N-terminal Brain Natriuretic Peptide Levels Research Articles

Correlation between troponin T and N-Terminal brain natriuretic peptide levels and cardiac structure and function and cardiovascular disease in elderly maintenance hemodialysis patients

With the development of chronic kidney disease (CKD), the patients showed a gradual decline in renal function, which eventually progressed to end-stage renal disease (ESRD), accompanied by various cardiovascular and cerebrovascular events. Maintenance hemodialysis (MHD) is one of the effective methods to treat ESRD, but some patients still die from cardiovascular and cerebrovascular complications. The purpose of this study was to investigate the relationship between troponin T (TnT), n-terminal brain natriuretic peptide (NT-proBNP), cardiac structure and function and cardiovascular disease in maintenance hemodialysis patients. In this experimental study, 100 patients with MHD were randomly selected as research objects. According to the level of NT-proBNP before dialysis, they were divided into two groups, namely the low NT-proBNP group and the high NT-proBNP group. The clinical and biological indicators and the average value of echocardiography were detected in the two groups. The degree of CKD disease was divided into six stages according to GFR, and the influence of different stages on the cardiac function of CKD patients was detected. The experimental results showed that the levels of TnT and NT-proBNP in MHD patients were significantly increased, and the levels of TnT and NT-proBNP and cardiac function were correlated with the patients with cardiovascular diseases. Cardiac ultrasound confirmed that the NT-proBNP level of patients with left ventricular hypertrophy was significantly higher than that of patients without left ventricular hypertrophy, and the difference between the two was statistically significant (P<0.005).

Sacubitril/valsartan reduces endoplasmic reticulum stress in a rat model of doxorubicin-induced cardiotoxicity.

The induction of endoplasmic reticulum (ER) stress has been reported as a key contributor to the cardiotoxicity of doxorubicin. Previous in vitro and in vivo studies suggest that sacubitril/valsartan, a novel angiotensin receptor-neprilysin inhibitor, could be effective against doxorubicin-induced cardiotoxicity. However, the precise mechanisms are not fully understood. Therefore, we investigated whether the cardioprotective effects of sacubitril/valsartan are associated with ER stress modulation in a rat model of doxorubicin-induced cardiotoxicity. Male Sprague-Dawley rats were treated with intraperitoneal injections of doxorubicin (15mg/kg; cumulative) or saline for 3weeks. From the day before the first treatment, control animals were gavaged daily with water (n = 8), whereas doxorubicin-treated animals were gavaged daily with water (n = 8) or sacubitril/valsartan (60mg/kg/day; n = 8) for 6weeks. Echocardiography was performed 6weeks after the initiation of doxorubicin. In addition, serum troponin I and N-terminal brain natriuretic peptide levels were determined, and the extent of apoptosis and protein levels related to ER stress in the cardiac tissue and doxorubicin-treated H9c2 cardiomyocytes were analyzed. Sacubitril/valsartan significantly reduced doxorubicin-induced cardiac dysfunction and apoptosis in the myocardium. In addition, sacubitril/valsartan significantly downregulated the expression levels of proteins related to apoptosis and ER stress, including BAX, caspase 3, GRP78, PERK, IRE-1α, ATF-6, eIF-2α, ATF-4, and CHOP, in the myocardium of a rat model of doxorubicin-induced cardiotoxicity in vivo and doxorubicin-treated H9c2 cardiomyocytes in vitro. Sacubitril/valsartan significantly alleviated doxorubicin-induced cardiotoxicity, which may be associated with the reduction of ER stress.

