Association between plasma B-type natriuretic peptide and anaemia in heart failure with or without ischaemic heart disease: a retrospective study

Abstract

ObjectivesAnaemia is a risk of worsening heart failure. However, anaemia sometimes remains undetected because the superficial cardiac function does not precisely reflect the adverse impact of anaemia. Plasma B-type natriuretic peptide (BNP) could be helpful in these cases. However, the direct anaemic effects on BNP remain unknown. Herein, we compared the direct effect of anaemia on BNP and left ventricular ejection fraction (LVEF) using an advanced statistical procedure.DesignA retrospective study.SettingSecondary care (cardiology), single-centre study.ParticipantsThe study consisted of 3756 inpatients, including 684 without ischaemic heart disease (IHD) and 3072 with IHD.Primary and secondary outcome measuresRelationship between plasma BNP levels and LVEF values.ResultsA path model was constructed to simultaneously examine the adverse impact of anaemia on LVEF and plasma BNP, allowing for renal function. The path model revealed that LVEF increased in response to low haemoglobin (Hb), and the phenomenon was prominent in non-IHD (standardised regression coefficients (St.β): −0.264, p<0.001) rather than in IHD (St.β: 0.015, p=0.531). However, the response of BNP was commonly observed in both groups (non-IHD St.β: −0.238, IHD St.β: −0.398, p<0.001, respectively). Additionally, this study showed a direct link between low estimated glomerular filtration rate and high BNP independently of LVEF. Incrementally, Bayesian structural equation modelling in covariance structure analysis clearly supported this result. The scatter plots and simple regression analysis revealed that an adequate blood supply was approximately Hb 110 g/L and over in the non-IHD patients, whereas blood was not supplied in sufficient quantities even by Hb 130 g/L in patients with IHD.ConclusionThe current study demonstrated that anaemia was a substantial risk for worsening cardiac overload as estimated by plasma BNP. The anaemic response of LVEF likely changed depending on underlying cardiac disorders (IHD or not). However, the response of BNP was robustly observed.

Can Anemia Be a Confounder in Nt-Probnp Interpretation?

“…On the other hand, a study found that after examining patients with heart failure, there was an inverse relationship between both BNP and Hb level. Despite the fact that it is expected to find an elevation in the BNP level, nevertheless, their reported value for correlation coefficient (r) between both variables was close to that reported by this study (0.41 vs 0.39) [13].…”

Haemodynamic Effects of Anaemia in Patients with Acute Decompensated Heart Failure

“…Our results support recommendation to carefully investigate the causes of anaemia in HF patients, especially the potentially reversible ones (e.g., iron deficiency, chronic bleeding, and medications) [1,24]. It is suggested that the treatment for anaemia should be initiated at an early stage before systolic function begins to decline [4]. Intravenous iron infusions seem to be the most efficient therapy for anaemia in HF.…”

“…e haemodynamic response to tissue hypoxia induced by severe anaemia in patients without cardiac disease presents as tachycardia, high cardiac output induced by the activation of the sympathetic nervous system, low vascular resistance caused by generalised vasodilation, and fluid retention [3][4][5]. In extreme cases, it can manifest as "noncardiac circulatory congestion" with pulmonary oedema and hypotension [3,5].…”

“…A rise in sympathetic and renin-angiotensin-aldosterone system activity provokes vasoconstriction and reduces renal perfusion. e heart is burdened with an increased volume workload as a result of water and salt retention [4]. Animal studies have revealed that chronic anaemia leads to eccentric cardiac hypertrophy, interstitial fibrosis, increased left ventricular end-diastolic pressure, and decreased systolic functional reserve [5,6].…”

“…e reaction of the heart to anaemia may differ depending on HF aetiology. Tominaga et al [4] revealed that, in nonischaemic HF, cardiac output could be increased to deliver sufficient oxygen in response to anaemia, while in ischaemic HF, this standby capacity in the heart seems to be exhausted [4]. e adverse haemodynamic effects of anaemia itself might be frequently missed or underestimated in clinical practice, mostly because of the lack of a simple bedside diagnostic tool.…”