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Eur J Cardiothorac Surg 2004;25:941-945
© 2004 Elsevier Science NL

Changes in type B natriuretic peptide (BNP) concentrations during cardiac valve replacement

A. Georgesa*, F. Forestierb, N. Vallia, A. Plogina, G. Janvierb, L. Bordenavea

a Nuclear Medicine Department, Hôpital Haut-Lévêque, Avenue Magellan, 33604 Pessac, Cedex, France
b Department of Anesthesia II, Hôpital Haut-Lévêque, Avenue Magellan, 33604 Pessac, Cedex, France

Received 6 November 2003; received in revised form 3 February 2004; accepted 25 February 2004.

* Corresponding author. Tel.: +33-5-57-65-68-25; fax: +33-5-57-65-68-39
e-mail: agnes.georges{at}chu-bordeaux.fr


   Abstract
Top
 Abstract
1. Introduction
 2. Methods
 3. Results
 4. Discussion
 References
 
Objective: The aim of our study was to investigate the ability of BNP levels to reveal the immediate post-surgery cardiac function improvement. We measured the perioperative variations in BNP concentrations in patients scheduled for cardiac surgery with cardiopulmonary bypass (CPB), chronic mitral regurgitation, valvular aortic stenosis, or myocardial ischaemia. Methods: Three groups were included: patients with coronary artery bypass graft (CABG, group I, n=14), aortic (AVR, group II, n=14) or mitral (MVR, group III, n=7) valve replacement. BNP assay was performed at the induction of anesthesia, immediately after the CPB, at the arrival in the intensive care unit, 4 h, 8 h and 12 h after the arrival in ICU. Results and conclusion: The occurring variation in BNP levels after the operation is an increase whatever the corrective surgery, underlying the relative lack of specificity of BNP with regard to the cardiac pathology. Besides iatrogenic cardioplegia one can supposes that cardiac surgery involves other major stimuli such as anesthesia, sternotomia, hemodynamics, post-operative that could influence in a non specific way BNP levels.

Key Words: B-type natriuretic peptide • Coronary artery bypass graft • Cardiac surgery


   1. Introduction
Top
 Abstract
 1. Introduction
2. Methods
 3. Results
 4. Discussion
 References
 
Chronic mitral regurgitation and aortic stenosis are two valve diseases leading, by different mechanisms, to myocardial decompensation in the absence of corrective surgery. In the chronic mitral regurgitation, the left ventricular muscle dysfunction is the result of a progressive increase of end-diastolic volumes. This muscle dysfunction impairs the emptying of the ventricle during the systole, leading to a left atrial pressure increase and to pulmonary congestion. Aortic stenosis is characterized by left ventricular outflow tract obstruction resulting in a systolic pressure gradient between the left ventricle and the aorta. Differing from the chronic mitral regurgitation, systolic pressure overload in the left ventricle progressively leads to an increase in ventricular wall thickness (i.e. concentric hypertrophy), with an impairment of diastolic compliance. However, in severe aortic stenosis these changes finally lead to increased left ventricular end-diastolic pressure, impaired contractility and left ventricular failure.

The natriuretic peptides are a group of structurally similar but genetically distinct peptides that have diverse actions in cardiovascular, renal, and endocrine homeostasis. Atrial natriuretic peptide (ANP) and B-type (or brain) natriuretic peptide (BNP) have a myocardial cell origin. BNP is predominantly secreted by the cardiac ventricles in response to increases in ventricular wall stress, and its measurement is a guide for the diagnosis of cardiac overload. BNP has been shown to be a potential marker of left ventricular dysfunction and heart failure while limiting expensive cardiac imaging modalities, for review [1,2]. Moreover, BNP and N-terminal proBNP measurement provide prognostic informations [3–6] and the pharmacotherapy for heart failure might be guided by plasma concentration of BNP [7] or N-terminal proBNP [8]. Some studies have focused on plasma levels of BNP or N-terminal proBNP in valvular aortic stenosis [9–12] or in patients with mitral regurgitation [13]. Their results show that plasma BNP concentration could serve as a non invasive monitor of disease progression [11] and as an early marker of left ventricular dysfunction [12,13]. In two studies BNP was determined in patients with aortic stenosis before and after corrective surgery. All of them report high BNP concentrations with increasing severity of symptoms.

The aim of our study was to investigate the ability of BNP levels to detect the immediate post-surgery cardiac function improvement in patients with mild cardiac failure in relation with valvulopathy. The patients were scheduled for cardiac surgery with cardiopulmonary bypass (CPB) for chronic mitral regurgitation or valvular aortic stenosis or myocardial ischaemia.


