Fluid balance in patients with chronic renal failure assessed with N-terminal proatrial natriuretic peptide, atrial natriuretic peptide and ultrasonography

The N-terminal proatrial natriuretic peptide (proANP) has become an important parameter for assessing the prognosis of patients with cardiac disease. Its use for evaluating the hydration status in patients with chronic renal failure, however, is still under investigation. The present study comprised 12 haemodialysis (HD) and 17 pre-dialysis patients. In the HD patients, the inferior vena cava diameter during quiet expiration (IVCe) was estimated by ultrasonography and plasma concentrations of N-terminal proANP, atrial natriuretic peptide (ANP) and cyclic guanosine monophosphate (cGMP) were measured before and 4 h after termination of HD. In the pre-dialysis patients venous blood samples were taken during rest to measure plasma N-terminal proANP and ANP and serum creatinine. Normal values for N-terminal proANP and ANP were obtained from 18 healthy volunteers. The plasma concentrations of N-terminal proANP and ANP in healthy volunteers were 328 +/- 92 and 11.4.0 +/- 3.1 pM L-1, respectively. In pre-dialysis patients, serum creatinine ranged from 110 to 447 microM L-1 and was significantly correlated to plasma N-terminal proANP (r = 0.60, P < 0.05) but not to ANP. This may indicate that N-terminal proANP is more dependent on renal function for its clearance than ANP, which is probably cleared by extrarenal mechanisms as well. In HD patients, IVCe was significantly correlated to the three hormones before HD, most strongly to N-terminal proANP. After dialysis, IVCe was significantly correlated to ANP and cGMP but was not correlated to N-terminal proANP. This may suggest that proANP takes a longer time than other hormones to reflect changes in intravascular volume. In conclusion, N-terminal proANP is a hormone closely related to degree of renal function. Furthermore, it is a sensitive marker reflecting the interdialytic hydration status in HD patients, as indicated by its high correlation to IVCe, a standard method which is used frequently nowadays to assess the body hydration. However N-terminal proANP could not reflect the acute changes in fluid volume induced by HD, probably because it is slowly metabolized.     

Relationship between N-terminal pro-B-type natriuretic peptide levels and metabolic syndrome

Introduction

Previous studies have shown that obese individuals have reduced natriuretic peptide levels. But conflicting data exist on the relation of natriuretic peptide levels to other metabolic risk factors.

Material and methods

We investigated the relationship between plasma N-terminal pro-B-type natriuretic peptide levels (NT-proBNP) and metabolic syndrome (MetS) and metabolic risk factors in 469 patients free of heart failure. Two hundred thirty diagnosed MetS cases and 239 non-MetS cases were included in this study. Echocardiography examinations were performed and left ventricular mass index was calculated according to the Devereux correction formula. NT-proBNP was measured by electrochemiluminescence. The log-transformed NT-proBNP levels were used for abnormal distribution. Multiple linear regression analysis was performed to assess the association between levels of NT-proBNP and metabolic factors. Covariance analysis was used for group comparisons.

Results

Log NT-proBNP levels were independently related to age, gender, body mass index, systolic blood pressure, diastolic blood pressure, fasting blood glucose, triglyceride, high density lipoprotein cholesterol, low density lipoprotein cholesterol, left ventricular mass index and left ventricular ejection fraction in multiple linear regression analysis (p < 0.05). Adjusted log NT-proBNP levels were lower in persons with MetS compared with those without MetS (p < 0.05). Individuals with hyperlipidaemia, elevated body mass index, diastolic blood pressure and fasting plasma glucose had lower levels of log NT-proBNP than those without MetS (p < 0.05).

Conclusions

There is a relationship between metabolic components and lower plasma NT-proBNP concentration. These findings raise the possibility that reduced plasma NT-proBNP levels are a manifestation of MetS, which might possess significant clinical and pathophysiological implications.     

