been expected that a high plasma BNP level would lead to an increase in diuretic dosage. In fact, the use of plasma BNP levels led also to an increase in ACEIs and beta-blockers. During the trial, we found that the association of abnormal BNP levels plus clinical examination was more meaningful to the cardiologist and led to more optimization in medications than clinical examination alone. Whether knowledge of BNP plasma level is beneficial through better evaluation of the CHF status of the patient or acts as a supplementary stimulus for increasing all drugs remains to be determined.

Study limitations.   In our study, the benefit of the BNP-guided strategy was tested after medical therapy had been optimized by highly qualified cardiologists. The benefit might actually be larger in routine clinical practice.

Similarly, baseline LVEF tended to be lower in the BNP group, which would be expected to increase the number of clinical events. This actually strengthens the results of our study.

As in other randomized studies, our population was young, mostly male, and limited to systolic dysfunction (LVEF <45%). Medical registers demonstrate that CHF patients are older and frequently female and diastolic dysfunction is increasingly prevalent. Our results only apply to the selected population included.


   Conclusions
Top
 Abstract
 Methods
 Results
 Discussion
 Conclusions
References
 
In optimally treated CHF patients with left ventricular systolic dysfunction, a BNP-guided strategy reduces the incidence of a combined end point (death and hospital stay related to heart failure) compared with a standard strategy. The result is mainly obtained through an increase in ACEI and beta-blocker dosages.


   Acknowledgments
 
The following is a list of the French investigators involved in the STARS-BNP study: National Coordinator: Patrick Jourdain (Pontoise); Investigators: Marie-Claude Aumont (Paris), Jean-François Aupetit (Lyon), Jean-Marc Davy (Montpellier), Michel Desnos (Paris), Erwan Donal (Poitiers), Jean-Christophe Eicher (Dijon), François Funck (Pontoise), Pascal De Groote (Lille), Michel Galinier (Toulouse), Pierre Gibelin (Nice), Jean-Yves Gueffet (Nantes), Guillaume Jondeau (Boulogne-Billancourt), Yves Juillière, Chairman of the French Working Group on Heart Failure (Nancy), Yves Kettelers (Armentières), Michel Komajda (Paris), Alain Le Helloco (Rennes), and Damien Logeart (Clichy).


   Footnotes
 
The STARS study was supported by an unrestricted grant from Biosite Inc. (San Diego, California) to the French Working Group on Heart Failure. Gary Francis, MD, FACC, served as Guest Editor for this article.


