Original article
BNP in septic patients without systolic myocardial dysfunction

https://doi.org/10.1016/j.ejim.2006.07.013Get rights and content

Abstract

Background

We tested our hypothesis that serum BNP levels rise in sepsis and septic shock patients as a result of an inflammatory state and not only because of left ventricular dysfunction.

Methods

Twenty-one patients with sepsis or septic shock were enrolled in the study. Echocardiography was performed in every patient on admission and at discharge. Laboratory data were evaluated on admission, during hospitalization, and at discharge. Serum IL-1β, IL-6, TNFα, and BNP concentrations were determined.

Results

BNP values on admission (r = 0.47, p = 0.03), during hospitalization (r = 0.64, p = 0.014), and on the day of discharge (r = 0.54, p = 0.015) were all positively correlated with CRP values. Mean BNP (r = 0.07, p = 0.006) and BNP level at discharge (r = 0.68, p = 0.001) were also positively associated with IL-1 at discharge. Mean CRP (17.7 mg/dL ± 1.5 vs. 9.2 mg/dL ± 3.6, p = 0.002), IL-6 (46.6 pg/mL ± 2.2 vs. 25.6 pg/mL ± 16.3, p = 0.003), and SAPS II levels (41.3 ± 4.7 vs. 33.9 ± 6.5 p = 0.01) were also higher in patients who died versus those who survived. No difference in BNP levels was recorded in subjects who died versus those who survived. There was no clinical or echocardiographic evidence of left ventricular systolic dysfunction (mean EF% on admission 55.1 ± 21.7 vs. 61.3 ± 8.6 on discharge, p = 0.123). Serum BNP levels at discharge were inversely associated with EF values on admission (r = −0.475, p = 0.046) and positively associated with E/A ratio on admission (r = 0.565, p = 0.028). No association was found between BNP values and death.

Conclusion

BNP is positively correlated with CRP levels in septic patients without clinical or echocardiographic evidence of systolic dysfunction. No association was found between death and BNP values. It seems that, in septic patients, BNP is less accurate as a measure of ventricular dysfunction.

Introduction

Atrial and brain natriuretic peptides (ANP and BNP) are cardiac hormones with natriuretic and vasodilator actions. Three peptides – ANP, BNP, and CNP – constitute the NP family. ANP and BNP act via NP receptor A (NPR-A), which activates cGMP production through two particulate guanylate cyclases (PGC) involved in their signal transduction [1], [2].

BNP is considered to be an effective marker of severity and prognosis of acute coronary syndromes and congestive heart failure. It has also been recognized as a diagnostic marker of left ventricular dysfunction [3], [4], [5]. There is a possibility that myocardial dysfunction is not the only trigger responsible for BNP release.

Sepsis and septic shock are increasing in incidence and are frequently accompanied by myocardial dysfunction [6], [7]. Although previously described as a preterminal event, ventricular dysfunction with reduced ejection fraction (EF) and biventricular dilatation is present in most patients with severe sepsis and septic shock [6], [7]. ANP, BNP, and IL-6 levels have been reported to be elevated in patients with septic shock. This increase in BNP was usually reported to reflect left ventricular dysfunction, while ANP was related to IL-6 production rather than to cardiovascular dysfunction [8], [9].

In the present study, we tested our hypothesis that BNP levels rise in sepsis and septic shock patients as a result of an inflammatory state and not only because of left myocardial dysfunction.

Section snippets

Materials and methods

A prospective, observational study was conducted. Consecutive patients (n = 21) with the diagnosis of sepsis or septic shock who were admitted to the internal medicine ward over a period of 6 months were enrolled in the study. The diagnosis of sepsis or septic shock was made according to the ACCP/SCCM consensus conference definitions of sepsis, severe sepsis, and septic shock [6]. An echocardiographic study was performed on every patient on admission and at discharge (M-mode guided 2D; the

Results

Eight patients (38%) in the study population were male (Table 1) and eight patients (38%) died during follow-up. No by-gender difference in death was observed.

Mean CRP, IL-6, and SAPS II levels were higher in patients who died than in survivors (17.7 mg/dL ± 1.5 vs. 9.2 mg/dL ± 3.6, p = 0.002; 46.6 pg/mL ± 2.2 vs. 25.6 pg/mL ± 16.3, p = 0.003; and 41.3 ± 4.7 vs 33.9 ± 6.5, p = 0.01, respectively).

Discussion

BNP was found to be positively correlated to CRP levels in septic patients without systolic left ventricular dysfunction, both clinically and echocardiographically. Up until now, BNP was considered to be an index of left ventricular systolic dysfunction and prognosis in heart failure [10]. This consideration made sense since BNP secretion was known to be stimulated mechanically by atrial and ventricular stretch, as occurs with volume overload [1], [3]. However, heart failure is also a state of

References (21)

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