(Hypertension. 1996;28:988-994.)
© 1996 American Heart Association, Inc.
Articles |
Superiority of Brain Natriuretic Peptide as a Hormonal Marker of Ventricular Systolic and Diastolic Dysfunction and Ventricular Hypertrophy
The Division of Cardiovascular Diseases and Internal Medicine, Mayo Clinic, Rochester, Minn (K.Y., J.C.B., M.J., R.A.N., K.R.B., M.M.R.), and the Department of Medicine and Clinical Science, Kyoto (Japan) University Graduate School of Medicine (Y.S., K.N.).
Correspondence to Margaret M. Redfield, MD, The Division of Cardiovascular Diseases and Internal Medicine, Mayo Clinic, 200 First St SW, Rochester, MN 55905. E-mail redfield.margaret@mayo.edu.
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionReferences |
|---|
Atrial and brain natriuretic peptides (ANP and BNP) are produced by the heart, and their plasma concentrations are increased in human chronic congestive heart failure. Although separate studies have suggested that circulating levels of the biologically active C-terminal ANP, the biologically inactive N-terminal ANP, and BNP may have diagnostic utility in the detection of left ventricular systolic dysfunction or left ventricular hypertrophy, no studies have directly assessed the relative value of these peptides prospectively. We therefore designed this study to compare the relative ability of the different natriuretic peptides to detect abnormal left ventricular systolic and diastolic function and left ventricular hypertrophy. Using a prospective study design, we investigated 94 patients referred for cardiac catheterization and 15 age-matched normal subjects. The diagnostic abilities of elevated plasma C-terminal ANP, N-terminal ANP-(1-30), and BNP concentrations to identify systolic dysfunction (ejection fraction <45%), diastolic dysfunction (time constant of left ventricular relaxation >55 milliseconds, left ventricular end-diastolic pressure >18 mm Hg), and left ventricular hypertrophy (left ventricular mass index >120 g/m2) were objectively compared by receiver operating characteristic analysis. The areas under the receiver operating characteristic curve of BNP for detecting each of these abnormalities ranged from 0.715 to 0.908 and were significantly greater than those of C-terminal ANP or N-terminal ANP-(1-30). The sensitivity and specificity of an elevated plasma BNP, which we defined as greater than the mean+3 SD of the 15 age-matched normal subjects, were 0.83 and 0.77, respectively, for detecting ejection fraction less than 45%, 0.85 and 0.70 for detecting the time constant of left ventricular relaxation greater than 55 milliseconds, 0.63 and 0.76 for detecting left ventricular end-diastolic pressure greater than 18 mm Hg, and 0.81 and 0.85 for detecting left ventricular mass index greater than 120 g/m2. The use of BNP and one other peptide increased sensitivity (0.90 to 0.96), albeit with lower specificity (0.56 to 0.71). An elevated plasma BNP was a more powerful marker of left ventricular systolic dysfunction, left ventricular diastolic dysfunction, and left ventricular hypertrophy than C-terminal ANP or N-terminal ANP-(1-30) in this population of patients with suspected cardiac disease. Measurement of BNP alone or in combination with C-terminal ANP or N-terminal ANP-(1-30) has potential utility for the detection of altered left ventricular structure and function in a patient population at risk for cardiovascular disease.