新活素在重症病毒性心肌炎心力衰竭中的作用

目的 观察新活素在重症病毒性心肌炎心力衰竭中的疗效及安全性.方法 选取2010年1月至2013年12月在我科诊断的重症病毒性心肌炎患者27例,分为新活素组和对照组,新活素组在强心、利尿、扩血管基础上加用新活素治疗,观察两组患者脑利钠肽（BNP）、肌钙蛋白（cTnT）、肌酸激酶同工酶（CK-MB）、心脏彩超改变情况并比较两组的疗效.结果 新活素组能明显降低BNP [（203.1±39.8）vs.（1185.5±48.3） pg/ml]、cTnT [（13.5±9.8）vs.（24.8±13.2） μg/L]、CK-MB [（32.9±10.7）vs.（195.3 ±48.2） U/L],改善左室射血分数[（59.2±9.2）％vs.（38.1±8.8）％],并且疗效优于对照组（P＜0.05）,没有出现明显不良反应.结论 新活素对重症病毒性心肌炎心力衰竭是一个有效安全的治疗措施.     

Low levels of B-type natriuretic peptide predict poor clinical outcomes in patients with chronic and advanced heart failure

B-type natriuretic peptide (BNP) is a neurohormone produced mainly by ventricular myocytes in response to increased left ventricular end-diastolic pressure. Patients with acute decompensated heart failure often have elevated plasma BNP. However, recent clinical observations have demonstrated that in patients with advanced heart failure, the plasma level of BNP is lower than those with acute heart failure. We hypothesized that a lower circulating BNP level in patients with chronic and advanced heart failure is due to the exhaustion of the biosynthesis mechanisms and is associated with a poor outcome in these patients.     

Brain natriuretic peptide in diagnosis and treatment of heart failure

Currently we are in the midst of a chronic disease epidemic of congestive heart failure (CHF) worldwide. This epidemic is marked by a rapid rise in prevalent cases over the past decade that is due in part to the aging population and improved survival in patients with other cardiovascular conditions. At present there are 5 million Americans with congestive heart failure, with nearly 500000 new cases every year. To provide cost-effective treatment for patients with congestive heart failure, rapid and accurate differentiation of congestive heart failure from other causes of dyspnea must be accomplished. Although echocardiography is considered the gold standard for the detection of left ventricular dysfunction, it is expensive, is not always easily accessible, and may not always reflect an acute condition. B-type natriuretic peptide (BNP) is a cardiac neurohormone specifically secreted from the cardiac ventricles as a response to ventricular volume expansion, pressure overload, and resultant increased wall tension. BNP can be used in the diagnosis of CHF. However, the present American College of Cardiology/American Heart Association practice guidelines (2001) for the evaluation and management of CHF state that the role of blood BNP in the identification of patients with CHF remains to be fully clarified. We have discussed the role of BNP in the diagnosis and management of CHF.     

Interpretation of plasma concentrations of human atrial natriuretic peptide (hANP) in congestive heart failure

The present study reports about novel findings concerning the interrelationship between release of human atrial natriuretic factor (hANP) and the clinical situation of patients suffering from congestive heart failure. Estimations of plasma hANP were done by specific and sensitive extraction-based RIA. The normal range was 5 to 80 ng/l, mean +/- SEM = 30 +/- 15 ng/l, n = 106. Influence of response to therapy on hANP-release was studied in altogether 14 patients. 12 of these patients had elevated plasma hANP at admittance, surprisingly peptide levels were normal in 2 patients throughout the study. 9 out of the 14 patients responded well to therapy (shift from NYHA IV/III to NYHA II within about 10 days), hANP-levels decreased to normal values: 235 +/- 104 ng/l vs. 65 +/- 13 ng/l; p less than 0.001. The 5 residual patients responded to therapy only partially (shift from HYHA IV to NYHA III within an observation interval of about 2 weeks). Plasma hANP values decreased from 225 +/- 94 ng/l to 137 +/- 22 ng/l (p less than 0.02), but were still supranormal. Atrial fibrillation, which persisted in 8 out of the 14 patients after therapy did not influence hANP levels: hANP levels paralleled clinical signs of improvement, irrespective of atrial fibrillation. Right heart catheterization revealed very high mean right atrial pressures in those 2 patients mentioned above, who had normal pretherapeutic hANP.(ABSTRACT TRUNCATED AT 250 WORDS)     

Atrial natriuretic peptide and atrial pressure in patients with congestive heart failure

