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European Journal of Heart Failure 2007 9(6-7):667-673; doi:10.1016/j.ejheart.2007.01.003
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© 2007 European Society of Cardiology

Direct comparison of transcardiac difference between brain natriuretic peptide (BNP) and N-terminal pro-BNP in patients with chronic heart failure

Takayoshi Tsutamoto*, Hiroshi Sakai, Chitose Ishikawa, Masanori Fujii, Toshinari Tanaka, Takashi Yamamoto, Hiroyuki Takashima, Masato Ohnishi, Atsuyuki Wada and Minoru Horie

Cardiovascular and Respiratory Medicine, Shiga University of Medical Science, Tsukinowa, Seta, Otsu 520–2192, Japan

* Corresponding author. Tel: +81 77 548 2213; fax: +81 77 543 5839. E-mail address: tutamoto{at}belle.shiga-med.ac.jp


   Abstract
Top
 Abstract
1. Introduction
 2. Methods
 3. Results
 4. Discussion
 References
 
Background: Direct comparison of transcardiac increase in brain natriuretic peptide (BNP) and NT-pro-BNP has not been performed previously.

Aims: To evaluate the relation between BNP and NT-pro-BNP secretion, plasma levels and renal function.

Methods: We measured the plasma levels of BNP and NT-pro-BNP in the aortic root and coronary sinus in 326 consecutive patients with chronic heart failure (CHF). Patients were divided into two groups [group I: estimated glomerular filtration rate (eGFR)≥60 mL/min and group II: eGFR<60mL/min].

Results: The molar level of the transcardiac increase in NT-pro-BNP is lower than that of BNP. There were no differences in haemodynamics or the transcardiac gradient of BNP and NT-pro-BNP between group I and group II. The molar ratio of the plasma NT-pro-BNP to BNP was significantly higher in group II than in group I. By stepwise multivariate analyses, not only the left ventricular (LV) ejection fraction and LV end-diastolic pressure, but also eGFR, LV mass index (LVMI) and haemoglobin were independent predictors of plasma NT-pro-BNP and BNP.

Conclusion: The molar level of the transcardiac increase in NT-pro-BNP is lower than that of BNP; however, the influence of renal function on plasma NT-pro-BNP is greater than that on BNP.

Key Words: Brain natriuretic peptide • N-terminal pro brain natriuretic peptide • Haemodynamic parameters • Renal failure • Glomerular filtration rate • Chronic heart failure

Received August 7, 2006; Revised November 1, 2006; Accepted January 10, 2007


   1. Introduction
Top
 Abstract
 1. Introduction
2. Methods
 3. Results
 4. Discussion
 References
 
Plasma levels of brain natriuretic peptide (BNP) and N-terminal pro-BNP (NT-pro-BNP) are useful as diagnostic objective markers of chronic heart failure (CHF) due to systolic and diastolic dysfunction. High plasma BNP and NT-pro-BNP levels are important prognostic predictors not only in patients with CHF [1-3] and acute coronary syndrome but also in the general population. Glomerular filtration rate (GFR) as well as BNP and NT-pro-BNP has been shown to be related to prognosis in patients with CHF [4,5]. Therefore, evaluation of BNP and NT-pro-BNP and estimated GFR (eGFR) is important to estimate the severity of CHF.

Although BNP and NT-pro-BNP are thought to be secreted from the heart in equimolar amounts during mechanical stimulation of the heart [6,7], there are no previous studies of transcardiac differences between BNP and NT-pro-BNP using commercially available kits. Both BNP and NT-pro-BNP are markedly influenced by renal dysfunction [8-10]. We recently reported that decreased clearance from the kidney contributes to the elevated BNP in CHF patients [11]. However, in this previous study [11], we did not evaluate plasma NT-pro-BNP and left ventricular mass index (LVMI), a possible independent stimulator of BNP and NT-pro-BNP [12,13]. The aim of the present study was therefore to evaluate the relationship between transcardiac increases in BNP and NT-pro-BNP, their plasma levels and renal function in a head-to-head comparison using commercially available assays; and also to assess whether other factors such as age, gender, body mass index (BMI), LVMI, anaemia, and atrial fibrillation [12-17] affect the secretion of BNP and NT-pro-BNP from the failing heart in CHF patients.