Protocol for a systematic review and meta-analysis of studies on the use of brain natriuretic peptide and N-terminal brain natriuretic peptide levels in the diagnosis of cardiopulmonary edema in acute respiratory failure

BackgroundDyspnea with bilateral pulmonary edema is common among patients in emergency departments (EDs) or intensive care units (ICUs). For the initial management of patients with this condition, cardiopulmonary edema (CPE) must be differentiated from acute respiratory distress syndrome (ARDS) in clinical settings. Brain natriuretic peptide (BNP) and N-terminal brain natriuretic peptide (NT-proBNP) are useful in distinguishing these conditions. However, current data about the use of these indexes are limited. Hence, we planned to perform a systematic review and meta-analysis to determine the accuracy of the two indexes for the diagnosis of CPE.MethodsWe designed and registered a study protocol for a systematic review and meta-analysis. This study aims to determine the diagnostic accuracy of BNP and NT-proBNP based on the standards of the methodology of the Cochrane Handbook for Systematic Reviews of Diagnostic Test Accuracy and the Preferred Reporting Items for a Systematic Review and Meta-analysis of Diagnostic Test Accuracy Studies in reporting the findings of this review. We will search PubMed (MEDLINE), Cochrane Library, Embase, www.ClinicalTrials.gov, International Clinical Trials Registry Platform, and Google Scholar. Randomized controlled trials, cross-sectional studies, and observational cohort studies reporting the accuracy in diagnosing CPE among adult patients with dyspnea and bilateral pulmonary edema will be included in the analysis. There will be no limits regarding language and publication date for this review. Two reviewers will independently screen articles, extract data, evaluate for quality and bias using the Quality Assessment of Diagnostic Accuracy Studies (QUADAS-2), and use Grading of Recommendations Assessment, Development and Evaluation to summarize the strength of body of evidence. Then, a meta-analysis will be performed, and different statistical methods will be used to investigate heterogeneity among studies. A subgroup analysis of elderly patients with left ventricular dysfunction or chronic renal dysfunction will be performed. In the meta-analysis, a hierarchical summary receiver operating characteristic model or a bivariate model will be used in each index test, as appropriate.DiscussionA systematic review and meta-analysis of the accuracy of BNP and NT-proBNP for the diagnosis of CPE will be conducted. The result of this study can help clinicians to identify an appropriate initial treatment for patients with acute respiratory failure, including those with ARDS and CPE. To the best of our knowledge, this will be the first comprehensive systematic review focusing on ARDS management in a specific population.Systematic review registrationPROSPERO ID CRD42020201576

Peak Early Diastolic Transmitral Velocity As A Surrogate Marker Of Short-Term Atrial Fibrillation Recurrence After Electrical Cardioversion.

The aim of this study was to assess if peak early diastolic transmitral velocity (E-wave) can be used as a surrogate marker of short-term atrial fibrillation (AF) recurrence. We prospectively studied 57 consecutive patients who underwent electrical cardioversion (ECV) for AF and successfully converted to sinus rhythm. N-terminal brain natriuretic peptide levels (BNP) before and after ECV was measured in all patients. The follow-up included physical examination and a 12-lead electrocardiogram 14 days and one month after the ECV. In 42.1% patients AF recurred during one-month follow-up period. Gender, presence of mitral regurgitation, treatment with angiotensin II receptor blocker and left atrium diameter independently influenced E-wave velocity before ECV. E-wave velocity fell immediately after successful ECV (94.0±27 cm/s vs 79.7±23 cm/s, P<0.0001). E-wave velocity before ECV>94 cm/s and E-wave velocity after ECV >80 cm/s were predictors of one-month AF recurrence [(Hazard Ratio) HR=3.62 with 95% CI=1.49-8.78 and HR=3.76 with 95% CI=1.40-10.10, respectively]. E-wave velocity before and E-wave velocity after ECV remained predictors of AF recurrence but only in non-hypertensive patients (HR=1.01 with 95% C.I=1.01-1.03 and HR=1.03 with 95% C.I=1.01-1.06, respectively). Similarly, BNP levels before and after ECV were associated with an increased the risk of AF recurrence (HR=1.14 with 95% C.I 1.01-1.28 and HR= 1.16 with 95% C.I 1.03- 1.31, respectively). The addition of BNP levels to E-wave velocity before ECV appeared to have incremental value on short-term AF recurrence but at a marginally statistical significance (LR chi2=3.28, p=0.07). E-wave velocity before and after ECV appears to be a marker of short-term recurrence of AF.

Glycemia Lowering and Risk for Heart Failure: Recent Evidence from Studies of Dipeptidyl Peptidase Inhibition.