To define the relation between atrial pressures and the release of atrial natriuretic peptide, we measured plasma concentrations of the peptide in 26 patients with cardiac disease--11 with normal atrial pressures and 15 with elevated atrial pressures (11 of these 15 had elevated pressures in both atria). Mean peptide levels (+/- SEM) in the peripheral venous blood were increased in the 11 patients with cardiac disease and normal atrial pressures, as compared with 60 healthy controls (48 +/- 14 vs. 17 +/- 2 pmol per liter). In the patients with elevated atrial pressures, peptide concentrations were increased twofold in peripheral venous, right atrial, pulmonary arterial, and systemic arterial plasma, as compared with the concentrations in the patients with normal atrial pressures. A step-up in peptide concentration was seen between the venous and right atrial plasma (P less than 0.002) and between the pulmonary and systemic arterial plasma (P less than 0.01), suggesting release of the peptide from the atria. A linear relation was found between right atrial pressure and right atrial peptide concentration (r = 0.835, P less than 0.001) and between pulmonary wedge pressure and the systemic arterial peptide concentration (r = 0.866, P less than 0.001). Right atrial pressure and the peptide concentration both increased with exercise testing in the nine patients evaluated. We conclude that the release of atrial natriuretic peptide is at least partly regulated by right and left atrial pressures. Distinguishing the relative contributions of the two atria and defining the role of peptide release in the pathogenesis of heart failure will require further investigation.     

Atrial natriuretic peptide during acute treatment of congestive heart failure

Atrial natriuretic peptide (ANP) induces potent diuretic/natriuretic, vasorelaxing and aldosterone inhibitory effects. Increased plasma levels in congestive heart failure (CHF) have been reported. The aim of this study was to investigate plasma immunoreactive ANP (ir-ANP) levels during acute treatment of CHF. Seven patients with CHF underwent cardiac catheterization. Ir-ANP plasma levels were followed up to two h after administration of an orally given phosphodiesterase inhibitor (Milrinone); a substance with positive inotropic and peripheral vasodilating properties. In all patients cardiac output increased and cardiac filling pressures decreased markedly. Initially high ir-ANP plasma levels decreased. Our patients did not have an increased blood volume. It is concluded that plasma ir-ANP levels in the pulmonary artery rapidly decrease when atrial pressure is reduced. These data suggest that atrial pressure is the major determinant for release of ir-ANP in man and that the ability to respond quickly to changes in cardiac filling pressures is maintained in patients with severe CHF. Plasma ir-ANP levels may also become useful as an index of the degree of heart failure and serve as a tool in monitoring response to drug therapy.     

Plasma atrial natriuretic factor in low output heart failure syndromes

Summary Plasma atrial natriuretic factor, aldosterone, renin activity, and antidiuretic hormone were studied in low output heart failure syndromes: cardiogenic shock in ten patients with acute myocardial infarction of the anterior wall (first group), hypovolemic shock after melena from peptic ulcer in ten subjects (second group), and hypotension with bradycardia syndrome in ten patients with acute myocardial infarction of the inferior wall (third group). Circulating atrial natriuretic factor in patients with cardiogenic shock (102.4±7.4 pg/ml) was significantly higher than in healthy volunteers matched for sex and age (8.4±0.3 pg/ml). In these patients there was a positive correlation between atrial natriuretic factor and central venous pressure values. Atrial natriuretic factor and central venous pressure values in the second and third groups were within normal range. Plasma aldosterone was high in all groups, plasma renin activity was elevated in the first and third groups, and high antidiuretic hormone was observed in the first and second groups. These findings indicate that in low output heart failure syndromes only hemodynamic changes affecting the atria stimulate atrial natriuretic factor release. No correlations were found between plasma atrial natriuretic factor and other hormones. In particular, high atrial natriuretic factor levels in the patients with cardiogenic shock did not inhibit release of aldosterone, renin, or antidiuretic hormone. It may be surmised that in these patients the hemodynamic effects override the inhibitory effects of atrial natriuretic factor.Abbreviations ANF atrial natriuretic factor - ANP atrial natriuretic peptide - ANOVA analysis of variance - ACTH adrenocorticotropin hormone     

Plasma brain natriuretic peptide levels in coronary heart disease with preserved systolic function

