| Backgrounds and aims:Measurable B-type natriuretic peptides (BNPs), which are largely produced by the left ventricle, include BNP and N-terminal prohormone BNP (NT-proBNP). These proteins are released from cardiomyocytes in response to wall tension and neurohumoral signals. These proteins are used as the tools for the diagnosis and prognosis of heart failure (HF).The level of NT-proBNP, a biomarker of cardiac function and heart failure, has become an important diagnostic tool for assessing patients who present acutely with dyspnea, and provides important prognostic information in both acute and chronic heart failure. Also, monitoring NT-proBNP plasma level is expected to improve patient care and outcomes. Secretion and plasma level of NT-proBNP respond to intracardiac distending pressures, with other modulating influences including age, sex, renal function and other aspects of neurohormonal status. Single measurement of NT-proBNP shows promise in diagnosis of heart failure.Minor increase in urinary albumin excretion (MAU) is known to predict adverse renal and cardiovascular events in diabetic and hypertensive patients. Recent findings show that MAU is an early and sensitive marker of future cardiovascular events even in healthy subjects. Albumin transition is indicative of a disturbance of the barrier function of endothelial cells, and vascular alterations are not confined to the kidney but can also be observed in the myocardium. MAU is now considered to be an atherosclerotic risk factor and predicts future cardiovascular disease risk in diabetic patients, in elderly patients, as well as in the general population. Lowering of MAU using rennin angiosin aldosterone sysyem (RAAS) inhibitors and others drugs appears to lower the risk for heart failure.Both of the plasm levels of NT-proBNP and MAU increased in patient with heart failure. The costs of monitoring MAU and NT-proBNP are different. Therefore, measurement of MAU instead of NT-proBNP in inpatients and outpatients with heart failure maybe a economic and easy way to monitor the progress of heart failue.Therefore, the aims of this study are as follows:1. NT-proBNP at cutpoints of>450 pg/ml was highly sensitive and specific for the diagnosis of heart failure and NT-proBNP level<300 pg/ml was optimal for ruling out acute chronic heart failure(CHF), with a negative predictive value of 99%. To investigate whether is the plasma levels of NT-proBNP increased synchronously in pace with the aggravation of heart failure.2. MAU is associated with increased heart failure risk. To investigate whether is the plasma levels of MAU increased synchronously in pace with the aggravation of heart failure.3. To evaluate whether is the plasm levels of NT-proBNP and MAU increased synchronously with the aggravation of heart failure.Methods:1. Ninety-one patients enrolled came from in-patient in this study with primary heart failure (NYHA stageâ… -â…£; NT-proBNP>450pg/ml; LVEF<50%; LVED>55mm), a normal renal function (GFR>90 ml/min/1.73 m2), and MAU (>30mg/L). All enrolled subjects were without diabetic signs, liver dysfunction, other causes of dyspnea and dyslipoproteinemia. All subjects were enrolled without any acute illness.2. Ninety-one patients with heart failure were devided into different groups according to different stage of heart failure.As per standard guidelines, all patients were processed for measuring left ventricular ejection fraction (LVEF) and left ventricular end diastolic diameter (LVEDD) by Doppler echocardiograph (HP Sonos 7500). Serum creatinine was also determined. Glomerular filtration rate (GFR) was calculated by using the Modification of Diet in Renal Disease (MDRD). Plasma levels of NT-proBNP was determined at baseline by electrochemiluminescence immunoassay in COB AS (sensitivity 10pg/ml) and MAU at baseline by immune scattering turbidimetry (ICTM)(sensitivity 2mg/L).Results:1. In all the groups, significant difference in every stage of heart failure was noted from the last baseline values of NT-proBNP and MAU among the subjects with the progress of heart failure (P<0.05).2. For all enrolled subjects with heart failure, there was a significant negative correlation in MAU and LVEF (r= -0.733, P<0.001). There were all positive correlation for MAU with LVEDD and NT-proBNP. The values of r and P were 0.704, <0.001,0.885,<0.001, respectively.Conclusions:1. The plasma levels of NT-proBNP and MAU increased synchronously in pace with the aggravation of heart failure, at the same time there was positive correlation for MAU with NT-proBNP (r=0.885,P<0.001). For all enrolled suhjects, there was a significant negative correlation between MAU and LVEF (r=-0.733, P<0.001).These phenomena indicated that a disturbance of the barrier function of vascular endothelial cells gradually increased with the aggravation of heart failure. Very likely, generalized endothelial dysfunction plays an important role on the mechanisms of the linking MAU and NT-proBNP with end-organ damage.2. The plasm levels of NT-proBNP and MAU increased synchronously with the aggravation of heart failure. Monitoring MAU might takes the place of monitoring NT-proBNP in patients with heart failure. |
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