   References
Top
 Abstract
 Methods
 Results
 Discussion
 Conclusions
 References
 

  1. The Task Force for the Diagnosis and Treatment of Chronic Heart Failure ESC guidelines for the diagnosis and treatment of chronic heart failure Eur Heart J 2001;22:1527-1560.[Free Full Text]
  2. Hunt SA, Baker DW, Chin MH, et al. ACC/AHA guidelines for the evaluation and management of chronic heart failure in the adult: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines Circulation 2001;104:2996-3007.[Free Full Text]
  3. Cleland JGF, Swedberg K, Follath F, et al. The EuroHeart Failure survey program—a survey on the quality of care among patients with heart failure in EuropePart 1: patient characteristics and diagnosis. Eur Heart J 2003;24:442-463.[Abstract/Free Full Text]
  4. McCullough PA, Philbin EF, Spertus JA, et al. Confirmation of a heart failure epidemic: findings from the Resource Utilization Among Congestive Heart Failure (REACH) study J Am Coll Cardiol 2002;39:60-69.[Abstract/Free Full Text]
  5. Redfield MM. Heart failure, an epidemic of uncertain proportions N Engl J Med 2002;347:1442-1444.[Free Full Text]
  6. Nakao K, Ogawa Y, Suga SI, et al. Molecular biology and biochemistry of the natriuretic peptide system J Hypertension 1992;10:907-912.[ISI][Medline]
  7. 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.[Abstract/Free Full Text]
  8. Hosoda K, Nakao K, Mukoyama M, et al. Expression of brain natriuretic peptide gene in human heart: production in the ventricle Hypertension 1991;17:1152-1156.[Abstract/Free Full Text]
  9. Levin ER, Gardner DG, Samson W. Natriuretic peptides N Engl J Med 1998;339:321-328.[Free Full Text]
  10. 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]
  11. McCullough PA, Nowak RM, McCord J, et al. B-type natriuretic peptide and clinical judgment in emergency diagnosis of heart failure: analysis from Breathing Not Properly (BNP) multinational study Circulation 2002;106:416-422.[Abstract/Free Full Text]
  12. Stanek B, Frey B, Hulsmann M, et al. Prognostic evaluation of neurohumoral plasma levels before and during beta-blocker therapy in advanced left ventricular dysfunction J Am Coll Cardiol 2001;38:436-442.[Abstract/Free Full Text]
  13. Koglin J, Pehlivanli S, Schwaiblmair M, et al. Role of brain natriuretic peptide in risk stratification of patients with congestive heart failure J Am Coll Cardiol 2001;38:1934-1941.[Abstract/Free Full Text]
  14. Bettencourt P, Ferreira A, Dias P, et al. Predictors of prognosis in mild to moderate heart failure J Card Fail 2000;6:306-313.[CrossRef][ISI][Medline]
  15. Gardner RS, Ozalo F, Murday AJ, Robb SD, McDonagh TA. N terminal pro-brain natriuretic peptideA new gold standard in predicting mortality in patients with advanced heart failure. Eur Heart J 2003;24:1735-1743.[Abstract/Free Full Text]
  16. Yoshimura M, Mizuno Y, Nakayama M, et al. B-type natriuretic peptide as a marker of the effects of enalapril in patients with heart failure Am J Med 2002;112:716-720.[CrossRef][ISI][Medline]
  17. Ferreira A, Bettencourt P, Dias P, et al. Neurohormonal activation, the renal dopaminergic system and sodium handling in patients with severe heart failure under vasodilator therapy Clin Sci (Lond) 2001;1:100-105.
  18. Murdoch DR, McDonagh TA, Byrne J, et al. Titration of vasodilator therapy in chronic heart failure according to plasma brain natriuretic peptide concentration: randomized comparison of the hemodynamic and neuroendocrine effects of tailored versus empirical therapy Am Heart J 1999;138:1126-1132.[CrossRef][ISI][Medline]
  19. Latini R, Mason S, Anand I, et al. Effects of valsartan on circulating brain natriuretic peptide and norepinephrine in symptomatic chronic heart failure: the Valsartan Heart Failure Trial (Val-HeFT) Circulation 2002;106:2454-2458.[Abstract/Free Full Text]
  20. Tsutamoto T, Wada A, Maeda K, et al. Effect of spironolactone on plasma brain natriuretic peptide in patients with congestive heart failure J Am Coll Cardiol 2001;37:1228-1233.[Abstract/Free Full Text]
  21. Bettencourt P, Frioes F, Azevedo A, et al. Prognostic information provided by serial measurements of brain natriuretic peptide in heart failure Int J Cardiol 2004;93:45-48.[CrossRef][ISI][Medline]
  22. Richards AM, Doughty R, Nicholls MG, et al. Plasma N-terminal pro-brain natriuretic peptide and adrenomedullin: prognostic utility and prediction of benefit from carvedilol in chronic ischemic left ventricular dysfunction J Am Coll Cardiol 2001;37:1781-1787.[Abstract/Free Full Text]
  23. Richards A, Doughty R, Nicholls M. Neurohumoral prediction of benefit from carvedilol in ischaemic left ventricular dysfunction Circulation 1999;99:786-792.[Abstract/Free Full Text]
  24. Fung JW, Yu CM, Yip G, et al. Effect of beta-blockade (carvedilol or metoprolol) on activation of the renin-angiotensin-aldosterone system and natriuretic peptides in chronic heart failure Am J Cardiol 2003;92:406-410.[CrossRef][ISI][Medline]
  25. 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.[Abstract/Free Full Text]
  26. Troughton RW, Frampton CM, Yandle TG. Treatment of heart failure guided by plasma aminoterminal brain natriuretic peptide (N-BNP) concentrations Lancet 2000;355:1126-1130.[CrossRef][ISI][Medline]
  27. Richards M, Throughton RW. NT pro-BNP in heart failure therapy decision and monitoring Eur J Heart Failure 2004;6:351-354.[CrossRef][ISI][Medline]
  28. Vogeser M, Jacob K. B-type natriuretic peptide (BNP)—validation of an immediate response assay Clin Lab 2001;47:29-33.[Medline]
  29. The Study Group of Diagnosis of the Working Group on Heart Failure of the European Society of Cardiology The EuroHeart Failure Survey program—a survey on the quality of care among patients with heart failure in EuropePart 2: treatment. Eur Heart J 2003;24:464-474.[Abstract/Free Full Text]
  30. Packer M, Coats AJ, Fowler MB, et al. Effect of carvedilol on survival in severe chronic heart failure N Engl J Med 2001;344:1651-1658.[Abstract/Free Full Text]
  31. Poole-Wilson PA, Swedberg K, Cleland JGF, et al. Comparison of carvedilol and metoprolol on clinical outcomes in patients with chronic heart failure in the Carvedilol Or Metoprolol European Trial (COMET): randomised controlled trial Lancet 2003;362:7-13.[CrossRef][ISI][Medline]
  32. Maeda K, Tsutamoto T, Wada A. Plasma brain natriuretic peptide as a biochemical marker of high left ventricular end-diastolic pressure in patients with symptomatic left ventricular dysfunction Am Heart J 1998;135:825-832.[CrossRef][ISI][Medline]



