atrial-natriuretic-factor and Pleural-Effusion

Previous studies have reported that natriuretic peptides in the blood and pleural fluid (PF) are effective diagnostic markers for heart failure (HF). These natriuretic peptides include N-terminal pro-brain natriuretic peptide (NT-proBNP), brain natriuretic peptide (BNP), and midregion pro-atrial natriuretic peptide (MR-proANP). This systematic review and meta-analysis evaluates the diagnostic accuracy of blood and PF natriuretic peptides for HF in patients with pleural effusion.. PubMed and EMBASE databases were searched to identify articles published in English that investigated the diagnostic accuracy of BNP, NT-proBNP, and MR-proANP for HF. The last search was performed on 9 October 2014. The quality of the eligible studies was assessed using the revised Quality Assessment of Diagnostic Accuracy Studies tool. The diagnostic performance characteristics (sensitivity, specificity, and other measures of accuracy) were pooled and examined using a bivariate model.. In total, 14 studies were included in the meta-analysis, including 12 studies reporting the diagnostic accuracy of PF NT-proBNP and 4 studies evaluating blood NT-proBNP. The summary estimates of PF NT-proBNP for HF had a diagnostic sensitivity of 0.94 (95% confidence interval [CI]: 0.90-0.96), specificity of 0.91 (95% CI: 0.86-0.95), positive likelihood ratio of 10.9 (95% CI: 6.4-18.6), negative likelihood ratio of 0.07 (95% CI: 0.04-0.12), and diagnostic odds ratio of 157 (95% CI: 57-430). The overall sensitivity of blood NT-proBNP for diagnosis of HF was 0.92 (95% CI: 0.86-0.95), with a specificity of 0.88 (95% CI: 0.77-0.94), positive likelihood ratio of 7.8 (95% CI: 3.7-16.3), negative likelihood ratio of 0.10 (95% CI: 0.06-0.16), and diagnostic odds ratio of 81 (95% CI: 27-241). The diagnostic accuracy of PF MR-proANP and blood and PF BNP was not analyzed due to the small number of related studies.. BNP, NT-proBNP, and MR-proANP, either in blood or PF, are effective tools for diagnosis of HF. Additional studies are needed to rigorously evaluate the diagnostic accuracy of PF and blood MR-proANP and BNP for the diagnosis of HF.

Topics: Atrial Natriuretic Factor; Biomarkers; Exudates and Transudates; Heart Failure; Humans; Natriuretic Peptide, Brain; Natriuretic Peptides; Peptide Fragments; Pleural Effusion; Sensitivity and Specificity

The purpose of this study was to compare the diagnostic utility of pleural fluid N-terminal pro-B-type natriuretic peptide (NT-proBNP), midregion pro-atrial natriuretic peptide (MR-proANP) and midregion pro-adrenomedullin (MR-proADM) for discriminating heart failure (HF)-associated effusions.. NT-proBNP, MR-proANP and MR-proADM were measured by commercially available methodologies in the pleural fluid of a retrospective cohort of 185 consecutive patients with pleural effusions, of whom 95 had acute decompensated HF. Receiver-operating characteristic and area under the curve (AUC) analyses allowed comparisons of the discriminative properties of these biomarkers to be made at their optimal cut-off points.. The diagnostic accuracy of NT-proBNP and MR-proANP for HF as quantified by the AUC was 0.935 and 0.918, respectively, whereas MR-proADM was of limited value (AUC = 0.62). A pleural fluid MR-proANP >260 pmol/L or NT-proBNP >1700 pg/mL argues for HF (likelihood ratio (LR) positive >5), while levels below these cut-off values significantly decrease the probability of having the disease (respective LR negative 0.19 and 0.10). The optimal cut-off points for natriuretic peptides were influenced by age, renal function and body mass index. Finally, both NT-proBNP and the albumin gradient correctly identified more than 80% of those cardiac effusions misclassified as exudates by standard criteria.. MR-proANP is as valuable a diagnostic tool as NT-proBNP for diagnosing or excluding HF as the cause of pleural effusion.