   2. Methods
Top
 Abstract
 1. Introduction
 2. Methods
3. Results
 4. Discussion
 References
 
2.1. Patients
Between January to December 2002 all patients who were undergoing corrective surgery for aortic stenosis (AVR for aortic valve replacement) or mitral regurgitation (MVR for mitral valve replacement) were prospectively enrolled in this study. For a purpose of comparison, we also studied patients with coronary artery disease undergoing coronary artery bypass (CABG) surgery. During this period, a total of 35 patients undergoing cardiac surgery gave informed consent to the study. Eighteen patients were on a diuretic, two on digoxin, seven on a calcium-blocker, eighteen on a ß-blocker and seventeen on an ACE inhibitor. Three groups of patients were constituted as follows: 14 patients with CABG (group I), 14 patients with AVR (group II) and 7 patients with MVR (group III). Among group I, 5 patients described a family history of coronary artery disease. Among all patients, 18 described a history of hypertension, 17 were smokers, 6 gave a history of diabetes mellitus and 15 of hypercholesterolemia. Other clinical characteristics are given in Table 1. In all patients, anesthesia, CPB and post-operative management were similarly done. Patients with acute or chronic renal failure were excluded from the study. The study was approved by the local ethics committee.


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  		Table 1. Clinical characteristics of the patients

 
2.2. Operative details
Anesthesia was induced and maintained by propofol i.v. (target controlled infusion), sufentanil citrate and atracurium. A prophylactic ultra-low dose of aprotinin was administered (5x105 KIU before skin incision, and 5x105 KIU during initiation of CPB). Patients blood was heparinized before CPB with 300 UI/kg of heparin, and the activated clotting time, using kaolin as the activating agent (Medtronic, ACT II HemoTec, Rueil Malmaison, France) was maintained during CPB at a value greater than 450 s with additional doses of heparin as required. The extracorporeal circuit was primed with 1000–1200 ml of a lactated Ringer's solution (Bioluz, St Jean de Luz, France) containing 4000 units of heparin. A membrane oxygenator was used and flows of 1.8–2.2 l min–1 m–2 were obtained with a roller pump (Stöckert Instrumente, Munich, Germany) under mild hypothermia to normothermic conditions (32–37 °C). After discontinuation of CPB, anticoagulation was reversed with protamine sulfate. Blood remaining in the CPB circuit was collected and infused to the patient before arrival in intensive care unit (ICU).

2.3. Measurement of plasma BNP concentrations
Blood was sampled from the venous ports of the CPB. For each patient, six 7 ml blood samples were taken: at the induction of anesthesia (T0), immediately after the CPB (T1), at the arrival in the ICU (T2), 4 h (T3), 8 h (T4) and 12 h (T5) after the arrival in ICU. The blood was transferred into tubes containing potassium EDTA (1 mg/ml blood) and placed at +4 °C before centrifugation, as BNP is stable for at least several hours without aprotinine at room temperature [14]. Plasma separated after centrifugation were frozen at –70 °C until assayed. The plasma BNP concentration was measured in duplicate by a solid phase sandwich immunoradiometric assay for human BNP (IRMA BNP Schering CIS bio international, Gif s/Yvette, France). The range of expected normal values is <5.9 pg/ml. The coefficient of variability of the assay is less than 10% in the range 3–100 pg/ml, and the detection limit is 3 pg/ml. Cross-reactivity with human ANP was <0.005%.

2.4. Statistics
Clinical variables were normally distributed and expressed as mean±standard deviation (SD). BNP levels were not normally distributed and expressed as medians with ranges, and thus log-transformed for statistical analysis. The difference in variables were evaluated by the ANOVA test. The time course of BNP within each group was tested by ANOVA for repeated measures followed by a Bonferroni post-hoc test. P values <0.05 were considered to be statistically significant.


   3. Results
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
4. Discussion
 References
 
The subjects of group II are significantly older than those of the other two groups (P=0.005) (Table 1). There is no significant difference in body mass index, NYHA score, left ventricular ejection fraction, CPB duration and aortic crossclamp duration between groups. Mean systemic arterial pressure is significantly lower at T5 than at induction in group I only (78.8±10.0 vs 104.0±20.7 mm Hg, respectively, P<0.01).

The distribution of the baseline values of BNP concentrations corresponding to T0 are presented in Fig. 1 according to the undertaken surgery. At the induction of anesthesia, BNP values are similar in the groups I, II and III. The time course of changes in BNP levels is presented in Table 2 and as a profile normalized to T0 values in Fig. 2 . Concerning patients of group I, the plasma BNP concentration becomes significantly increased 8 h and 12 h after the induction of anesthesia to 91.7 and 148.3 pg/ml, respectively, (P<0.001) when compared with T0. This pattern of the plasma BNP level is almost similar to patients of group III reaching values of 82.3 and 143.0 pg/ml 8 and 12 h after the induction of anesthesia (P<0.01 and <0.001, respectively). BNP values in group II are not significantly different 12 h after the induction of anesthesia than at time T0, but one has indeed to notice the large dispersion of the BNP levels in this group. Interestingly, there is a significant correlation between the induction BNP concentration (T0) and the BNP concentration 12 h after the arrival in ICU (T5) (r2=0.87,P<0.0001).



