Skip Navigation

European Journal of Echocardiography 2007 8(1):30-36; doi:10.1016/j.euje.2005.12.009
This Article
Right arrow Abstract Freely available
Right arrow FREE Full Text (PDF) Freely available
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 PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Scardovi, A. B.
Right arrow Articles by Ceci, V.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Scardovi, A. B.
Right arrow Articles by Ceci, V.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2005, The European Society of Cardiology

Brain natriuretic peptide plasma level is a reliable indicator of advanced diastolic dysfunction in patients with chronic heart failure

Angela Beatrice Scardovia,*, Claudio Colettaa, Nadia Aspromontea, Silvia Pernab, Manuela Greggia, Paola D'Errigoc, Augusto Sestilia and Vincenzo Cecia

aCardiology Department, S. Spirito Hospital, Lungotevere in Sassia 1, 00196 Rome, Italy
bCardiology Department, S. Andrea Hospital, Rome, Italy
cIstituto Superiore di Sanità, Rome, Italy

Received 6 August 2005; received in revised form 13 October 2005; accepted after revision 15 December 2005.

* Corresponding author. Tel.: +39 06 68352264; fax: +39 06 68354880. ab.scardovi{at}libero.it


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 Conclusion
 References
 
The aim of the study was to determine the value of brain natriuretic peptide for the identification of diastolic dysfunction status in congestive heart failure.

We studied 204 patients with stable heart failure. Brain natriuretic peptide plasma levels were correlated with echocardiographic parameters of diastolic dysfunction. Diastolic dysfunction was classified as mild (abnormal echocardiographic relaxation pattern) and severe (pseudo-normal or restrictive pattern). A significant correlation between brain natriuretic peptide levels and the other parameters was detected.

Brain natriuretic peptide dosage, then, seems to be a reliable tool for the assessment of diastolic dysfunction status in patients with congestive heart failure.

Keywords: Brain natriuretic peptide; Heart failure; Doppler echocardiography; Diastole


   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 Conclusion
 References
 
Congestive heart failure is one of the main causes of hospitalization in industrialized countries, with a five-year survival rate as low as 50%. The clinical syndrome of congestive heart failure occurs over a broad range of underlying left ventricular systolic functional status.1,2 Conversely, diastolic dysfunction plays a primary role in determining individual prognosis.3,4 Although Doppler echocardiography is widely used to determine left ventricular diastolic filling, this method has several limitations and pitfalls, related to the clinical status of the patient and to the unavoidable technical difficulties. In this setting an alternative marker, whenever related to the diastolic functional status, could give useful information for a first-step outcome assessment of congestive heart failure patients.

Brain natriuretic peptide, a marker of neurohormonal activation secreted by cardiomyocytes in response to ventricular wall stretch, has a basic role in cardiovascular remodelling and volume homeostasis. High plasma brain natriuretic peptide levels in resting conditions act as sensitive and specific markers for the diagnosis of heart failure from other causes of dyspnea.5 Moreover, their levels are closely related to the NYHA functional class and the individual prognosis6–10 and seem to reflect diastolic functional status,11 but no definite data exist about the relationship between BNP levels and severe diastolic dysfunction.

Indeed, the aim of our study was to investigate the relationship between brain natriuretic peptide levels and the severity of diastolic dysfunction as assessed by Doppler echocardiography in stable outpatients with congestive heart failure.


   Methods
Top
 Abstract
 Introduction
 Methods
Results
 Discussion
 Conclusion
 References
 
Patients
Two hundred and seventy-six consecutive outpatients referred to our tertiary cardiology centre between February 2002 and January 2003 were considered for the study. All patients were in clinically stable conditions since at least four weeks before admission. For the purpose of the study, the following exclusion criteria were defined: (a) renal insufficiency (serum creatinine≥2mg/dl), (b) any mitral stenosis or previous mitral valve surgery, (c) significant aortic stenosis (peak systolic velocity≥4m/s) and/or insufficiency, (d) significant pulmonary or liver disease, (e) recent (≤3 months) myocardial infarction or unstable angina, (f) New York Heart Association (NYHA) functional class IV, (g) atrial fibrillation or flutter at the moment of the study or documented paroxysmal atrial fibrillation in the last three months, (h) Moreover, 24 patients (9%) were excluded from the study due to a low technical quality of Doppler echocardiography with unavailability of reliable pulmonary artery pressure or pulmonary venous flow velocity assessment.