Topics: Adrenomedullin; Aged; Aged, 80 and over; Atrial Natriuretic Factor; Biomarkers; Diagnosis, Differential; Disease Progression; Female; Follow-Up Studies; Heart Failure; Humans; Immunoassay; Male; Middle Aged; Natriuretic Peptide, Brain; Peptide Fragments; Pleural Effusion; Protein Precursors; Reproducibility of Results; Retrospective Studies; Severity of Illness Index

We focused on neurohumoral activity and its clinical correlates early and late after fenestrated, lateral intra-atrial total cavopulmonary connection (TCPC). Between 2007 and 2010, we prospectively studied 28 early and 48 late postoperative TCPC patients. Plasma concentrations of vasopressin, endothelin-1, proBNP, proANP were determined. We reviewed clinical data to determine relationship between neurohumoral activation and clinical status after TCPC. There was a significant influence of preoperative ventricular end-diastolic pressure (VEDP) (P=0.008) and vasopressin concentration (P=0.02) on the appearance of prolonged pleural effusions. A significant correlation between a combined predictor (a product of preoperative vasopressin concentration and VEDP) and time of effusions (r=0.59, P=0.006) was found. The mean respiratory equivalent of carbon dioxide at peak exercise (VE/VCO(2peak)) was significantly lower in patients operated before the second year of life compared to patients operated after two years of age (27.5±1.39 vs. 48.6±3.86; P=0.039). There was a significant correlation of endothelin-1 (r=0.84; P=0.008) and proBNP (r=0.88; P=0.02) concentrations with VE/VCO(2peak). The prolonged postoperative pleural effusions can be predicted based on the product of preoperative vasopressin concentration and VEDP. Exercise performance is related to the age at TCPC. Endothelin-1 and proBNP can be useful for identification of high-risk Fontan patients.

Topics: Analysis of Variance; Atrial Natriuretic Factor; Biomarkers; Child, Preschool; Endothelin-1; Exercise Tolerance; Female; Fontan Procedure; Heart Defects, Congenital; Humans; Infant; Length of Stay; Logistic Models; Male; Natriuretic Peptide, Brain; Pleural Effusion; Poland; Prospective Studies; Risk Assessment; Risk Factors; Time Factors; Treatment Outcome; Vasopressins; Ventricular Pressure

Neurohormonal activation has been shown to be a major factor in congestive heart failure progression and mortality. The beneficial effects obtained in clinical trials with angiotensin converting enzyme (ACE) inhibitors, beta-blockers and aldosterone antagonists have confirmed this hypothesis. 5,6-Diisobutirroyloxy-2-methyl-aminotetraline hydrochloride (nolomirole) is a selective agonist of prejunctional D(2)-dopaminergic and alpha(2)-adrenergic receptors. The stimulation of these receptors inhibits catecholamine release from sympathetic nerve endings. To confirm that this mechanism can be useful in congestive heart failure, we studied the effects of nolomirole on monocrotaline-induced congestive heart failure. The ACE inhibitor trandolapril was used as reference compound. Rats were given single intraperitoneal injection of either saline (control group; n=20) or monocrotaline (50 mg kg(-1)). Three days later, the monocrotaline-treated animals were randomly allocated (n=50 per group) to oral treatment with distilled water (vehicle group), nolomirole (0.25 mg kg(-1)) twice a day, or trandolapril (0.3 mg kg(-1)) once a day up to sacrifice. On the fourth week after monocrotaline injection, animals with signs of congestive heart failure were sacrificed for evaluation of heart hypertrophy and neuroendocrine alterations. Atrial natriuretic peptide (ANP) and alderosterone were determined by radioimmunoassay in plasma. Tissue norepinephrine concentration was quantified by high-pressure liquid chromatography. Nolomirole and trandolapril significantly reduced (a) hypertrophy of right atria and ventricles, (b) plasma levels of ANP and presence of pleural/peritoneal effusions and (c) norepinephrine depletion of right ventricle. These findings confirmed that nolomirole, like trandolapril, is able to attenuate the heart failure signs in the monocrotaline-induced congestive heart failure model.

Topics: Administration, Oral; Adrenergic alpha-Agonists; Aldosterone; Animals; Ascitic Fluid; Atrial Natriuretic Factor; Body Weight; Disease Models, Animal; Dopamine Agonists; Drug Evaluation, Preclinical; Esters; Female; Heart Atria; Heart Failure; Heart Ventricles; Hypertrophy, Right Ventricular; Indoles; Monocrotaline; Norepinephrine; Pleural Effusion; Rats; Rats, Sprague-Dawley; Tetrahydronaphthalenes