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  		Fig. 1. Plot of baseline BNP concentrations at T0 against groups of patients.

 

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  		Table 2. Plasma BNP concentrations (median pg/ml (range)) for each group of patients (*P<0.05)

 


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  		Fig. 2. Time courses of plasma BNP levels after CPB normalized to baseline values at T0. {triangleup} indicates patients with CABG, {diamondsuit} indicates patients with AVR, {square} indicates patients with MVR.

 

   4. Discussion
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
References
 
From a huge amount of work, it has been proposed that B type natriuretic peptide measurement could identify either heart failure or left ventricular systolic dysfunction In fact, BNP is really an indicator of raised intracardiac pressure, irrespective of the etiology: left ventricular hypertrophy, left ventricular systolic dysfunction or valve disease [2].

One can supposes that valve replacement elicits pressure variations. As BNP is rapidly released by myocytes and disappears rapidly from plasma because of its short half-life (22 min), we investigated its use as an index of pressure variations in patients undergoing valvular cardiac surgery. Our study obviously cannot include healthy subjects undergoing such a surgery. Thus, we used patients with CAD as a control group despite a baseline BNP value higher than that recently reported by us or others in normal subjects [15–17] even if a recent paper suggests to adjust plasma BNP concentration to the patient's age [18]. For this group, our results are consistent with the findings of Chello et al. in a group of 31 coronary patients before operation [19]. Two recent studies investigated BNP concentrations pattern following cardiac surgery with cardioplegic arrest. An enhanced release is observed 5 min after aortic unclamping [1]. For Avidan et al. [20], BNP decreases when the aortic clamp is applied then increases following aortic clamp removal and termination of CPB. In our hands, a significant increase in BNP compared to values before aortic clamping is only observed several hours after the end of CPB, these findings being partially consistent with others suggesting that the operation causes cardiac ischemia from aortic crossclamp and cardioplegic arrest after termination of CPB [1,10,20].

In groups II and III, the plasma BNP concentrations are elevated after CPB suggesting an increased ventricular production related to hemodynamic conditions. One can supposes that myocardial ischemia can compromise left ventricular function and decrease the contractile function of the ventricle i.e. hibernating myocardium. Moreover, stunned myocardium is probably of importance the first hours after operation inducing reduced myocardial contraction, increased ventricular pressure and and secretion of BNP. Whatever the valvular heart disease (mitral, aortic or tricuspid) blood ANP and BNP concentrations are elevated when compared to either healthy subjects or coronary heart disease patients [9,13,21–24]. However, due to the natural history of the disease, patients presenting aortic stenosis are elderly subjects and not age-matched for the other two groups. In patients with aortic stenosis, N-terminal proBNP and BNP are elevated when compared to those of control subjects or patients with coronary artery disease [9–12]. Among these four studies, only one of them examined BNP concentrations before and immediately after aortic valve replacement [10]. Ikeda et al. [10] studied the time courses of BNP levels until 120 h after operation. They observe that a rapid and important decrease of BNP occurs especially for the patients whose preoperative values are markedly elevated, whereas for other aortic stenosis patients and those with coronary artery disease, a transient increase of BNP level is observed after the operation. Our results appear consistent with those of Ikeda et al. [10] over a comparable period of time. However, our study was focused on perioperative values and stopped at 12 h after admission in ICU, it could be interesting to measure BNP levels the day after surgery. Additionally to Ikeda's work we provide a group of 7 MVR for which we observe as high baseline BNP levels as those from literature, and an identical pattern over time to that of group I. In this group, the BNP baseline value although non significantly different than that of group II seems higher. This can probably be attributable to the different pathophysiological mechanisms taking place between chronic mitral regurgitation and aortic stenosis. The main limitation of our study is the lack of echocardiographic measurements and calculations or results of cardiac catheterization. The latter could improve the classification of patients especially in the group II where the BNP levels varied greatly with no obvious reason.

In conclusion, we observe that the occurring variation in BNP levels after the operation is an increase whatever the undergone corrective surgery, underlying the relative lack of specificity of BNP with regard to the cardiac pathology. Besides iatrogenic cardioplegia one can supposes that cardiac surgery involves other major stimuli such as anesthesia, sternotomia, hemodynamics, post-operative that could influence in a non specific way BNP levels. In our study all patients improved their cardiac function after the surgery (data not shown). What clearly needs to be established is whether the persistence of elevated BNP concentrations could predict critical surgery before the occurrence of clinical symptoms.


   Acknowledgments
 
We thank Schering CIS bio international for support and H. Filliatre and MF. Dubernet for their excellent technical assistance. We also thank Dr JB Corcuff for his participation in the manuscript preparation.


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

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