   2. Methods
Top
 Abstract
 1. Introduction
 2. Methods
3. Results
 4. Discussion
 References
 
2.1. Patients
Consecutive symptomatic CHF patients (n=326) with left ventricular dysfunction undergoing cardiac catheterization for clinical indications were included. Patients with acute myocardial infarction, hypertrophic cardiomyopathy, congenital heart disease, valvular heart disease, primary pulmonary hypertension, lung disease, or pacemaker implantation and those on dialysis therapy were excluded. This was the same study population as in our previously reported study (n=366) [11]; however, 40 patients in whom an echocardiogram could not be performed were excluded. NYHA functional class was evaluated on the day of cardiac catheterization. Informed consent was obtained from all patients for participation in the study, according to a protocol approved by the Committee on Human Investigation at our institution.

2.2. Study protocol
All patients were premedicated with an oral dose of diazepam (5 mg) and rested in bed in a supine position for at least 20 min. Left-sided cardiac catheterization was performed and blood pressure was measured. Heart rate was monitored by electrocardiography. Blood samples for measurement of plasma BNP and NT-pro-BNP were collected simultaneously from the aortic root (AO) and coronary sinus (CS). A 6Fr catheter for blood sampling was positioned in the CS, and the position of the catheter was confirmed as previously reported [18]. Blood samples for measurement of creatinine and haemoglobin were also collected from the AO. Left ventriculography was performed using contrast medium or radioisotope, before or at least one week after the haemodynamic measurements and blood sampling. A two-dimensionally guided M-mode echocardiogram was performed by an experienced cardiologist who was blinded to BNP and NT-pro-BNP data. LV mass index (LVMI) was calculated from M-mode echocardiograms according to the formula by Devereux et al [19]. Renal function was represented by the estimated glomerular filtration rate (eGFR) according to the Cockcroft-Gault equation [20]. Preserved renal function was defined as eGFR≥60 ml/min and impaired renal function as eGFR<60 ml/min. Elevated left ventricular end-diastolic pressure (LVEDP) was defined as LVEDP≥12 mmHg [21].

2.3. Measurement of BNP and NT-pro-BNP
Samples for the assay of plasma BNP and NT-pro-BNP concentrations were transferred to chilled disposable tubes containing aprotinin (500 kallikrein inactivator units/ml). The blood samples were immediately placed on ice and centrifuged at 4 °C, and the plasma was frozen in aliquots and stored at –30 °C until assay. Plasma BNP concentrations were measured with a specific immunoradiometric assay for human BNP using a commercial kit (Shionogi, Osaka, Japan) as previously reported [1]. Plasma levels of NT-pro-BNP were measured using the Elecsys pro-BNP sandwich immunoassay (Roche Diagnostics, Mannheim, Germany).

2.4. Statistical analysis
All results are expressed as the mean±SD. A Chi-square test was used to determine differences between groups. Univariate analyses were performed using Student's t test with two-tailed p values of <0.05. Differences in mean BNP and NT-pro-BNP concentrations between subgroups were tested for significance using the Kruskal-Wallis test because BNP and NT-pro-BNP levels were not normally distributed. Differences in mean levels of BNP and NT-pro-BNP between the two groups were tested by Wilcoxon rank-sum test for paired values and by Mann-Whitney U test for unpaired values with two-tailed p values of <0.05 and log BNP and log NT-pro-BNP was used for correlations and regression models. To evaluate the contribution of BNP and NT-pro-BNP levels, univariate and stepwise multivariate analyses were used to compare 11 variables including haemodynamic parameters and eGFR. The sensitivity and specificity of BNP and NT-pro-BNP for predicting patients with an elevated LVEDP (≥12 mmHg) were determined, and receiver operating characteristics curves were constructed. Linear regression analysis was used to determine the relationship between continuous variables. A p value <0.05 was regarded as significant.


