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

ABSTRACT: OBJECTIVES:Anaemia 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. DESIGN:A retrospective study. SETTING:Secondary care (cardiology), single-centre study. PARTICIPANTS:The study consisted of 3756 inpatients, including 684 without ischaemic heart disease (IHD) and 3072 with IHD. PRIMARY AND SECONDARY OUTCOME MEASURES:Relationship between plasma BNP levels and LVEF values. RESULTS:A 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. CONCLUSION:The 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.

SUBMITTER: Tominaga M

PROVIDER: S-EPMC6429955 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:ObjectivesThis study sought to characterize urinary and plasma C-type natriuretic peptide (CNP) in acute decompensated heart failure (ADHF) to define their relationship with clinical variables and to determine whether urinary and plasma CNP together add prognostic value.BackgroundCNP is a protective hormone that is synthesized in the kidney and endothelium and possesses antiremodeling properties. Urinary and plasma CNP levels are elevated in pathophysiological conditions; however, their regulation and prognostic value in heart failure (HF) is unclear.MethodsUrinary and plasma CNP were measured in 109 healthy subjects and 208 patients with ADHF; the 95th percentile of CNP values from healthy subjects established the normal contemporary cutoffs. Patients with ADHF were stratified based on urinary and plasma CNP levels for clinical characterization and the assessment of risk for adverse outcomes.ResultsThere was no significant correlation between urinary and plasma CNP in both cohorts. Urinary and plasma CNP were significantly elevated in patients with ADHF, and both increased with disease severity and were positively correlated with plasma N-terminal pro-B-type natriuretic peptide (NT-proBNP). Of the patients with ADHF, 23% had elevations in both urinary and plasma CNP, whereas 24% had normal CNP levels. During a median follow-up of 3 years, patients with elevated urinary and plasma CNP had a significantly higher risk of rehospitalization and/or death (HR: 1.79; P = 0.03) and rehospitalization (HR: 2.16; P = 0.01) after adjusting for age, sex, left ventricular ejection fraction, renal function, and plasma NT-proBNP. The C-statistic and integrated discrimination analyses further supported that the addition of urinary and plasma CNP to established risk models improved the prediction of adverse outcomes in patients with ADHF.ConclusionsUrinary and plasma CNP are differentially regulated in ADHF, and elevations in both provided independent prognostic value for predicting adverse outcomes.

Project description:ObjectivesThis study was conducted to determine whether urinary excretion of C-type natriuretic peptide (CNP) is elevated in acute decompensated heart failure (ADHF) and whether elevated levels predict adverse outcomes.BackgroundUrinary CNP has been detected in patients with heart failure, but its clinical significance and prognostic utility, compared to established kidney injury biomarkers, in ADHF is unknown.MethodsWe measured 24-h urinary excretion and concurrent plasma concentrations of CNP22, CNP53, and NT-CNP53 in 58 ADHF patients and 20 healthy control subjects. Urinary kidney injury molecule (KIM)-1 and neutrophil gelatinase–associated lipocalin (NGAL) and plasma N-terminal pro-B type natriuretic peptide (NT-proBNP) were also measured. Mortality and all-cause rehospitalization/death were assessed over a follow-up of 1.5 ± 0.9 years.ResultsADHF patients had higher urinary excretion of all 3 CNP molecular forms than did controls. Plasma CNP22 and CNP53 were elevated in ADHF but showed limited correlation with urinary excretion, suggesting that mainly renal-derived CNP appears in urine. Plasma NT-proBNP and urinary KIM-1 were also elevated in ADHF (p < 0.0001); urinary NGAL was similar to that in controls. At 6 months, event-free survival values in ADHF patients were 86% for mortality and 59% for all-cause rehospitalization/death. On Cox regression analysis, urinary NT-CNP53 was the only predictor of mortality (hazard ratio: 1.7; 95% confidence interval: 1.1 to 2.4; p = 0.01) and all-cause rehospitalization/death (hazard ratio: 1.8; 95% confidence interval: 1.3 to 2.4; p = 0.0004), even after adjustment. Integrated discrimination analysis suggested that urinary NT-CNP53 combined with plasma NT-proBNP improved the prediction of adverse outcomes.ConclusionsThe findings from this study support the clinical utility of urinary CNP molecular forms. In ADHF, urinary NT-CNP53 correlated with prognosis, better predicted outcomes than did urinary NGAL and KIM-1, and improved the prognostic value of plasma NT-proBNP.

Project description:BACKGROUND:Numerous experimental studies suggest that B-type natriuretic peptide (BNP) is cardioprotective; however, in clinical studies, higher plasma BNP concentrations have been associated with incident cardiovascular disease and higher left ventricular mass. Genetic association studies may allow us to determine the true causal directions without confounding by compensatory mechanisms. METHODS AND RESULTS:We performed a meta-analysis of 2 genome-wide association results from a total of 2790 blacks. We assumed an additive genetic model in an association analysis of imputed 2.5 million single-nucleotide polymorphism dosages with residuals generated from multivariable-adjusted logarithmically transformed BNP controlling for relevant covariates and population stratification. Two loci were genome-wide significant, a candidate gene locus NPPB (rs198389, P=1.18×10(-09)) and a novel missense variant in the KLKB1 locus (rs3733402, P=1.75×10(-11)) that explained 0.4% and 1.9% of variation in log BNP concentration, respectively. The observed increase in BNP concentration was proportional to the number of effect allele copies, and an average of 8.1 pg/mL increase was associated with 2 allele copies. In a companion study, single-nucleotide polymorphisms in this loci were cross-checked with genome-wide association results for the aldosterone/renin ratio in individuals of European ancestry, and rs3733402 was genome-wide significant (P<5.0×10(-8)), suggesting possible shared genetic architecture for these 2 pathways. Other statistically significant relations for these single-nucleotide polymorphisms included the following: rs198389 with systolic blood pressure in blacks (COGENT consortium) and rs198389 and rs3733402 with left ventricular mass in whites (EchoGEN consortium). CONCLUSIONS:These findings improve our knowledge of the genetic basis of BNP variation in blacks, demonstrate a possible shared allelic architecture for BNP with aldosterone-renin ratio, and motivate further studies of underlying mechanisms.

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

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