The study was approved by the local Ethical Committee and all patients gave written consent.

Doppler echocardiography
Comprehensive transthoracic Doppler echocardiography was performed on the standard left parasternal and apical views by experienced operators (CC, AS) in blind conditions. The pulsed-wave Doppler approach was used for the transmitral flow velocity analysis using a 2–4mm sample volume placed at the mitral leaflet tip level in the apical four-chamber view. The transmitral pulsed-wave Doppler blood flow velocities were calculated off-line from five consecutive cardiac cycles and the following measurements were performed: early diastolic flow (E) peak velocity (cm/s), late diastolic flow (A) peak velocity (cm/s), E/A velocity ratio and E-velocity deceleration time (ms). In patients without return of E velocity slope to baseline, extrapolation of the deceleration signal to the zero line was accepted. Diastolic function, as determined from the pattern of transmitral and pulmonary venous blood flow, was classified into three categories:

Type I: identified by the abnormal relaxation pattern (E/A velocity ratio<0.75);
Type II: identified by the pseudo-normal pattern (E/A velocity ratio≥0.75 and <1.5; E-velocity deceleration time>140ms and pulmonary vein peak diastolic velocity>peak systolic velocity);
Type III: identified by the restrictive pattern (E/A velocity≥1.5, E-velocity deceleration time≤140ms).

For the purposes of the study, types II and III were classified as severe diastolic dysfunction. In our laboratory, interobserver reproducibility data for transmitral early- and late peak diastolic velocity have been detected in 20 consecutive patients with symptoms of congestive heart failure and demonstrated to be 5±4% and 4±4%, respectively. In the same setting, interobserver variability of E-velocity deceleration time was 6±7%.

Left ventricular ejection fraction (%) was measured off-line using the modified Simpson's biplane method by the apical four and two chambers views as recommended by the American Society of Echocardiography.12

All images and clips were stored on a magneto-optical disc.

Finally, peak systolic pulmonary arterial pressure (mmHg) was empirically calculated using the formula: right ventricle–right atrium peak systolic gradient (mmHg)+10mmHg.

Brain natriuretic peptide plasma levels
In all patients blood was collected by venipuncture from antecubital vein after 10min of sitting rest, in tubes containing ethylene diamine tetracetic acid before echocardiography examination. The blood samples were kept at room temperature and analyzed within 4h of the draw time. Before analysis, each tube was inverted several times to ensure homogeneity. A point-of-care test for determination of brain natriuretic peptide (Triage BNP test, Biosite Diagnostics®) based on immunofluorometric assay in whole blood or plasma was used in our study. The range of detectable levels, at the time of the study, was 1–1.300pg/mL. The average 95% confidence limit of the analytical sensitivity of the test is less than 5pg/mL (95% confidence interval 0.2–4.8pg/mL). The average total error is 10% at mean values of 28pg/mL and 16.2% at mean levels of 1080.4pg/mL. No significant cross-reactivity with endothelin-1, atrial natriuretic peptide or aldosterone is present.13

Brain natriuretic peptide concentrations were determined by nurses who were blinded to echocardiography results.