The global epidemic of type 2 diabetes mellitus (T2DM) has substantial implications for cardiovascular disease–related morbidity and mortality.1 The prevalence of T2DM in patients with heart failure (HF) is high, with strong and independent association between T2DM and incident HF observed in multiple prospective studies and in randomized-controlled clinical trials. In the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT), which enrolled subject’s ≥55 years of age with hypertension and ≥1 risk factor, patients with T2DM had a 2-fold risk for HF hospitalization or death after adjustment for other risk factors (RR, 1.95). The association with T2DM was independent of coronary artery disease and at least equivalent in magnitude and greater than that for electrocardiographic left ventricular (LV) hypertrophy.2 All measures of glycemia including fasting, postprandial, measures of insulin resistance, and hemoglobin A1c (HbA1c) have been associated with risk of developing HF, with the association extending to both HF with preserved ejection fraction and to HF with reduced ejection fraction.3,4 A substantial body of evidence from preclinical studies, endomyocardial biopsies in humans and more recently with cardiac MRI, support increased myocardial stiffness in T2DM related to alteration in extracellular matrix. There are multiple proximate mediators that have been hypothesized to play a role including advanced glycation end product deposition and reactive oxygen species that may increase myocardial stiffness during diastole, by cross-linking collagen or by enhancing collagen formation.5,6 Another pernicious proximal mediator is the elevation in postprandial lipids, such as remnant lipoproteins, characteristic of atherogenic dyslipidemia, a highly prevalent abnormality in T2DM, that may result in direct myocellular deposition of lipid, leading to microcirculatory dysfunction, alteration in substrate use and mitochondrial dysfunction.7,8 Indeed, positron emission tomography studies show reduced myocardial glucose uptake in favor of fatty acid …

Predictors of 30‐Day Readmission in Patients Hospitalized With Decompensated Heart Failure

Heart failure (HF) is the leading cause of hospitalizations and readmissions in the United States. Approximately one-third of patients admitted for HF are readmitted within 3 months; however, there are few markers that can identify those at highest risk for readmission. The purpose of this study was to identify clinical and laboratory markers associated with hospital readmission in decompensated HF. Clinical and laboratory markers are associated with readmission rates in decompensated HF. Clinical and laboratory data from 412 patients admitted with HF were analyzed using a multivariable logistic regression analysis to find predictors of HF readmission by 30 days. HF readmission rates at 30 days were lowest in those with at least 2 of the following discharge criteria: net fluid reduction >1.3 L (odds ratio [OR]: 0.27, P = 0.019), serum sodium level >135 (OR: 0.46, P = 0.034), and N-terminal brain natriuretic peptide level reduction >23% (OR: 0.11, P = 0.048). In multivariate analysis, those patients meeting ≥2 criteria had a very low risk of 30-day readmission (OR: 0.10, 95% confidence interval: 0.01-0.68, P = 0.019) compared to patients who failed to meet 2 criteria. A negative fluid balance, normal serum sodium, and net reduction in N-terminal brain natriuretic peptide level during hospitalization may be important indices to target to help reduce the likelihood of HF readmission within 30 days.

Ghrelin and Its Relation with N-Terminal Brain Natriuretic Peptide, Endothelin-1 and Nitric Oxide in Patients with Idiopathic Pulmonary Hypertension

Objectives: To investigate ghrelin levels in patients with idiopathic pulmonary arterial hypertension (IPAH) and the association of ghrelin with N-terminal brain natriuretic peptide (N-BNP), endothelin-1 (ET-1) and nitric oxide (NO). Methods: Plasma ghrelin, N-BNP, ET-1 and NO were measured, and echocardiography was performed in 20 IPAH patients and in 20 control subjects matched for age, sex and body mass index. Results: Plasma ghrelin and NT-proBNP levels were significantly higher in IPAH patients compared with values in control subjects (p < 0.05). In IPAH patients, ghrelin levels correlated positively with N-BNP (r = 0.616, p = 0.004), NO (r = 0.464, p = 0.039), right ventricle diameter (RVD; r = 0.485, p = 0.030) and pulmonary arterial systolic pressure (PASP; r = 0.591, p = 0.006). N-BNP levels correlated positively with RVD (r = 0.551, p = 0.012) and ET-1 (r = 0.451, p = 0.046). Conclusions: Plasma ghrelin levels were elevated in IPAH. Increased ghrelin levels correlated positively with N-BNP, PASP, RVD and NO, and N-BNP levels correlated positively with RVD and ET-1. Pulmonary vascular pathology is a complex imbalance of opposing forces. Ghrelin may not only provide a novel prognostic biomarker for IPAH but also be a potential new therapeutic strategy.