Key Words: natriuretic hormone • ventricular function • hypertrophy, left ventricular • hemodynamics
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Enhanced production of the natriuretic peptides by the heart is a hallmark of congestive heart failure, and the pathophysiological significance of these peptides in the regulation of renal, humoral, and cardiovascular function in heart failure is well recognized. The reinduction of the embryonic genome with expression of the ANP gene and subsequent peptide production is a highly conserved and cardinal feature of ventricular hypertrophy,1 and there is similar evidence that BNP production is upregulated early in the hypertrophic process.2 3 4 The enhanced production of these peptides in the presence of altered LV function and structure is now recognized, and interest is growing in their potential diagnostic use. Plasma concentrations of the natriuretic peptides have emerged as potential noninvasive markers for the detection of abnormal LV structure and function.5 6 7 8 9 The proform of ANP is produced predominantly in the atrium10 and is released in two molecular forms: the biologically active C-ANP, which has a short half-life, and the biologically inactive N-ANP, which has a longer half-life.11 12 ANP is released by atrial myocytes in response to stretch associated with increased atrial pressure.13 Ventricular production of ANP occurs only in the presence of ventricular hypertrophy.1 BNP is predominantly of ventricular origin,10 and its production is enhanced in the presence of chronic congestive heart failure or LV hypertrophy.10 14 15 Although several studies have examined the utility of a single natriuretic peptide in the detection of LV systolic dysfunction or LV hypertrophy and have reported favorable findings, especially with regard to the detection of asymptomatic LV systolic dysfunction, no study has compared C-ANP, N-ANP, and BNP to determine which assay may best detect the presence of LV systolic dysfunction and LV hypertrophy. Furthermore, no study has focused on the ability of the peptides to detect LV diastolic dysfunction, which occurs frequently in individuals with hypertension and other types of cardiac disease.16 17
We designed this study to prospectively determine whether one of the natriuretic peptides—C-ANP, N-ANP, or BNP—is superior to the others for the detection of LV systolic dysfunction, LV diastolic dysfunction, or LV hypertrophy in patients with suspected cardiac disease referred for cardiac catheterization. We also examined the role of combined analysis of the natriuretic peptides. We used echocardiography to assess LV systolic function and LV mass. We analyzed LV pressure tracings to characterize LV diastolic function. Normal values for the peptides were determined in age-matched subjects without cardiovascular disease, and an elevated value used as a partition value of each peptide was prospectively defined as greater than the mean value in normal subjects plus 3 SD. To avoid effects of the definition of an elevated value on the comparison of the abilities of these peptides, we also performed ROC analysis, which can compare the combined sensitivity and specificity of the natriuretic peptides for the detection of altered LV structure and function independently of partition values.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Study Population
Ninety-four consecutive patients referred for cardiac catheterization were studied. Patients with acute myocardial infarction, active ischemia, or renal failure (plasma creatinine concentration >201 µmol/L) were not included. The clinical record of each patient was reviewed for determination of their New York Heart Association (NYHA) class regarding symptoms of heart failure. All studies were done electively, and nearly all were outpatient procedures. This protocol was approved by the Mayo Clinic Institutional Review Board, and all patients provided written informed consent.
Echocardiography
Transthoracic echocardiographic examinations18 were conducted within 3 hours before catheterization. All patients were in the fasting state, and medications were not withheld before the study for ethical reasons.
Cardiac Catheterization
Blood samples for humoral assay were obtained from the side arm of the sheath in the femoral artery. LV pressure was recorded with a 7F high-fidelity manometer-tipped catheter in 63 patients or a 6F pigtail catheter connected to a fluid-filled transducer in the other 31 patients. The high-fidelity LV pressure was calibrated to the fluid-filled LV pressure measured by the lumen of the catheter just before the recording.19 LV pressure was digitized at 5-millisecond intervals onto an off-line computer.
Data Analysis
From the LV pressure tracing, LVEDP was measured.19 In the patients with high-fidelity pressure recordings, the time constant of LV relaxation (
) was calculated for assessment of LV relaxation rate by the method of Weiss et al20 using zero asymptote from peak -dP/dt to 5 mm Hg above LVEDP.19 21 From the echocardiographic recordings, EF and LV mass were calculated. EF was assessed in all patients by a modification of the method of Quinones et al22 as previously described.18 23 Measurements that allowed the calculation of LV mass with the formula derived from the data of the American Society of Echocardiography24 were possible in 74 patients. LV mass index was calculated as the ratio of LV mass to body surface area as previously described.25 Averaged values of echocardiographic and pressure-derived parameters of more than three consecutive beats were used for statistical analysis.