   3. Results
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
4. Discussion
 References
 
3.1. Patient characteristics
Table 1 summarizes patient characteristics according to eGFR. The mean age of patients was 64.1 years, 74% were men, and 145 patients (44%) had a preserved left ventricular ejection fraction (LVEF>40%). Patients were divided into two groups, those with preserved renal function (group I: eGFR≥60 ml/min) and those with impaired renal function (group II: eGFR<60 ml/min). One hundred and twenty-three patients (38%) had chronic kidney disease (CKD) as indicated by a decrease in eGFR (<60 ml/min). Patients with CKD were older, female, more likely to have a lower BMI, more likely to have anaemia, and more likely to be receiving loop diuretics. There were no differences in NYHA class, aetiology of CHF, or haemodynamic parameters between the two groups. The transcardiac difference between BNP and NT-pro-BNP was similar in both groups. Plasma levels of BNP and NT-pro-BNP were significantly higher in group II than in group I. The molar ratio of plasma NT-pro-BNP to BNP was significantly higher in group II than in group I.


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  		Table 1 Patient characteristics according to estimated glomerular filtration rate (eGFR)

 
3.2. Direct comparison of the transcardiac increase in BNP and NT-pro-BNP in patients with CHF
Plasma levels of NT-pro-BNP were significantly higher than BNP (202±39 vs. 55±5 pmoL/L, p<0.0001) and correlated with BNP in the AO (r=0.874, p<0.0001). The transcardiac increase in BNP and NT-pro-BNP increased with the severity of CHF and cardiac secretion of NT-pro-BNP was significantly lower than BNP (47.8±89 vs. 67.3±73 pmoL/L, p<0.0001) (Fig. 1). The molar ratio of transcardiac increase in NT-pro-BNP to BNP secretion was significantly lower than that of the NT-pro-BNP to BNP in the AO (0.64±0.7 vs. 2.5±2.2, p<0.0001) (Table 1).


Figure 01
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  		Fig. 1 Comparison of the transcardiac increase in brain natriuretic peptide (BNP) and N-terminal pro brain natriuretic peptide (NT-pro-BNP) in patients with chronic heart failure. The white box indicates the value of (CS-AO) BNP and the black box indicates the value of (CS-AO) NT-pro-BNP. The box defines the interquartile range with the median indicated by the crossbar, differences between groups were analyzed using Kruskal-Wallis testing. NYHA=New York Heart Association, AO=aortic root, CS=coronary sinus *=p<0.001, #=p<0.05 vs. the value of the (CS-AO) BNP in the same NYHA class by Wilcoxon rank-sum test.

 
3.3. Relation between the severity of CHF and the molar ratio of BNP to NT-pro-BNP
There was no difference in the molar ratio of transcardiac increase in NT-pro-BNP to BNP by severity of CHF. There was no difference in the molar ratio of plasma NT-pro-BNP to BNP in the AO by severity of CHF (Fig. 2).


Figure 02
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  		Fig. 2 A. Comparison of the molar ratio of transcardiac increase in brain natriuretic peptide (BNP) and that of N-terminal pro brain natriuretic peptide (NT-pro-BNP) in patients with chronic heart failure. B. Comparison of the molar ratio of brain natriuretic peptide (BNP) and N-terminal pro brain natriuretic peptide (NT-pro-BNP) in the aortic root (AO) in patients with chronic heart failure. The box defines the interquartile range with the median indicated by the crossbar. CS=coronary sinus.