Low Plasma Level of Atrial Natriuretic Peptide Predicts Development of Diabetes: The Prospective Malmö Diet and Cancer Study

The cardiac natriuretic peptides are involved in blood pressure regulation, and large cross-sectional studies have shown lower plasma levels of N-terminal pro-natriuretic peptide levels [N-terminal atrial natriuretic peptide (N-ANP) and N-terminal brain natriuretic peptide (N-BNP)] in patients with insulin resistance, obesity, and diabetes. In this study, we prospectively tested whether plasma levels of mid-regional ANP (MR-ANP) and N-BNP predict new-onset diabetes and long-term glucose progression. MR-ANP and N-BNP were measured in 1828 nondiabetic individuals of the Malmö Diet and Cancer cohort (mean age 60 yr; 61% women) who subsequently underwent a follow-up exam including an oral glucose tolerance test after a median follow-up time of 16 yr. Logistic regression was used to adjust for covariates. During follow-up, 301 subjects developed new-onset diabetes. After full multivariate adjustment, MR-ANP was significantly inversely associated with incident diabetes (OR = 0.85; 95% CI = 0.73-0.99; P = 0.034) but not N-BNP (OR = 0.92; 95% CI = 0.80-1.06; P = 0.262). In fully adjusted linear regression models, the progression of fasting glucose during follow-up was significantly inversely related to baseline levels of MR-ANP (P = 0.004) but not N-BNP (P = 0.129). Quartile analyses revealed that the overall association was mainly accounted for by excess risk of incident diabetes in subjects belonging to the lowest quartile of MR-ANP. After full adjustment, the odds ratio for incident diabetes in the bottom compared with the top quartile of MR-ANP was 1.65 (OR = 1.08-2.51, P = 0.019) and 1.43 (OR = 1.04-1.96, P = 0.027) compared with all other subjects. Low plasma levels of MR-ANP predict development of future diabetes and glucose progression over time, suggesting a causal role of ANP deficiency in diabetes development.

Effects of admission serum urea, glomerular filtration rate, proteinuria and diabetes status on 3-month mortality after acute stroke

from hypovolemia, renovascular disease or reduced cardiac output. Our finding from this study predicting short-term mortality is in contrast to the findings from another study which showed that creatinine was a independent predictor of long-term mortality post-stroke. This large well-conducted study looking at biochemical predictors of longterm outcome after stroke however did not include serum urea as a prognostic determinant. Another study has implicated congestive cardiac failure as a mechanism of raisedurea-induced poor outcome. Interestingly, N-Terminal Brain Natriuretic Peptide level, a sensitive marker of cardiac dysfunction, has also been shown to independently predict short-term mortality post-stroke. It is therefore tempting to speculate the presence of underlying occult heart failure in patients with acute stroke and that interventions with pharmacotherapy to target cardiac disorders may confer shortand longer-term benefits. Our study has also shown that diabetes predicts poor stroke outcome, but it remains unclear whether hyperglycaemia is simply a cause or a marker of poor outcome. In conclusion, serum urea and diabetes status independently predict short-term mortality following an acute stroke. These parameters should therefore be included in developing future models of quality and prognosis of post-stroke care in predicting short-term mortality.