Blood for humoral analysis was placed in tubes containing EDTA, which were immediately placed on ice. After centrifugation at 2500 rpm and 3°C, the plasma was decanted and stored at -80°C until analysis. Plasma concentration of C-ANP was measured by radioimmunoassay with the use of antibody to preproANP-(124-151) (Peninsula Laboratories)26 27 ; interassay and intra-assay variabilities were 9% and 6%, respectively. Plasma concentration of N-ANP was determined by radioimmunoassay with the use of antibody to preproANP-(26-55), which is also known as proANP-(1-30) [N-ANP-(1-30)] (Phoenix Pharmaceuticals Inc). For the assay, 1 mL of plasma was preacidified with 1 mL of 0.5% trifluoroacetic acid. C8 cartridges (Analytichem) were washed with 4 mL of 100% methanol and 4 mL water. Plasma was applied to the cartridge, washed with 2 mL normal saline and 6 mL water, and eluted with 2 mL of 90% methanol and 1% trifluoroacetic acid. This antibody does not cross-react with higher molecular weight forms of N-ANP or C-ANP. Recovery is 78% to 85% and is determined with the use of synthetic preproANP-(26-55) at 0.003, 0.023, and 0.091 pmol per tube (Phoenix Pharmaceuticals Inc). Plasma concentration of BNP was determined by immunoradiometric assay with antibody to human BNP (Shionogi Co Ltd)10 28 ; the interassay and intra-assay variabilities were both 8%. There was no cross-reactivity among these assays.
Echocardiographic and catheterization data were interpreted blindly with respect to natriuretic peptide levels.
Plasma was also collected from 15 age-matched control subjects (mean age, 67 years) for measurement of C-ANP, N-ANP-(1-30), and BNP and calculation of the mean and SD of these peptides in normal individuals. These subjects were vigorously screened by the Mayo Clinic Department of Laboratory Medicine, Normal Values Laboratory, to be without cardiac or other systemic disease. For the purpose of this study, an elevated value was defined as greater than the mean normal value plus 3 SD. Normal values were determined from venous samples, and arterial samples were collected in patients referred for cardiac catheterization. As previously shown,10 the difference between arterial and venous plasma concentrations of C-ANP is slightly larger compared with that of BNP or N-ANP. Thus, the partition value for C-ANP may differ between arterial and venous sampling and may affect sensitivity and specificity. However, ROC analysis compares the diagnostic value of the peptides independently of the partition value.
Statistical Analysis
Values are expressed as mean±SD. The linear association of each peptide with physiological variables was assessed by simple linear regression and correlation as well as by Spearman rank correlation. Correlations were compared by Williams' modification of Hotelling's statistics.29 For the correlation analysis, we used the natural logarithm (ln) of BNP, C-ANP, and N-ANP-(1-30) to normalize the distribution of their plasma concentrations.
We assessed the relative ability of natriuretic peptides to identify EF less than 45%, LV mass index greater than 120 g/m2, LVEDP greater than 18 mm Hg, and greater than 55 milliseconds by ROC analysis. To assess whether natriuretic peptide assays have any information content, we compared the areas under the ROC curves with 0.5 (area under the line of no information) using the Wilcoxon rank sum statistics.30 We compared the areas under the ROC curves for detecting each abnormality between peptides by the method of Delong et al.31 We explored the question of whether measuring two peptides enhances the ability to detect abnormal physiological variables by determining the sensitivity and specificity of the combined analysis of two peptides for the detection of each abnormality. Statistical significance was judged at the .05 level of significance.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Patient Characteristics
Table 1
reports the clinical characteristics of the patient population. Table 2 reports LV function, LV mass, and natriuretic peptides in the patient population and the natriuretic peptides in the age-matched normal control population. Ten of the 24 patients with EF less than 45%, 8 of the 20 patients with greater than 55 milliseconds, 18 of the 35 patients with LVEDP greater than 18 mm Hg, and 11 of the 26 patients with LV mass index greater than 120 g/m2 had mild or no (NYHA class II or less) symptoms of dyspnea. Thus, significant structural and functional abnormalities were frequently unassociated with frank clinical evidence of heart failure.
|
|
Correlation Study
The pairwise linear associations between each peptide and each physiological variable were significant with the exception of the association between ln N-ANP-(1-30) and EF (Table 3). For each physiological variable, the strongest correlate was ln BNP. Spearman rank correlation provided identical findings.
|
ROC Analysis
The Figure presents the findings of the ROC analysis. The areas under the ROC curves were significantly greater than 0.5, with the exception of that of C-ANP for detecting greater than 55 milliseconds or LVEDP greater than 18 mm Hg and that of N-ANP-(1-30) for detecting EF less than 45%. The areas for BNP detecting abnormal EF, LV mass index, and were significantly larger than those for C-ANP and N-ANP-(1-30). The area for BNP detecting abnormal LVEDP was significantly larger than that for C-ANP and tended to be larger, but not significantly, than that for N-ANP-(1-30).
|
P<.05 vs area under the ROC curve of N-ANP-(1-30).