This article has been cited by other articles:


Home page
 Eur Heart JHome page
Authors/Task Force Members, K. Dickstein, A. Cohen-Solal, G. Filippatos, J. J.V. McMurray, P. Ponikowski, P. A. Poole-Wilson, A. Stromberg, D. J. van Veldhuisen, D. Atar, et al.
ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2008: The Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2008 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association of the ESC (HFA) and endorsed by the European Society of Intensive Care Medicine (ESICM)
Eur. Heart J., October 1, 2008; 29(19): 2388 - 2442.
[Full Text] [PDF]

Home page
 J Am Coll CardiolHome page
S. Masson, R. Latini, I. S. Anand, S. Barlera, L. Angelici, T. Vago, G. Tognoni, J. N. Cohn, and for the Val-HeFT Investigators
Prognostic Value of Changes in N-Terminal Pro-Brain Natriuretic Peptide in Val-HeFT (Valsartan Heart Failure Trial)
J. Am. Coll. Cardiol., September 16, 2008; 52(12): 997 - 1003.
[Abstract] [Full Text] [PDF]

Home page
 Eur Heart JHome page
L. Frankenstein, A. Remppis, M. Nelles, B. Schaelling, D. Schellberg, H. Katus, and C. Zugck
Relation of N-terminal pro-brain natriuretic peptide levels and their prognostic power in chronic stable heart failure to obesity status
Eur. Heart J., September 2, 2008; (2008) ehn388v1.
[Abstract] [Full Text] [PDF]

Home page
 Eur Heart JHome page
D. Kelly, S. Q. Khan, M. Thompson, G. Cockerill, L. L. Ng, N. Samani, and I. B. Squire
Plasma tissue inhibitor of metalloproteinase-1 and matrix metalloproteinase-9: novel indicators of left ventricular remodelling and prognosis after acute myocardial infarction
Eur. Heart J., September 1, 2008; 29(17): 2116 - 2124.
[Abstract] [Full Text] [PDF]

Home page
 J. Am. Soc. Nephrol.Home page
A. Y.-M. Wang and K.-N. Lai
Use of Cardiac Biomarkers in End-Stage Renal Disease
J. Am. Soc. Nephrol., September 1, 2008; 19(9): 1643 - 1652.
[Abstract] [Full Text] [PDF]

Home page
 J. Thorac. Cardiovasc. Surg.Home page
A. A. Fox, S. K. Shernan, C. D. Collard, K.-Y. Liu, S. F. Aranki, S. M. DeSantis, P. Jarolim, and S. C. Body
Preoperative B-type natriuretic peptide is as independent predictor of ventricular dysfunction and mortality after primary coronary artery bypass grafting.
J. Thorac. Cardiovasc. Surg., August 1, 2008; 136(2): 452 - 461.
[Abstract] [Full Text] [PDF]

Home page
 QJMHome page
P. Ray, S. Delerme, P. Jourdain, and C. Chenevier-Gobeaux
Differential diagnosis of acute dyspnea: the value of B natriuretic peptides in the emergency department
QJM, July 29, 2008; (2008) hcn080v1.
[Abstract] [Full Text] [PDF]

Home page
 J Am Coll CardiolHome page
M. Nishii, T. Inomata, H. Takehana, T. Naruke, T. Yanagisawa, M. Moriguchi, S. Takeda, and T. Izumi
Prognostic utility of B-type natriuretic peptide assessment in stable low-risk outpatients with nonischemic cardiomyopathy after decompensated heart failure.
J. Am. Coll. Cardiol., June 17, 2008; 51(24): 2329 - 2335.
[Abstract] [Full Text] [PDF]