 
3.4. Independent predictors of BNP and NT-pro-BNP in CHF patients with renal insufficiency
Among 11 variables including eGFR, BMI and LVMI, only LVEF (p<0.0001), LVEDP (p<0.0001) and cardiac index (p=0.0087) were independent predictors of transcardiac increase in BNP and NT-pro-BNP (Table 2). Among 11 variables, not only LVEF (p=0.0292) and LVEDP (p<0.0001) but also eGFR (p<0.0001), LVMI (p<0.0001) and haemoglobin (p=0.014) were independent predictors of BNP and NT-pro-BNP in the AO (Table 3). There was a significant correlation between LVMI and BNP and NT-pro-BNP (Fig. 3). There was no correlation between eGFR and the molar ratio of NT-pro-BNP to BNP secretion (r=–0.103, p=0.064), but there was a significant negative correlation between eGFR and the molar ratio of NT-pro-BNP to BNP in the AO (r=–0.327, p<0.0001).


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  		Table 2 Univariate and multivariate linear model of transcardiac increase in log NT-pro-BNP

 


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  		Table 3 Univariate and multivariate linear model of plasma Log NT-pro-BNP Level

 


Figure 03
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  		Fig. 3 Correlations between left ventricular mass index (LVMI) and transcardiac increase in brain natriuretic peptide (BNP) and N-terminal pro brain natriuretic peptide (NT-pro-BNP) and plasma levels of BNP and NT-pro-BNP.

 
3.5. BNP and NT-pro-BNP as a predictor of elevated LVEDP
Receiver operating characteristics curves of BNP and NT-pro-BNP to detect patients with elevated LVEDP (12≥mmHg, n=148) were evaluated. The cut-off level of BNP was determined as 63 pg/mL for group I and 220 pg/mL for group II giving a sensitivity of 91% and specificity of 63% for group I [area under the curve (AUC)=0.830, 95%CI, 0.773-0.887], and a sensitivity of 62% and specificity of 87% for group II(AUC=0.800, 95%CI, 0.722-0.878). The cut-off level of NT-pro-BNP was determined as 295 pg/mL for group I and 699 pg/mL for group II, giving a sensitivity of 86% and specificity of 63% for group I (AUC=0.805, 95%CI, 0.745-0.866), and a sensitivity of 78% and specificity of 74% for group II (AUC=0.735, 95%CI, 0.648-0.824).


   4. Discussion
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
References
 
BNP is synthesized as pro-BNP in cardiac myocytes, and then pro-BNP is transformed to hormonally active BNP and inactive NT-pro-BNP. BNP and NT-pro-BNP are thought to be secreted from the heart in equimolar amounts [6,7]. In addition BNP and NT-pro-BNP and also pro-BNP are secreted in the blood stream [22]. Therefore, at least three molecular forms, pro-BNP, BNP and NT-pro-BNP, are found in the plasma. In this study we have evaluated for the first time, the transcardiac increase in BNP and NT-pro-BNP in a head-to-head comparison between two commercially available assays (BNP: Shionogi and NT-pro-BNP: Roche). Plasma BNP and NT-pro-BNP levels in the present study were comparable with the baseline values of BNP and NT-pro-BNP shown in a recent study [23] by the Val-HeFT group using the same commercial kits. The Triage Biosite BNP assay gives a value approximately 50% higher than that of the Shionogi assay (Triage BNP=1,579 (Shionogi) –2.947, r=0.963) [24]. Therefore, if the Triage BNP assay kit is used, the molar ratio of the transcardiac increase in NT-pro-BNP to the transcardiac increase of BNP would be lower than that reported in the present study. Surprisingly, in our study the molar ratio of the transcardiac increase in NT-pro-BNP to the transcardiac increase in BNP showed wide variation with a mean value less than one, suggesting that the secretion pattern of BNP from the failing heart, as judged from these assays, is not uniform and that other molecular forms of BNP may be secreted. In fact, molecular forms of human BNP other than these three have been reported in plasma [22,25,26].