Table 4 shows the sensitivity and specificity and their 95% confidence intervals of an elevated value of each peptide as prospectively defined for the identification of each parameter. Table 5 shows the plasma peptide concentration at the point closest to that of perfect separation on each ROC curve and the sensitivity and specificity of each peptide with that partition value. The optimal BNP levels shown in Table 5 are close to the prospectively determined partition value (mean+3 SD of the normal values), and the use of the optimal BNP levels as partition values slightly improved specificity.
|
|
In our patient population, the sensitivity and specificity of BNP greater than 14.7 pmol/L (mean+3 SD of the normal control value) for detecting any abnormality of LV structure or function (ie, the presence of EF <45%, >55 milliseconds, or LV mass index >120 g/m2) were 0.73 and 0.83, respectively.
Combined Analysis of Natriuretic Peptides
Table 6 shows the sensitivity and specificity when another peptide was analyzed along with BNP. The optimal peptide concentrations as determined by the ROC analysis (shown in Table 5
) were used as partition values in this analysis. Proper combination of BNP and another peptide allowed the detection of abnormal EF, , and LV mass index with very high sensitivity (0.90 to 0.96) while retaining moderate specificity (0.56 to 0.71).
|
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
The present study compared the ability of plasma concentrations of C-ANP, N-ANP-(1-30), and BNP to detect LV systolic dysfunction (decreased EF), LV diastolic dysfunction (prolonged
, increased LVEDP), and LV hypertrophy (increased LV mass index) in patients with suspected cardiac disease. When the relative diagnostic utility of the three peptides was determined by either comparative ROC analysis or comparative correlation analysis, BNP emerged as the single best marker of LV systolic dysfunction, LV diastolic dysfunction, and LV hypertrophy compared with C-ANP and N-ANP-(1-30). Measurement of BNP and another peptide provided better sensitivity, with moderate specificity. Congestive heart failure is caused by LV systolic or diastolic dysfunction.16 17 It is an extremely common condition, especially in the elderly, where the prevalence approaches 10%,32 and is very costly as it is the most common discharge diagnosis for hospitalized patients in the United States.33 Thus, new strategies must be developed to identify and treat patients with or at risk for the development of congestive heart failure in a more cost-effective way.34 These new strategies must include an emphasis on early treatment to delay and hopefully prevent the progression to end-stage heart failure.34 35 Such an emphasis requires the ability to identify patients with LV dysfunction before the development of severe symptoms. Considering the large number of patients suspected of having cardiac disease who are at risk for LV dysfunction, interest is growing in the use of the natriuretic peptides as diagnostic, potentially cost-effective, markers of altered LV structure and function.9 36
Plasma C-ANP concentration is elevated in patients with overt heart failure26 37 and in some patients with LV dysfunction without overt heart failure.38 However, the biologically inactive N-ANP has reduced clearance compared with C-ANP and circulates at a concentration 10- to 20-fold higher than that of C-ANP,39 and previous studies have reported that N-ANP is superior to C-ANP in the detection of asymptomatic LV systolic dysfunction in selected cardiac populations8 40 and as a prognostic factor after acute myocardial infarction.5 The current study did not demonstrate that N-ANP-(1-30) was superior to C-ANP in detecting LV systolic dysfunction. A previous study by Lerman et al8 focused on the ability of N-ANP-(1-30) to detect asymptomatic LV dysfunction, whereas the current study included patients with and without symptoms. Lerman et al used a different technique to assess EF and a different definition of LV systolic dysfunction that included patients with a resting EF of greater than 50% if they had a peak exercise EF of less than 55%. Indeed, the mean EF in the patients with asymptomatic LV dysfunction was 49%, and the population of patients with exercise-induced but not resting LV systolic dysfunction may be unique. The current study was confined to patients referred for cardiac catheterization, and this population may differ in other respects from one consisting of patients referred for radionuclide angiography. These differences may be responsible for the discrepancy between our results and previous results. Also, the current study measured proANP-(1-30), not proANP-(1-98), as N-ANP, and thus, the measurement of proANP-(1-98)5 12 might have provided different results.