Relationship Between Obesity and N-Terminal Brain Natriuretic Peptide Level as a Prognostic Value After Acute Myocardial Infarction

Background and ObjectivesRecently, the prognostic value of N-terminal brain natriuretic peptide (NT-proBNP) in acute coronary syndrome has been demonstrated in many studies. However, NT-proBNP levels are influenced by various factors such as sex, age, renal function, heart failure severity, and obesity. NT-proBNP concentrations tend to decrease with higher body mass index (BMI). The aim of this study was to examine the influence of obesity on NT-proBNP as a predictive prognostic factor in acute myocardial infarction (AMI) patients.Subjects and MethodsUsing data from the Korea Acute Myocardial Infarction Registry (January 2005 to September 2008), 2,736 AMI patients were included in this study. These patients were divided into men (n=1,972, 70%) and women (n=764, 30%), and were grouped according to their BMIs. Major adverse cardiac events (MACE) during 1 year clinical follow-up were evaluated.ResultsNT-proBNP was significantly higher in lower BMI (p<0.001). Mean NT-proBNP levels of each obesity group were 2,393±4,022 pg/mL in the lean group (n=875), 1,506±3,074 pg/mL in the overweight group (n=724) and 1,100±1,137 pg/mL in the obese group (n=1,137) (p<0.01). NT-proBNP was an independent prognostic factor of AMI in obese patients by multivariative analysis of independent risk factors of MACE (p=0.01).ConclusionNT-proBNP is lower in obese AMI patients than in non-obese AMI patients, but NT-proBNP is still of independent prognostic value in obese AMI patients.

Analysis of N-terminal pro-B-type natriuretic peptide in patients with acute coronary syndromes

The N-terminal portion of brain natriuretic peptide (NT-proBNP) has been identified as an indicator of prognosis in different cardiovascular diseases. The objective of this study was to determine the utility of measuring plasma NT-proBNP levels in patients with acute coronary syndromes. We studied 66 patients admitted in our division for acute coronary syndromes. Patients underwent a venous blood sample within 24 h from the admission to determine NT-proBNP levels. Increasing plasma levels of NT-proBNP (in tertiles) was associated with a greater history of hypertension and current smoking, whereas biochemical parameters were associated with higher level of creatine kinase-MB mass, cardiac troponin I, and renal insufficiency. We detected correlations between the values of NT-proBNP and several variables; positive correlations were found between the values of NT-proBNP and creatinine (r=+0354; P=0.0024), cardiac troponin I levels (r=0320; P=0.0111), and creatine kinase-MB mass values (r=0261; P=0.035). An interesting result of our study was a significantly longer hospitalization in those patients belonging to the third tertile compared with those belonging to the first one (P=0.02). Finally, we showed a higher N-terminal brain natriuretic peptide level in patients with poor outcome during the hospitalization (left-ventricular systolic dysfunction, recurrent ischemic events, or death) compared with those who did not (3204+/-1841 vs. 836+/-1136, P=0.003). Measurement of B-type natriuretic peptide provides predictive information during the hospitalization in patients with acute coronary syndromes.

An evaluation of blood volume changes during ultrafiltration pulses and natriuretic peptides in the assessment of dry weight in hemodialysis patients

Changes in blood volume (BV) during dialysis as well as plasma levels of brain natriuretic peptide (BNP) and N-terminal (NT) pro-BNP levels are possible tools to assess dry weight in hemodialysis (HD) patients. The aim of the study was to compare these parameters with other non-invasive techniques used to assess dry weight in HD patients, and to study their relation with intradialytic hypotension (IDH) and the presence of cardiovascular disease BV changes during HD, both during regular dialysis and during an ultrafiltration pulse, plasma levels of NT pro-BNP and BNP, and vena cava diameter index (VCDI) were assessed in a cohort of 66 HD patients, which was subdivided according to tertiles of total body water (TBW) corrected for body weight, assessed by bioimpedance analysis. Parameters were also related to the presence of IDH and history of cardiovascular disease. The decline in BV during regular dialysis and during an ultrafiltration pulse, as well as VCDI and BNP were significantly different between the tertiles of normalized TBW, but refill after the ultrafiltration pulse and NT pro-BNP were not. Only VCDI and the decline in BV during regular dialysis were significantly different between patients with or without IDH. Vena cava diameter index, BNP, and NT pro-BNP were significantly higher in patients with cardiovascular disease. Using bioimpedance as the reference method, changes in BV, either during regular dialysis or during an ultrafiltration pulse, as well as VCDI and BNP are all indicative of hydration state in dialysis patients, but refill after an ultrafiltration pulse is not. Only VCDI and BV changes were related to IDH. The presence of cardiovascular disease appears to influence both VCDI as well as BNP.