Statistical analysis
Categorical variables are presented as mean values±standard deviation (SD). Mean values and their SD were compared by the Student's t test or by ANOVA with Bonferroni post-hoc test for multiple groups. Analysis of correlation among the parameters of the study was performed using a Pearson's correlation and results are presented by the r coefficient of correlation. The receiver-operating characteristic curves were also calculated for determining the best diagnostic accuracy of brain natriuretic peptide levels. The results are expressed in terms of the areas under the curve with their 95% confidence intervals. Sensitivity, specificity and accuracy for identification of severe diastolic dysfunction were computed using a selection of multiple cut-off points of brain natriuretic peptide level. All statistical tests were based on a two-tailed models and a p value<0.05 was considered statistically significant. Data were analyzed using the SPSS 11 for Microsoft Windows package (SPSS Inc., Chicago).


   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 Conclusion
 References
 
The final population of the study was constituted by 204 patients. Mean age was 70±11 years, most subjects were males (135/204, 66%) (Table 1).


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

  		Table 1 Clinical data of the study population (n=204)

 
Average left ventricular ejection fraction and systolic pulmonary arterial pressure, in our study population, were 41±13% and 47±14mmHg, respectively.

One-hundred and twenty-four (61%) patients had a diastolic function type I, 33 patients (16%) had type II and 47 patients (23%) had type III, so that a severe diastolic dysfunction was detected in 80 out of 204 patients (39%).

The prevalence of severe diastolic dysfunction was lower in patients on beta-blocker therapy (23% vs 36%, p=0.061). Mean ejection fraction was lower and the E-velocity deceleration time was shorter in patients with severe diastolic dysfunction than in those without (35+11% vs 44+11%, p<0.001, and 152+41 vs 236+63ms, p<0.001, respectively) (Table 2).


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

  		Table 2 BNP values and echocardiography – Doppler results in the study population

 
Average brain natriuretic peptide plasma level was 266±351pg/mL (median value: 122pg/mL). Plasma levels were within the standardized normal limit (40pg/mL) in 37 out of 204 patients (18%). Conversely, a level<100pg/mL was detected in 83 patients (41%). Fourteen (17%) patients had preserved systolic function and severe diastolic dysfunction (types II and III). In this subgroup mean ejection fraction was 54+6% and average brain natriuretic peptide level was 168+97pg/mL (median: 166pg/mL, range: 16–361). Ejection fraction and diastolic dysfunction were significantly correlated (r=–413; p<0.01).

Diastolic function and brain natriuretic peptide
Brain natriuretic peptide was significantly higher in patients with severe diastolic dysfunction than in those without (459±462pg/mL vs 142±166pg/mL, p<0.001).

A significant correlation between brain natriuretic peptide and left atrium (r=0.311; p<0.01), E velocity (r=0.369; p<0.01), E/A velocity ratio (r=0.515; p<0.01) and pulmonary systolic arterial pressure (r=0.509; p<0.001) was found. The relationship between brain natriuretic peptide and systolic pulmonary pressure appeared particularly evident in symptom-free patients (r=0.934; p<0.001).

Moreover, a reverse correlation between brain natriuretic peptide level and ejection fraction (r=–0.445; p<0.01), A velocity (r=–0.358; p<0.01) and E velocity deceleration time (r=–0.389; p<0.01) (Fig. 2) was present (Table 3).


Figure 1
View larger version (14K):
[in this window]
[in a new window]
[Download PowerPoint slide]
  		Figure 1 Scatter plots of brain natriuretic peptide (BNP) concentrations versus E/A ratio. BNP: brain natriuretic peptide; E/A ratio: early diastolic flow (E), peak velocity late diastolic flow (A), velocity ratio.

 


Figure 2
View larger version (14K):
[in this window]
[in a new window]
[Download PowerPoint slide]
  		Figure 2 Scatter plots of brain natriuretic peptide (BNP) concentrations versus E-velocity deceleration time (EDT). BNP: brain natriuretic peptide; EDT: E-velocity deceleration time.