Plasma BNP concentration is also elevated in patients with chronic congestive heart failure.14 37 As BNP is produced primarily in ventricular myocytes, elevated BNP concentrations may more accurately reflect alterations in the structure and function of the ventricle. Previous studies have reported that BNP can detect systolic dysfunction after acute myocardial infarction with more sensitivity than C-ANP or clinical history and examination.6 7 Davis et al9 found that the presence of an elevated BNP concentration was an excellent discriminator of cardiac and noncardiac dyspneas. The present study examined the relative abilities of C-ANP, N-ANP-(1-30), and BNP to detect LV systolic dysfunction and demonstrated that BNP is a better marker than C-ANP or N-ANP-(1-30) in patients with suspected cardiac disease.
Although recent studies examining the diagnostic utility of the natriuretic peptides have focused on the detection of systolic dysfunction, the stimulus for the enhanced production of these peptides partly reflects the structural changes (hypertrophy) and hemodynamic consequences (elevated intracardiac pressures) usually associated with systolic dysfunction. Kohno et al15 have reported that plasma BNP concentration is correlated with LV mass index in patients with hypertension. LV hypertrophy is a potent risk factor for cardiovascular morbidity and mortality.41 As LV hypertrophy cannot be reliably predicted from blood pressure level,42 a noninvasive and inexpensive method for the detection of LV hypertrophy would be clinically useful. The current study examined the utility of the natriuretic peptides in detecting LV hypertrophy and demonstrated that BNP concentration correlated well with LV mass index and that the sensitivity and specificity for the detection of LV hypertrophy were excellent and exceeded those for C-ANP and N-ANP-(1-30).
Patients with cardiac disease often have diastolic dysfunction, which can result in elevated filling pressures and symptoms of overt heart failure, sometimes in the absence of systolic dysfunction.43 44 Although studies have demonstrated that the concentrations of the natriuretic peptides correlate with filling pressures, the strength of these correlations vary,45 46 perhaps because filling pressures are determined by both LV diastolic function and loading conditions.47 LV relaxation is an important component of diastolic function47 and can be assessed invasively by but is difficult to assess noninvasively.19 48 49 Impaired relaxation precedes reduced EF in most cardiac diseases.50 In the present study, elevated BNP concentrations detected impaired relaxation with good sensitivity and specificity. However, although the area under the ROC curve of BNP for detecting elevated LVEDP was greater than those of C-ANP and N-ANP-(1-30), the overall sensitivity and specificity of BNP as a marker of elevated LVEDP was relatively poor compared with its ability to detect abnormal EF, , or LV mass index. These data suggest that BNP best reflects LV structural and functional abnormalities rather than abnormal loading conditions. The current study significantly extends previous studies and exhibits the utility of the natriuretic peptides in the detection of diastolic dysfunction.
Although BNP is the single best marker in the detection of LV functional and structural abnormalities and preload augmentation, the combined analysis of BNP and either C-ANP or N-ANP-(1-30) increased sensitivity. In some clinical situations, higher sensitivity may be desirable, and in this study, the combined use of BNP and another peptide increased sensitivity, particularly to more than 0.90 in detecting LV systolic dysfunction, LV diastolic dysfunction, and LV hypertrophy, with a moderate reduction in specificity. Although previous studies have focused on the utility of a single peptide, our study suggests the potential utility of a combination analysis.
Conclusions
The current study reports that elevated plasma BNP is a more powerful marker of LV systolic dysfunction, LV diastolic dysfunction, and LV hypertrophy than C-ANP or N-ANP-(1-30) in this population of patients with suspected cardiac disease. The combined use of BNP and another peptide increases the sensitivity while decreasing specificity moderately. These findings suggest that plasma BNP alone or together with C-ANP or N-ANP-(1-30) may have diagnostic utility for the detection of altered LV function or structure in patients with or at risk for cardiac disease. The subjects of this study were referred for cardiac catheterization and thus have a high prevalence of altered LV structure and function. Further studies in broader populations at risk for altered LV structure and function are needed for determination of the potential role of these peptides in clinical practice.
|
Selected Abbreviations and Acronyms |
|---|
|
|
Acknowledgments |
|---|
This study was supported in part by grants from the Joseph P. and Jeanne M. Sullivan Foundation, Chicago, Ill; the National Heart, Lung, and Blood Institute, Bethesda, Md (HL-033643); the Miami Heart Research Institute; and the Mayo Foundation. Dr Yamamoto was supported by the Fellowship of the Uehara Memorial Foundation.