To discuss the value of atrial natriuretic peptide (ANP) in differentiating benign and malignant pleural effusion.. Direct radioimmunoassay was used to detect ANP of pleural effusion and serum in 30 tuberculous and 26 cancerous pleural effusion patients.. The ANP in tuberculous and cancerous pleural effusion were (75 +/- 9) ng/L, (157 +/- 45) ng/L respectively, and significant difference was found (P < 0.001). The ANP of tuberculous pleural effusion was apparently lower [(75 +/- 9) ng/L] than serum [(170 +/- 37) ng/L], and significant difference was also found (P < 0.001). The ratio of ANP of pleural effusion to that of serum were 0.47 +/- 0.17, 0.99 +/- 0.46 respectively in tuberculous and cancerous pleural effusion patients. The sensitivity of ANP was 81% and specificity 100% in diagnosing malignant pleural effusion.. Detecting ANP of pleural effusion is one of important methods for differentiating benign and malignant pleural effusion.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Atrial Natriuretic Factor; Diagnosis, Differential; Female; Humans; Male; Middle Aged; Pleural Effusion; Pleural Effusion, Malignant

We studied plasma concentration, content, and mRNA for atrial natriuretic peptide (ANP-mRNA) in heart chambers of monocrotaline-treated rats. Three distinct groups emerged: group 1, with moderate congestive heart failure (CHF; pleural effusion < 1 ml; no peritoneal effusion); group 2, with severe CHF (pleural and peritoneal effusion > 1 ml); and group 3, with right hypertrophy and no CHF. Group 1 and 2 rats had right atrial and ventricular hypertrophy, raised plasma ANP (from 16.31 +/- 11.32 to 98.50 +/- 22.50 and 124.09 +/- 57.29 pg/ml, respectively; P < 0.001), and depletion of right atrial ANP (from 143.23 +/- 29.79 to 21.70 +/- 17.70 and 18.12 +/- 14.64 nmol/g, respectively; P < 0.001). Ventricular ANP concentration was unchanged. ANP-mRNA rose in the right atrium [10.6 (P < 0.02) and 7.9 (P < 0.01) times] and right ventricle (53.0 and 46.6 times; P < 0.01). In left unhypertrophied chambers it also increased, although to a smaller extent. Group 3 rats had isolated right ventricular hypertrophy, normal ANP levels in plasma and tissues, and no activation of synthesis. These data suggest that 1) plasma concentration and ANP synthesis are increased only in animals with CHF, 2) activation of ANP synthesis is maximal in early stages of CHF and is not related to the degree of hypertrophy, and 3) ANP-mRNA is also expressed in unhypertrophied heart chambers of rats with CHF but is not expressed in hypertrophied chambers of animals without CHF.

Topics: Animals; Ascitic Fluid; Atrial Natriuretic Factor; Cardiomegaly; Female; Gene Expression; Heart Failure; Hypertrophy, Right Ventricular; Monocrotaline; Myocardium; Organ Specificity; Pleural Effusion; Rats; Rats, Sprague-Dawley; RNA, Messenger

The renin-angiotensin and cardiac natriuretic systems play an important role in the pathophysiology of congestive heart failure (CHF). The status of the membrane-bound pulmonary and renal activities of three ectoenzymes involved in the regulation of these systems-angiotensin-converting enzyme (ACE), neutral endopeptidase (NEP), and aminopeptidase A (APA)-was investigated in Wistar rats 3 months after induction of myocardial infarction (MI) and in sham-operated (control) rats. Plasma renin activity and ACE activity, plasma angiotensin II (Ang II) levels, and atrial natriuretic factor levels were simultaneously determined. The lung ACE activity was decreased in MI rats compared with control rats (P < .0001), and this decrease depended on the severity of the heart failure. In contrast, plasma ACE activity was increased in MI rats (P < .01), and this increase was also proportional to the severity of MI. Northern blot analysis showed that the lung ACE mRNA level in severe MI rats was half that of the control rats. Renal ACE activity of the MI rats was not affected, and neither renal or pulmonary NEP nor pulmonary APA activities were altered. Thus, lung ACE gene expression appears to be both organ- and enzyme-specifically regulated during CHF. Whereas plasma renin was increased in heart failure rats, plasma Ang II levels were not different from those of control rats. Thus, decreased lung ACE activity could possibly contribute to keeping plasma Ang II levels in the normal range. The decrease in lung ACE activity and mRNA levels, combined with increased plasma ACE activity, represents a novel aspect of endothelial dysfunction in CHF.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Analysis of Variance; Angiotensin II; Animals; Atrial Natriuretic Factor; Cell Membrane; Disease Models, Animal; Endothelium, Vascular; Gene Expression; Heart; Heart Failure; Kidney; Lung; Male; Myocardial Infarction; Organ Size; Peptidyl-Dipeptidase A; Pleural Effusion; Rats; Rats, Wistar; Renin; RNA, Messenger