We evaluated the circulating levels of brain natriuretic peptide (BNP) in stable angina, unstable angina, and myocardial infarction relating hormone levels to extension of coronary disease and number of vessels involved after angiographic examination. We studied 86 patients consecutively undergoing angiographic coronary examination and echocardiographic evaluation for coronary heart disease. These included 15 control subjects (group 0), 21 with stable angina (group I), 26 with unstable angina (group II), and 24 with non-Q myocardial infarction (group III). Patients with heart failure, a history of myocardial infarction, or recent myocardial damage with electrocardiographic S-T elevation were excluded. BNP levels in patients with unstable angina and myocardial infarction were significantly increased with respect to the group with stable angina (P<0.01). There were no differences between the groups with unstable angina and myocardial infarction. Analysis of peptide levels in relation to the number of involved vessels demonstrated a significant increase in patients with three-vessel disease compared with subjects with one or two vessels involved (P<0.03); among subjects with mono-vessel disease, patients with left descendent anterior stenosis had a more-marked BNP elevation than subjects with stenosis in other regions (P<0.01). Hence, BNP levels appear to be elevated in coronary disease, especially in acute coronary syndromes, even in the absence of systolic dysfunction. BNP levels also seem to be related to the severity of coronary atherosclerosis and number of vessels involved. BNP could prove a novel marker for risk stratification, not only in heart failure but also in coronary heart disease.     

Plasma brain natriuretic peptide levels in coronary heart disease with preserved systolic function

Abstract. We evaluated the circulating levels of brain natriuretic peptide (BNP) in stable angina, unstable angina, and myocardial infarction relating hormone levels to extension of coronary disease and number of vessels involved after angiographic examination. We studied 86 patients consecutively undergoing angiographic coronary examination and echocardiographic evaluation for coronary heart disease. These included 15 control subjects (group 0), 21 with stable angina (group I), 26 with unstable angina (group II), and 24 with non-Q myocardial infarction (group III). Patients with heart failure, a history of myocardial infarction, or recent myocardial damage with electrocardiographic S-T elevation were excluded. BNP levels in patients with unstable angina and myocardial infarction were significantly increased with respect to the group with stable angina (P<0.01). There were no differences between the groups with unstable angina and myocardial infarction. Analysis of peptide levels in relation to the number of involved vessels demonstrated a significant increase in patients with three-vessel disease compared with subjects with one or two vessels involved (P<0.03); among subjects with mono-vessel disease, patients with left descendent anterior stenosis had a moremarked BNP elevation than subjects with stenosis in other regions (P<0.01). Hence, BNP levels appear to be elevated in coronary disease, especially in acute coronary syndromes, even in the absence of systolic dysfunction. BNP levels also seem to be related to the severity of coronary atherosclerosis and number of vessels involved. BNP could prove a novel marker for risk stratification, not only in heart failure but also in coronary heart disease.     

Studies on plasma immunoreactive human brain natriuretic peptide (hBNP) levels in patients with congestive heart failure and present forms of hBNP in human cardiac ventricle

By using a specific radioimmunoassay (RIA) for human brain natriuretic peptide (hBNP), we measured immunoreactive hBNP (ir-hBNP) in plasma from patients with congestive heart failure (CHF). There appeared to be relationship between the enhanced ir-hBNP secretory activity and the severity of the failing heart as well as that of immunoreactive human atrial natriuretic peptide (ir-hANP). However, the secretion of ir-hBNP was augmented much more than that of ir-hANP in sever CHF patients. Gel permeation chromatography coupled with the RIA revealed that ir-hBNP in human ventricle is composed with gamma-hBNP and hBNP (1-32) as well as that of human atrium. However, we found differences of the gamma-hBNP/hBNP (1-32) ratio in atrial and ventricular tissues. These findings suggest that the hBNP secretion mechanism differ in the two areas of human heart.     

慢性心力衰竭患者血浆瘦素水平的变化

目的： 研究慢性心力衰竭（CHF）患者血浆瘦素（leptin）水平的变化。方法：应用放射免疫法测定了60例CHF患者和26例健康对照者的血浆瘦素水平，比较CHF组与对照组、CHF组不同心衰级别及不同病因亚组间的血浆瘦素水平。结果：CHF组患者血浆瘦素水平明显高于对照组（P＜0.01）；心功能Ⅳ级患者的血浆瘦素水平明显高于心功能Ⅲ级患者（P＜0.01）；CHF不同病因亚组间血浆瘦素水平无显著差异（P＞0.05）。结论：CHF患者血浆瘦素水平升高，并与心衰的严重程度相关，而与引起心衰的病因无关。