Home page
 J Am Coll CardiolHome page
R. M. Mills
Learning to use a biomarker. More about B-type natriuretic peptide.
J. Am. Coll. Cardiol., June 17, 2008; 51(24): 2336 - 2338.
[Full Text] [PDF]

Home page
 NEJMHome page
E. Braunwald
Biomarkers in Heart Failure
N. Engl. J. Med., May 15, 2008; 358(20): 2148 - 2159.
[Full Text] [PDF]

Home page
 Circ Heart FailHome page
J. J.V. McMurray, B. Pitt, R. Latini, A. P. Maggioni, S. D. Solomon, D. L. Keefe, J. Ford, A. Verma, J. Lewsey, and for the Aliskiren Observation of Heart Failure Tre
Effects of the Oral Direct Renin Inhibitor Aliskiren in Patients With Symptomatic Heart Failure
Circ Heart Fail, May 1, 2008; 1(1): 17 - 24.
[Abstract] [Full Text] [PDF]

Home page
 HeartHome page
G. W Yip
B-type natriuretic peptide: a treatment, not a diagnostic marker
Heart, May 1, 2008; 94(5): 542 - 544.
[Full Text] [PDF]

Home page
 Eur Heart JHome page
I. Squire
Assessing prognosis in heart failure: you can see a lot if you look, but more if you look again ... ... ...
Eur. Heart J., April 2, 2008; 29(8): 959 - 960.
[Full Text] [PDF]

Home page
 Eur Heart JHome page
D. A. Pascual-Figal, M. Domingo, T. Casas, I. Gich, J. Ordonez-Llanos, P. Martinez, J. Cinca, M. Valdes, J. L. Januzzi, and A. Bayes-Genis
Usefulness of clinical and NT-proBNP monitoring for prognostic guidance in destabilized heart failure outpatients
Eur. Heart J., April 2, 2008; 29(8): 1011 - 1018.
[Abstract] [Full Text] [PDF]

Home page
 J Am Coll CardiolHome page
J. R. Teerlink
Learning the points of COMPASS-HF: assessing implantable hemodynamic monitoring in heart failure patients.
J. Am. Coll. Cardiol., March 18, 2008; 51(11): 1080 - 1082.
[Full Text] [PDF]

Home page
 J Am Coll CardiolHome page
L. B. Daniels and A. S. Maisel
Natriuretic Peptides
J. Am. Coll. Cardiol., December 18, 2007; 50(25): 2357 - 2368.
[Abstract] [Full Text] [PDF]

Home page
 J Am Coll CardiolHome page
P. Jourdain, G. Jondeau, and Y. Juilliere
Reply
J. Am. Coll. Cardiol., November 20, 2007; 50(21): 2098 - 2099.
[Full Text] [PDF]

Home page
 J Am Coll CardiolHome page
U. C. Hoppe
Plasma Brain Natriuretic Peptide-Guided Therapy Not Yet Justified
J. Am. Coll. Cardiol., November 20, 2007; 50(21): 2097 - 2098.
[Full Text] [PDF]

Home page
 J Am Coll CardiolHome page
A. Maisel
Biomarkers in Heart Failure: Does Prognostic Utility Translate to Clinical Futility?
J. Am. Coll. Cardiol., September 11, 2007; 50(11): 1061 - 1063.
[Full Text] [PDF]

Home page
 CirculationHome page
W.H. Wilson Tang, G. S. Francis, D. A. Morrow, L. K. Newby, C. P. Cannon, R. L. Jesse, A. B. Storrow, R. H. Christenson, COMMITTEE MEMBERS, R. H. Christenson, et al.
National Academy of Clinical Biochemistry Laboratory Medicine Practice Guidelines: Clinical Utilization of Cardiac Biomarker Testing in Heart Failure
Circulation, July 31, 2007; 116(5): e99 - e109.
[Full Text] [PDF]

Home page
 Journal Watch CardiologyHome page
B-type Natriuretic Peptide: The North Star of HF Treatment?
Journal Watch Cardiology, April 25, 2007; 2007(425): 2 - 2.
[Full Text]

This Article
Right arrow Abstract Freely available
Right arrow Figures Only
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
j.jacc.2006.10.081v1
49/16/1733    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (44)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Jourdain, P.
Right arrow Articles by Juillière, Y.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Jourdain, P.
Right arrow Articles by Juillière, Y.

HOME SUBSCRIPTIONS CURRENT ISSUE PAST ISSUES CARDIOSOURCE SEARCH HELP FEEDBACK