Based on our previous observations, there was no significant difference in plasma BNP and NT-pro-BNP levels between the AO and antecubital vein in CHF patients (data not shown). We recently reported that decreased clearance from the kidney contributes to elevated BNP in CHF patients with renal dysfunction, especially in patients with an eGFR less than 60 ml/min [11]. In the current study we extended our previous findings and measured NT-pro-BNP as well as LVMI by echocardiogram, as a possible independent stimulator of BNP and NT-pro-BNP secretion. The present study suggests that renal function has a direct effect on circulating BNP and NT-pro-BNP and that NT-pro-BNP is more influenced by renal function than BNP, which is consistent with recent findings in patients with CKD [27]. The finding that LVMI is an independent predictor of plasma BNP and NT-pro-BNP in CHF patients if we concomitantly measure LVEDP and LVEF is consistent with previous findings in patients with hypertension [12,13] and in patients after myocardial infarction [22]. Haemoglobin was also an independent predictor of BNP and NT-pro-BNP, which is consistent with previous reports [11,17,28]. In the present study 5 parameters, LVEDP, LVEF, LVMI, anaemia (haemoglobin) and renal function (eGFR), were confirmed as prognostic markers influencing plasma levels of BNP and NT-pro-BNP; therefore, a single measurement of BNP and NT-pro-BNP may be a strong prognostic indicator in CHF patients.

Regarding haemodynamic parameters; left ventricular diastolic dysfunction, which is common in old age and in women, is thought to be an important stimulator of BNP and NT-pro-BNP secretion. Therefore, neither age nor gender was an independent predictor of transcardiac increase in BNP or NT-pro-BNP from the heart when LVEDP was measured simultaneously in the present study. Regarding atrial fibrillation, which worsens left ventricular performance and elevates LVEDP, it has been observed that high BNP and NT-pro-BNP levels in AF patients with CHF may be due to haemodynamic overload [29,30]. BMI was lower in the group with lower eGFR and was not an independent predictor of transcardiac increase in BNP and NT-pro-BNP, suggesting that the impact of BMI on BNP and NT-pro-BNP level occurs via haemodynamics or decreased degradation of BNP and NT-pro-BNP due to renal insufficiency.

There are several limitations in this study. The molecular forms of the blood samples for the BNP and NT-pro-BNP assays could not be evaluated, and further studies are needed to clarify this issue using radioimmunoassay combined with gel chromatography or high performance liquid chromatography. Being unable to determine the total amount of cardiac secretion of BNP and NT-pro-BNP because coronary blood flow was not measured is also a limitation of this study. Other factors such as age, sex, BMI, and atrial fibrillation may not have been major factors affecting plasma BNP and NT-pro-BNP in the present study. However, further studies are needed to confirm our findings in a larger number of CHF patients.

There is currently a worldwide epidemic of CHF and CKD. Although many previous studies have supported the usefulness of BNP and NT-pro-BNP in the diagnosis and management of CHF, the present study demonstrates that renal function has a more direct effect on circulating BNP and NT-pro-BNP than previously recognized in CHF patients with CKD, especially for NT-pro-BNP. In other words, a single measurement of BNP and NT-pro-BNP may be a strong prognostic predictor due to its reflection of the severity of cardiorenal dysfunction and LVMI in CHF patients with CKD [23].

In conclusion, transcardiac increase in NT-pro-BNP is lower than that of BNP at a molar level and both plasma BNP and NT-pro-BNP levels are influenced by renal clearance with a greater influence of eGFR on NT-pro-BNP than on BNP. Anaemia (haemoglobin) and LVMI are independent regulators of plasma levels of BNP and NT-pro-BNP in CHF patients.


   Acknowledgements
 
We wish to thank Aoi Murata for excellent technical assistance. We also express thanks to Mr. Daniel Mrozek for assistance in preparing the manuscript. This study was supported by a Grant-in-Aid for Scientific Research in Japan.


   References
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
 References
 

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T. Tsutamoto, K. Nishiyama, H. Sakai, T. Tanaka, M. Fujii, T. Yamamoto, M. Yamaji, and M. Horie
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