Received April 8, 1996; first decision May 8, 1996; accepted July 22, 1996.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
1. Lee RT, Bloch KD, Pfeffer JM, Pfeffer MA, Neer EJ, Seidman CE. Atrial natriuretic factor gene expression in ventricles of rats with spontaneous biventricular hypertrophy. J Clin Invest. 1988;81:431-434.
2.
Dagnino L, Lavigne JP, Nemer M. Increased transcripts for B-type natriuretic peptide in spontaneously hypertensive rats: quantitative polymerase chain reaction for atrial and brain natriuretic peptide transcripts. Hypertension. 1992;20:690-700.
3.
Ogawa Y, Nakao K, Mukoyama M, Hosoda K, Shirakami G, Arai H, Saito Y, Suga S, Jougasaki M, Imura H. Natriuretic peptides as cardiac hormones in normotensive and spontaneously hypertensive rats: the ventricle is a major site of synthesis and secretion of brain natriuretic peptide. Circ Res. 1991;69:491-500.
4. Nakagawa O, Ogawa Y, Itoh H, Suga S, Komatsu Y, Kishimoto I, Nishino K, Yoshimasa T, Nakao K. Rapid transcriptional activation and early mRNA turnover of brain natriuretic peptide in cardiocyte hypertrophy. J Clin Invest. 1995;96:1280-1287.
5.
Hall C, Rouleau JL, Moye L, de Champlain J, Bichet D, Klein M, Sussex B, Packer M, Rouleau J, Arnold MO, Lamas GA, Sestier F, Gottlieb SS, Wun CCC, Pfeffer MA. N-terminal proatrial natriuretic factor: an independent predictor of long-term prognosis after myocardial infarction. Circulation. 1994;89:1934-1942.
6. Choy AMJ, Darbar D, Lang CC, Pringle TH, McNeill GP, Kennedy NSJ, Struthers AD. Detection of left ventricular dysfunction after acute myocardial infarction: comparison of clinical, echocardiographic, and neurohumoral methods. Br Heart J. 1994;74:16-22.
7. Motwani JG, McAlpine H, Kennedy N, Struthers AD. Plasma brain natriuretic peptide as an indicator for angiotensin-converting-enzyme inhibition after myocardial infarction. Lancet. 1993;341:1109-1113.[Medline] [Order article via Infotrieve]
8. Lerman A, Gibbons RJ, Rodeheffer RJ, Bailey KR, McKinley LJ, Heublein DM, Burnett JC Jr. Circulating N-terminal atrial natriuretic peptide as a marker for symptomless left-ventricular dysfunction. Lancet. 1993;341:1105-1109.[Medline] [Order article via Infotrieve]
9. Davis M, Espiner E, Richards G, Billings J, Town I, Neill A, Drennan C, Richards M, Turner J, Yandle T. Plasma brain natriuretic peptide in assessment of acute dyspnea. Lancet. 1994;343:440-444.[Medline] [Order article via Infotrieve]
10.
Yasue H, Yoshimura M, Sumida H, Kikuta K, Kugiyama K, Jougasaki M, Ogawa H, Okumura K, Mukoyama M, Nakao K. Localization and mechanism of secretion of B-type natriuretic peptide in comparison with those of A-type natriuretic peptide in normal subjects and patients with heart failure. Circulation. 1994;90:195-203.
11.
Glembotski CC, Dixon JE, Gibson TR. Secretion of atrial natriuretic factor-(1-98) by primary cardiac myocytes. J Biol Chem. 1988;263:16073-16081.
12.
Sundsfjord JA, Thibault G, Larochelle P, Cantin M. Identification and plasma concentrations of the N-terminal fragment of proatrial natriuretic factor in man. J Clin Endocrinol Metab. 1988;66:605-610.
13.
Brenner BM, Ballermann BJ, Gunning ME, Zeidel ML. Diverse biological actions of atrial natriuretic peptide. Physiol Rev. 1990;70:665-699.
14. Mukoyama M, Nakao K, Hosoda K, Suga S, Saito Y, Ogawa Y, Shirakami G, Jougasaki M, Obata K, Yasue H, Kambayashi Y, Inouye K, Imura H. Brain natriuretic peptide as a novel cardiac hormone in humans: evidence for an exquisite dual natriuretic peptide system, atrial natriuretic peptide and brain natriuretic peptide. J Clin Invest. 1991;87:1402-1412.