 


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

  		Table 3 Correlation coefficient between brain natriuretic peptide levels and echocardiographic parameters

 
In the receiver-operating curve analysis, the identification of severe diastolic dysfunction by brain natriuretic peptide levels showed overall area under the curve to be 0.764 (95% CI: 0.68–0.84), and a level≥138pg/mL appeared to be the best limit for severe diastolic dysfunction, with accuracy, 70%, sensitivity, 72%, and specificity, 70% (Fig. 1). Alternatively, a brain natriuretic peptide level≥402pg/mL had the highest sensitivity (93%) and positive predictive value (85%), but the specificity was low (38%). Finally, a ≤46pg/ml level, with a 93% negative predictive value, reliably identified patients free of severe diastolic dysfunction (Fig. 3).


Figure 3
View larger version (13K):
[in this window]
[in a new window]
[Download PowerPoint slide]
  		Figure 3 Receiver-operating characteristic curve comparing sensitivity and specificity of brain natriuretic peptide (BNP) and echocardiographic diagnosis of left ventricular diastolic dysfunction. AUROC: area under the receiver-operating characteristic curve; BNP: brain natriuretic peptide; DD II: diastolic dysfunction type II; DD III: diastolic dysfunction type III; DD II+DD III: severe diastolic dysfunction.

 

   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
Conclusion
 References
 
The results of our study confirm the moderate relationship between plasma brain natriuretic peptide values and severe diastolic dysfunction as defined by Doppler echocardiography in patients with established congestive heart failure. In this clinical setting, the selection of different cut-off values of brain natriuretic peptide allowed a reasonable identification of patients at higher and at lower risk of severe diastolic dysfunction.

Although diastolic dysfunction plays an important role in the risk stratification of CHF-patients, the ideal approach requires invasive measurement of left ventricular pressures and volumes, resulting in a time-consuming, high-cost and unpractical approach for the daily practice. As a consequence, non-invasive determination of left ventricular filling by Doppler blood flow velocity encoding has become a routine clinical tool for identifying diastolic function and predicting mortality in patients with clinically evident heart failure. However Doppler echocardiography, due to the well-known technical limitations, cannot provide unequivocal evidence of left ventricular diastolic functional status in any patient.14 As a consequence, alternative low-cost markers for identifying patients at higher risk of advanced diastolic dysfunction might be very useful in the first-step screening of large populations with congestive heart failure.

Brain natriuretic peptide is a cardiac neurohormone secreted from the ventricle walls as a response to chamber volume expansion and pressure overload, easily dosable by point-of-care systems15 and strictly correlated to prognosis16–18; high brain natriuretic peptide levels are detectable in symptomatic patients and, similarly, an activated neurohormonal status is present in patients with diastolic dysfunction19,20 and high pulmonary systolic pressure.21,22

The link among these variables is probably multifactorial. It is possible that brain natriuretic peptide levels act as a non-selective index of cardiac performance, reflecting the combined effects of left ventricular systolic and diastolic function as well as the severity of global cardio-pulmonary exercise impairment.

The results of our study demonstrate a correlation among brain natriuretic peptide levels, diastolic dysfunction and pulmonary artery pressure, suggesting the possible role of the neurohormone as a window on the hemodynamic status of the single patient. The r values found in this study were quite low, but elevated brain natriuretic peptide levels reliably indicated severe diastolic abnormality, in spite of the well-known, potentially confounding variability of neurohormonal levels among heart failure patients.

Elevated brain natriuretic peptide levels reliably indicate severe diastolic abnormality, but the well-known variability of neurohormonal levels among heart failure patients can still generate some confusion in interpreting the results. However, the correlation between brain natriuretic peptide level and severe diastolic dysfunction explains the independent prognostic value either in patients with normal or abnormal left ventricle systolic function.21 Although the isolated detection of abnormal brain natriuretic peptide levels cannot differentiate between systolic and diastolic dysfunction, a result within the range of normality in patients with preserved systolic function reliably rules out advanced diastolic dysfunction.19 Conversely, the combined and confounding effect of right ventricular performance, mitral and aortic functional status and pulmonary/systemic hypertension explains the lower accuracy of brain natriuretic peptide for the identification of pure systolic dysfunction.22–25