To investigate the possibility that the prohormone of atrial natriuretic factor might be secreted into the pleural fluid of patients with congestive heart failure who are known to have high concentrations of both the N-terminus and C-terminus of this prohormone circulating in their plasma, six patients with class 2 New York Heart Association classified congestive heart failure had the simultaneous measurement of plasma and pleural fluid N-terminal and C-terminal atrial natriuretic factor prohormone concentrations. The 98 amino acid (aa) N-terminus, the midportion of the N-terminus consisting of aa 31-67 of the 126 aa ANF prohormone (ie, pro ANF 31-67), and the C-terminus (aa. 99-126, ANF) were found in high concentrations in the pleural fluid of all of these patients. The concentrations of the N-terminus (ie, pro ANF 1-98), and pro ANF 31-67 in pleural fluid were nearly equal to their concentration in plasma of these patients. Their plasma levels were more than double the plasma concentrations of pro ANFs 1-98 and 31-67 in 54 persons without congestive heart failure. These preliminary findings demonstrate that all 126 amino acids of the ANF prohormone are present in pleural fluid of patients with congestive heart failure since both the 98 aa N-terminus and the C-terminus (aa 99-126) are present. Whether or not the N-terminus, which contains diuretic and natriuretic peptides, secretion into pleural fluid helps clear the fluid present in the lung in congestive heart failure could not be determined from the present investigation.

Topics: Atrial Natriuretic Factor; Diuretics; Heart Failure; Humans; Natriuresis; Peptide Fragments; Pleural Effusion; Protein Precursors; Radioimmunoassay

To investigate the possibility that atrial natriuretic factor might be secreted into the pleural fluid of patients with congestive heart failure who are known to have high concentrations of this new peptide hormone circulating in their plasma, six patients with class 2 New York Heart Association classified congestive heart failure had simultaneos measurement of plasma and pleural fluid atrial natriuretic factor concentrations. Atrial natriuretic factor was found in high concentrations in the pleural fluid of all of these patients. The concentration of atrial natriuretic factor in pleural fluid was nearly equal to the concentration in plasma of these patients. Their plasma levels were double the plasma concentration of this peptide hormone in 54 persons without congestive heart failure. These preliminary findings demonstrate that atrial natriuretic factor is present in pleural fluid of patients with congestive heart failure, but whether or not this secretion of atrial natriuretic factor into the pleural fluid helps the lung clear the fluid present in the lung in congestive heart failure cannot be determined from the present investigation.

Topics: Atrial Natriuretic Factor; Heart Failure; Humans; Lung; Pleural Effusion; Radioimmunoassay

To assess the response of atrial natriuretic peptide (ANP) to rapidly changing right atrial pressures in vivo, we measured ANP levels in 15 patients undergoing the Fontan procedure and compared them with control levels in nine patients undergoing cardiac surgery for lesions not associated with atrial hypertension. There were no significant differences in preoperative ANP levels: 57 +/- 15 pg/ml for patients undergoing the Fontan procedure, 43 +/- 8 pg/ml for control patients. There was no significant change in ANP during surgery or in the postoperative period in control patients. In contrast, ANP increased significantly to 333 +/- 70 pg/ml (p less than .0025) after establishment of right atrial-pulmonary artery continuity with the Fontan procedure and was related to right atrial pressure, which increased from 5 mm Hg before to 14 mm Hg after the Fontan procedure (p less than .001). There was no significant change in left atrial pressure. During the first postoperative day, ANP levels fell to 141 +/- 34 pg/ml (p less than .01) but later increased to 290 +/- 80 pg/ml (p less than .025), a finding that may suggest depletion of a readily releasable intracellular pool of ANP before mobilization of a storage pool. There was no direct relationship between ANP levels and effusions in patients undergoing the Fontan procedure. Pharmacologically significant increases in ANP occur in patients undergoing the Fontan procedure, correlating with increased right atrial pressures, but the relationship between ANP and the fluid derangements after the procedure remains unclear.

Topics: Atrial Natriuretic Factor; Blood Vessel Prosthesis; Child; Heart Atria; Heart Defects, Congenital; Humans; Pericardial Effusion; Pleural Effusion; Postoperative Period; Pulmonary Artery; Water-Electrolyte Balance