Adjunctive therapy with low-molecular-weight heparin in patients with chronic heart failure secondary to dilated cardiomyopathy: One-year follow-up results of the randomized trial

Defective endothelial function has been shown in dilated cardiomyopathy. Therefore, improvement in endothelial function after low-molecular-weight heparin (LMWH) therapy may be clinically beneficial. Consequently, the effect of adjunct enoxaparin, a LMWH, on standard treatment of dilated cardiomyopathy was investigated. This was a randomized, standard treatment-controlled, 2-center pilot trial of 102 patients (52 receiving adjunctive therapy with enoxaparin at a dosage of 1.5 mg/kg daily for 3 months and 50 receiving standard therapy with angiotensin-converting enzyme inhibitors, beta-blockers, and diuretics alone) with stable chronic heart failure secondary to dilated cardiomyopathy (New York Heart Association [NYHA] class II and III; left ventricular [LV] ejection fraction, < or = 40%). All patients underwent coronary angiography and endomyocardial biopsy and were clinically stable for at least 6 months before enrollment. The combined primary end point included mortality, urgent heart transplantation, and readmission to hospital due to heart failure progression. The secondary end point was to determine the severity of heart failure (serum level of N-terminal brain natriuretic peptide), cardiac function (LV ejection fraction by radionuclide ventriculography), LV diameters by echocardiography, exercise capacity (changes in NYHA class, changes in peak oxygen consumption), and changes in quality of life (Minnesota Living with Heart Failure questionnaire). The clinical outcome was assessed after 6 and 12 months of therapy. Baseline characteristics were comparable in both groups. Five patients dropped out during 12 months of the study. Twelve patients achieved primary end point (8 in the control group and 4 in the LMWH group). The free survival rate was 94% for the LMWH group and 90% for the controls (not statistically significant). After the 12-month period, in the LMWH group, N-terminal brain natriuretic peptide level and LV diameters decreased significantly (P < .001 and P = .006, respectively), whereas LV systolic function increased (P < .001). Changes in exercise capacity and subjective improvement did not differentiate the groups (nonsignificant). Adverse reactions to the enoxaparin therapy were minor and transient. In patients with chronic heart failure due to dilated cardiomyopathy, adjunct long-term enoxaparin therapy may offer additional clinical benefit without deleterious effects on major cardiac events.

Utility of N-Terminal Brain Natriuretic Peptide Plasma Concentrations in Comparison to Lactate and Troponin in Children with Congenital Heart Disease Following Open-Heart Surgery

We conducted a prospective study in a pediatric cardiac intensive care unit in order to determine the diagnostic value of N-terminal brain natriuretic peptide (N-BNP) plasma concentration in the perioperative care of children with congenital heart disease (CHD). N-BNP plasma concentrations were determined by using a validated enzyme immunoassay. We measured N-BNP the day before surgery and up to 15 days postoperatively in 23 children (age range, 0.25-11 years) undergoing cardiac surgery due to various CHDs. Supply and duration of catecholamines, vasodilators, and respiratory therapy were determined and correlated to N-BNP. In addition, troponin T (TnT) and arterial Lactat (aL) concentrations were measured simultaneously. We found a significant correlation between preoperative and maximal N-BNP levels and dosage of vasodilators (r = 0.41, p < 0.02 and r = 0.83, p < 0.01, respectively). Maximal TnT and aL levels were not correlated to dosage of vasodilators. The dosage and duration of catecholamines, the duration of respiratory therapy, and the plasma concentration of TnT and aL were not correlated to pre- or perioperative N-BNP. Maximal TnT and aL levels were correlated to duration (r = 0.53, p < 0.01 and r = 0.48, p < 0.02) and dosage (r = 0.52, p < 0.02 and r = 0.60, p < 0.01) of catecholamines and duration of respiratory therapy (r = 0.57, p < 0.01 and r = 0.50, p < 0.02). As recent studies show, N-BNP appears to be a powerful neurohumoral indicator of ventricular function and prognosis for guiding therapy in the outpatient department or for discriminating cardiac from noncardiac symptoms. In contrast, the value of N-BNP for guiding perioperative therapy in pediatric cardiac intensive care units is limited.