One important feature of our study was the high prevalence (41%) of patients with a brain natriuretic peptide level<100pg/mL (the accepted cut-off value for diagnosing decompensated heart failure), and the large group of patients (18%) with normal (<40pg/mL) levels. This seems due to the characteristics of our study population, constituted by clinically stable outpatients already receiving a point-of-care pharmacological treatment. In our population the high prevalence of long-term beta-blocker therapy probably played a role, reducing sympathetic influence on heart rate, myocardial contractility and vascular tone, as indirectly confirmed by the lower prevalence of severe diastolic dysfunction in patients taking beta-blockers. The high correlation found between brain natriuretic peptide level and pulmonary artery pressure in asymptomatic patients remains an unexplained task. Possibly due to a casual distribution in this small group (n=20) of patients, it could also reflect the ability of the neurohormone to identify abnormal tensive regimens of the pulmonary circulation, as confirmed by the established link between brain natriuretic peptide and pulmonary capillary wedge pressure.16,17

Based on the results of our study, brain natriuretic peptide dosage offers a simple and cost-saving tool for assessing patients at high risk of severe diastolic dysfunction and, consequently, of worse outcome in the first-step screening of large populations or in patients with technically inadequate Doppler echocardiography. Moreover, in the search of new strategies in patients with congestive heart failure, the combination of neurohormonal and echocardiographic parameters might represent a rational approach for a more accurate prognostic stratification, and further studies should be planned to assess this particular feature.

Study limitation
Our study acknowledges several limitations.

First, the study population included only outpatients in stable clinical conditions, presumably not representative of the clinical status of more general populations referred for clinical management of congestive heart failure. Patients with renal insufficiency were excluded from the study because of the non-specific elevation of plasma BNP in this clinical condition.26 Thus, whether different plasma BNP levels predict functional capacity and ventilatory response to exercise in HF patients with renal failure cannot be ascertained from our data.

The link between diastolic function and brain natriuretic activity observed in our study was in part dependent on the strong relationship in the asymptomatic or mildly symptomatic patients. Consequently, in patients with more advanced NYHA functional class new prospective studies should better define the accuracy of brain natriuretic peptide for the identification of severe diastolic dysfunction.

We did not measure plasma N-terminal pro-brain natriuretic peptide, which has been recently suggested to be more accurate for predicting left ventricular function and prognosis after myocardial infarction. However, the assay utilized in this study represents the most widely accepted method for rapid determination of neurohormonal activity in congestive heart failure patients.

Based on the design of our study, it remains unknown whether consecutive, multiple plasma brain natriuretic peptide levels, reducing the intrinsic variability of the method, would represent a more accurate approach for the identification of diastolic dysfunction in these patients. Finally, a relatively significant proportion of patients were a priori excluded for technical limitations of Doppler echocardiography. The aim of the study was to analyze the possible role of brain natriuretic peptide level as an indirect marker of diastolic dysfunction, and this information appears particularly useful in patients without reliable Doppler information. Therefore, this unavoidable limitation should be considered in the clinical application of our data.


   Conclusion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Conclusion
References
 
In clinically stable heart failure patients plasma brain natriuretic peptide values are closely related to the diastolic functional status and pulmonary systolic pressure, both reliable markers of poor prognosis.

Based on the results of our study, brain natriuretic peptide dosage could be considered a low-cost, widely available tool for the first-step screening of patients at higher risk of severe diastolic dysfunction, particularly in the presence of normal or mildly abnormal functional status. In this era of cost-saving management of chronic heart disease, brain natriuretic peptide determination, eventually combined with Doppler echocardiography in a sequential approach, could represent a reliable strategy for the screening of asymptomatic or mildly symptomatic patients with congestive heart failure.