15. Kohno M, Horio T, Yokokawa K, Murakawa K, Yasunari K, Akioka K, Tahara A, Toda I, Takeuchi K, Kurihara N, Takeda T. Brain natriuretic peptide as a cardiac hormone in essential hypertension. Am J Med. 1992;92:29-34.[Medline] [Order article via Infotrieve]
16. Bonow RO, Udelson JE. Left ventricular diastolic dysfunction as a cause of congestive heart failure. Ann Intern Med. 1992;117:502-510.
17. Goldsmith SR, Dick C. Differentiating systolic from diastolic heart failure: pathophysiologic and therapeutic consideration. Am J Med. 1993;95:645-655.[Medline] [Order article via Infotrieve]
18. Yamamoto K, Masuyama T, Tanouchi J, Naito J, Mano T, Kondo H, Nagano R, Hori M, Kamada T. Intraventricular dispersion of early diastolic filling: a new marker of left ventricular diastolic dysfunction. Am Heart J. 1995;129:291-299.[Medline] [Order article via Infotrieve]
19. Nishimura RA, Schwartz RS, Holmes DR Jr, Tajik AJ. Failure of calcium channel blockers to improve ventricular relaxation in humans. J Am Coll Cardiol. 1993;21:182-188.[Abstract]
20. Weiss JL, Frederiksen JW, Weisfeldt ML. Hemodynamic determinants of the time-course of fall in canine left ventricular pressure. J Clin Invest. 1976;58:751-760.
21.
Yamamoto K, Masuyama T, Doi Y, Naito J, Mano T, Kondo H, Nagano R, Tanouchi J, Hori M, Kamada T. Noninvasive assessment of left ventricular relaxation using continuous-wave Doppler aortic regurgitant velocity curve: its comparative value to the mitral regurgitation method. Circulation. 1995;91:192-200.
22.
Quinones MA, Waggoner AD, Reduto LA, Nelson JG, Young JB, Winters WL Jr, Ribeiro LG, Miller RR. A new simplified and accurate method for determining ejection fraction with two-dimensional echocardiography. Circulation. 1981;64:744-753.
23.
Rihal CS, Nishimura RA, Hatle LK, Bailey KR, Tajik AJ. Systolic and diastolic dysfunction in patients with clinical diagnosis of dilated cardiomyopathy: relation to symptoms and prognosis. Circulation. 1994;90:2772-2779.
24. Devereux RB, Alonso DR, Lutas EM, Gottlieb GJ, Campo E, Sachs I, Reichek N. Echocardiographic assessment of left ventricular hypertrophy: comparison to necropsy findings. Am J Cardiol. 1986;57:450-458.[Medline] [Order article via Infotrieve]
25. Klein AL, Burstow DJ, Tajik AJ, Zachariah PK, Bailey KR, Seward JB. Effects of age on left ventricular dimensions and filling dynamics in 117 normal persons. Mayo Clin Proc. 1994;69:212-224.[Medline] [Order article via Infotrieve]
26.
Burnett JC Jr, Kao PC, Hu DC, Heser DW, Heublein DM, Granger JP, Opgenorth TH, Reeder GS. Atrial natriuretic peptide elevation in congestive heart failure in the human. Science. 1986;231:1145-1147.
27.
Redfield MM, Edwards BS, McGoon MD, Heublein DM, Aarhus LL, Burnett JC Jr. Failure of atrial natriuretic factor to increase with volume expansion in acute and chronic congestive heart failure in the dog. Circulation. 1989;80:651-657.
28. Yasue H, Yoshimura M, Jougasaki M, Itoh H, Suga S, Ogawa Y, Nakao K. Plasma levels of brain natriuretic peptide in normal subjects and patients with chronic heart failure: measurement by immunoradiometric assay (IRMA). Horm Clin. 1993;41:397-403.
29. Neill JJ, Dunn OJ. Equality of dependent correlation coefficients. Biometrics. 1975;31:531-543.
30.
Murphy JM, Berwick DM, Weinstein MC, Borus JF, Budman SH, Klerman GL. Performance of screening and diagnostic tests: application of receiver operating characteristic analysis. Arch Gen Psychiatry. 1987;44:550-555.