Is plasma N‐BNP a good indicator of the functional reserve of failing hearts? The FRESH‐BNP study

Whether plasma N-terminal brain natriuretic peptide (N-BNP) is useful in the diagnosis of heart failure (HF) depends traditionally on whether it is as good as the putative 'gold-standard', left ventricular ejection fraction (LVEF), in indicating cardiac dysfunction. However, since HF is primarily an impairment of function of the cardiac pump, we explored the relationship between N-BNP and direct and indirect indicators of cardiac pump dysfunction. Eighty-six HF patients (mean age 56 years) with a range of LVEF's (mean 36.9+/-15.2%, range 15-66%) and 10 age-matched healthy controls were recruited into the study and had resting N-BNP measured. Cardiopulmonary exercise testing was performed to assess peak oxygen consumption (Vo(2)). A subgroup of 23 subjects underwent further exercise haemodynamic assessment to evaluate peak cardiac power output (CPO). The CHF group had significantly higher N-BNP (median [interquartile range]) levels (299 [705] fmol/ml) than the control group (7 [51] fmol/ml, P<0.005). Significant correlations between N-BNP and peak Vo(2), and N-BNP and peak CPO were observed (R> or =0.5, P<0.005). Although significant correlation was observed between N-BNP and LVEF (R=0.34, P=0.01), the correlations between LVEF and peak Vo(2) or peak CPO (all R<0.3, P>0.3) were not significant. Multivariate analysis identified plasma N-BNP and NYHA class, but not LVEF, as independent predictors of peak Vo(2). We have found that N-BNP was surprisingly good as a simple indicator of cardiac pump dysfunction. Since heart failure is an inadequacy of function, these results strongly support the notion that N-BNP is a useful blood test in estimating the extent of cardiac pump dysfunction and helpful in establishing positive diagnosis of heart failure.

Brain natriuretic peptide and n-terminal brain natriuretic peptide in the diagnosis of heart failure in patients with acute shortness of breath

ObjectivesThis study sought to compare the utility of measurement of plasma brain natriuretic peptide (BNP) and N-terminal brain natriuretic peptide (N-BNP) in the diagnosis of heart failure (HF) in patients with acute dyspnea. BackgroundPlasma BNP is useful in differentiating HF from other causes of dyspnea in the emergency department. The N-terminal component of BNP has a longer half-life, and in HF increases in plasma N-BNP are proportionately greater. MethodsWe studied 205 patients (average age 70 ± 14 years) presenting to the emergency department with acute dyspnea. Brain natriuretic peptide was analyzed using a point-of-care test and two locally developed radioimmunoassays. N-terminal BNP was measured using a locally developed radioimmunoassay and a commercially available assay. Final diagnosis of HF was adjudicated by two cardiologists. ResultsPatients with HF (n = 70) had higher mean levels of both hormones by all assays (p < 0.001 for all). Results with all assays correlated closely (r values between 0.902 and 0.969). Subjects with left ventricular (LV) dysfunction or left-sided valvular disease but no HF had intermediate levels of BNP and N-BNP (lower than subjects with HF, and higher than subjects without HF with no LV dysfunction or left-sided valvular disease) (p < 0.01 for all). Using optimum cut-offs, specificity for the diagnosis of HF ranged between 70% and 89% (highest for the N-BNP assays). Sensitivity ranged between 80% and 94% (highest for the point-of-care BNP assay). ConclusionsMeasurement of BNP or N-BNP is useful in the diagnosis of HF in acute dyspnea. Commercially available assays compare favorably with well-validated laboratory assays. Differences in sensitivity and specificity may influence the assay choice in this setting.