   References
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Conclusion
 References
 

  1. Senni M., Tribouilloy C.M., Rodeheffer R.J., Jacobsen S.J., Evans J.M., Bailey K.R., et al. Congestive heart failure in the community: a study of all incident cases in Olmsted Country, Minnesota, 1991. Circulation (1998) 98:2282–2289.[Abstract/Free Full Text]
  2. Vasan R.S., Larson M.G., Benjamin E.J., Evans J.C., Reiss C.K., Levy D. Congestive heart failure in subjects with normal versus reduced left ventricular ejection fraction. J Am Coll Cardiol (1999) 33:1948–1955.[Abstract/Free Full Text]
  3. Vasan R.S., Benjamin E.J., Levy D. Prevalence, clinical features and prognosis of diastolic heart failure: an epidemiologic perspective. J Am Coll Cardiol (1995) 26:1565–1574.[Abstract]
  4. Bonow R., Udelson J.E. Left ventricular diastolic dysfunction in patients with congestive heart failure. Ann Intern Med (1992) 117:502–510.[CrossRef][Web of Science][Medline]
  5. Maisel A.S., Krishnaswamy P., Nowak R.M., McCord J., Hollander J.E., Duc P., et al. Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure. N Engl J Med (2003) 347:161–167.[CrossRef][Web of Science]
  6. Richards AM, Nicholls MG, Yandle TG, Frampton C, Espiner EA, Turner JG, et al. Plasma N-terminal pro-brain natriureticpeptide and adrenomedullin: new neurohormonal predictors of left ventricular function and prognosis after myocardialinfraction. Circulation 1998 May 19;97(19):1921–9.
  7. Tsutamoto T., Wada A., Maeda K., et al. Attenuation of compensation of endogenous cardiac natriuretic peptide system in chronic heart failure: prognostic role of plasma brain natriuretic peptide concentration in patients with chronic symptomatic left ventricular dysfunction. Circulation (1997) 96:509–516.[Abstract/Free Full Text]
  8. Harrison A., Morrison L.K., Krishnaswamy P., Kazanegra R., Clopton P., Dao Q., et al. B-type natriuretic peptide predicts future events in patients presenting to the emergency department with dyspnea. Ann Emerg Med (2002) 39:131–138.[CrossRef][Web of Science][Medline]
  9. Maeda K., Tsutamoto T., Wada A., Mabuchi N., Hayashi M., Tsutsui T., et al. High levels of plasma brain natriuretic peptide and interleukin-6 after optimized treatment of failure are independent risk. J Am Coll Cardiol (2000) 36:1587–1593.[Abstract/Free Full Text]
  10. Gardner R.S., Ozlap F., Murday A.J., Robb S.D., McDonag T.A. N-terminal pro-brain natriuretic peptide. A new gold standard in predicting mortality in patients with advanced heart failure. Eur Heart J (Oct 2003) 24(19):1735–1743.[Abstract/Free Full Text]
  11. Yu C.M., Sanderson J.E., Shun I.O.L., Chan S., Yeung L.Y., Hung Y.T., et al. Diastolic dysfunction and natriuretic peptides in systolic heart failure. Eur Heart J (1996) 17:1694–1702.[Abstract/Free Full Text]
  12. Schiller N.B., Shah P.M., Crawford M., DeMaria A., Devereux R., Feigenbaum H., et al. Recommendations for quantitation of the left ventricle by two-dimensional echocardiography. American Society of Echocardiography Committee on Standards, Subcommittee on Quantitation of Two-Dimensional Echocardiograms. J Am Soc Echocardiogr (1989) 2:358–367.[Medline]
  13. Maisel A.S., Koon J., Krishnaswamy P., Kazenegra R., Clopton P., Gardetto N., et al. Utility of B–natriuretic peptide as a rapid, point–of–care test for screening patients undergoing echocardiography to determine left ventricular dysfunction. Am Heart J (2001) 141:367–374.[CrossRef][Web of Science][Medline]
  14. Yamamoto K., Redfield M.M., Nishimura R.A. Analysis of left ventricular diastolic function: a common and costly clinical entity. Heart (1996) 75(Suppl. 2):27–35.[Free Full Text]
  15. Cheng V., Kazanagra R., Garcia A., Lenert L., Krishnaswamy P., Gardetto N., 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]
  16. Silver M.A., Maisel A., Yancy C.W., McCullough P.A., Burnett J.C., Francis G.S., et al. BNP consensus panel 2004: a clinical approach for the diagnostic, prognostic, screening, treatment monitoring, and therapeutic roles of natriuretic peptides in cardiovascular diseases. Congest Heart Fail (2004) 10(Suppl. 3):S1–S30.
  17. Kazanegra R., Cheng V., Garcia A., Krishnaswamy P., Gardetto N., Clopton P., et al. A rapid test for B-type natriuretic peptide correlates with falling wedge pressures in patients treated for decompensated heart failure: a pilot study. J Card Fail (2001) 7:21–29.[CrossRef][Web of Science][Medline]
  18. Troughton R.W., Prior D.L., Pereira J.J., Martin M., Fogarty A., Morehead A., et al. Plasma B-type natriuretic peptide levels in systolic heart failure. J Am Coll Cardiol (2004) 43:416–422.[Abstract/Free Full Text]
  19. Lubien E., DeMaria A., Krishnaswamy P., Clopton P., Koon J., Kazanegra R., et al. Utility of Bnatriuretic peptide in detecting diastolic dysfunction. Comparison with Doppler velocity recordings. Circulation (2002) 105:595–601.[Abstract/Free Full Text]
  20. Dokainish H., Zoghbi W.A., Lakkis N.M., Quinones M.A., Nagueh S.F. Comparative accuracy of B-type natriuretic peptide and tissue Doppler echocardiography in the diagnosis of congestive heart failure. Am J Cardiol (May 1, 2004) 93(9):1130–1135.[CrossRef]
  21. Ghio S., Gavazzi A., Campana C., Inserra C., Klersy C., Sebastiani R., et al. Independent and additive prognostic value of right ventricular systolic function and pulmonary artery pressure in patients with chronic heart failure. J Am Coll Cardiol (2001) 37:183–188.[Abstract/Free Full Text]
  22. Nagaya N., Nishikimi T., Okano Y., Uematsu M., Satoh T., Kyotani S., et al. Plasma brain natriuretic peptide levels increase in proportion to the extent of right ventricular dysfunction in pulmonary hypertension. J Am Coll Cardiol (1998) 31:202–208.[Abstract/Free Full Text]
  23. Mayer S.A., De Lemos J.A., Murphy S.A., Brooks S., Roberts B.J., Grayburn P.A. Comparison of Btype natriuretic peptide levels in patients with heart failure with versus without mitral regurgitation. Am J Cardiol (Apr 15, 2004) 93(8):1002–1006.[CrossRef]
  24. Sutton T.M., Stewart R.A., Gerber I.L., West T.M., Richards A.M., Yandle T.G., et al. Plasma natriuretic peptide levels increase with symptoms and severity of mitral regurgitation. J Am Coll Cardiol (Jun 18, 2003) 41(12):2280–2287.[CrossRef]
  25. Troughton R.W., Prior D.L., Pereira J.J., Martin M., Fogarty A., Morehead A., et al. Plasma B-type natriuretic peptide levels in systolic heart failure: importance of left ventricular diastolic function and right ventricular systolic function. J Am Coll Cardiol (Feb 4, 2004) 43(3):416–422.[CrossRef]
  26. Ishizaka Y., Yamamoto Y., Fukanaga T., Yokota N., Kida O., Kitamura K., et al. Plasma concentration of human brain natriuretic peptide in patients on haemodialysis. Am J Kidney Dis (1994) 24:461–472.[Web of Science][Medline]

Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?



This Article
Right arrow Abstract Freely available
Right arrow FREE Full Text (PDF) Freely available
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 PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Scardovi, A. B.
Right arrow Articles by Ceci, V.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Scardovi, A. B.
Right arrow Articles by Ceci, V.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?