31. Delong ER, Delong DM, Clarke-Pearson DL. Comparing the area under two or more correlated receiver operating characteristic curves: a nonparametric approach. Biometrics. 1988;44:837-845.[Medline] [Order article via Infotrieve]
32. Kannel WB, Belanger AJ. Epidemiology of heart failure. Am Heart J. 1991;121:951-957.[Medline] [Order article via Infotrieve]
33. Yancy CW, Firth BG. Congestive heart failure. Dis Mon. 1989;34:467-536.
34.
Armstrong PW, Moe GW. Medical advances in the treatment of congestive heart failure. Circulation. 1993;88:2941-2952.
35. Cohn JN. The prevention of heart failure: a new agenda. N Engl J Med. 1992;327:725-727.[Medline] [Order article via Infotrieve]
36.
Struthers AD. Plasma concentration of brain natriuretic peptide: will this new test reduce the need for cardiac investigations? Br Heart J. 1993;70:397-398.
37.
Wei CM, Heublein DM, Perrella MA, Lerman A, Rodeheffer RJ, McGregor CGA, Edwards WD, Schaff HV, Burnett JC Jr. Natriuretic peptide system in human heart failure. Circulation. 1993;88:1004-1009.
38.
Francis GS, Benedict C, Johnstone DE, Kirlin PC, Nicklas J, Liang C, Kubo SH, Rudin-Toretsky E, Yusuf S. Comparison of neuroendocrine activation in patients with left ventricular dysfunction with and without congestive heart failure: a substudy of the Studies of Left Ventricular Dysfunction (SOLVD). Circulation. 1990;82:1724-1729.
39.
Itoh H, Nakao K, Mukoyama M, Sugawara A, Saito Y, Morii N, Yamada T, Shiono S, Arai H, Imura H. Secretion of N-terminal fragment of 
-human atrial natriuretic polypeptide. Hypertension. 1988;11(suppl I):I-52-I-56.
40.
Winters CJ, Sallman AL, Baker BJ, Meadows J, Rico DM, Vesely DL. The N-terminus and a 4,000-MW peptide from the midportion of the N-terminus of the atrial natriuretic factor prohormone each circulate in humans and increase in congestive heart failure. Circulation. 1989;80:438-449.
41. Ghali JK, Liao Y, Simmons B, Castaner A, Cao G, Cooper RS. The prognostic role of left ventricular hypertrophy in patients with or without coronary artery disease. Ann Intern Med. 1992;117:831-836.
42. Frohlich ED, Apstein C, Chobanian AV, Devereux RB, Dustan HP, Dzau V, Fauad-Tarazi F, Horan MJ, Marcus M, Massie B, Pfeffer MA, Re RN, Roccella EJ, Savage D, Shub C. The heart in hypertension. N Engl J Med. 1992;327:998-1008.[Medline] [Order article via Infotrieve]
43. Dougherty AH, Naccarelli GV, Gray EL, Hicks CH, Goldstein RA. Congestive heart failure with normal systolic function. Am J Cardiol. 1984;54:778-782.[Medline] [Order article via Infotrieve]
44. Soufer R, Wohlgelernter D, Vita NA, Amuchestegui M, Sostman HD, Berger HJ, Zaret BL. Intact systolic left ventricular function in clinical congestive heart failure. Am J Cardiol. 1985;55:1032-1036.[Medline] [Order article via Infotrieve]
45.
Richards AM, Crozier IG, Yandle TG, Espiner EA, Ikram H, Nicholls MG. Brain natriuretic factor: regional plasma concentrations and correlations with haemodynamic state in cardiac disease. Br Heart J. 1993;69:414-417.
46. Haug C, Metzele A, Kochs M, Hombach V, Grunert A. Plasma brain natriuretic peptide and atrial natriuretic peptide concentrations correlate with left ventricular end-diastolic pressure. Clin Cardiol. 1993;16:553-557.[Medline] [Order article via Infotrieve]
47.
Gilbert JC, Glantz SA. Determinants of left ventricular filling and of the diastolic pressure-volume relation. Circ Res. 1989;64:827-852.
48. Appleton CP, Hatle LK, Popp RL. Relation of transmitral flow velocity patterns to left ventricular diastolic function: new insights from a combined hemodynamic and Doppler echocardiographic study. J Am Coll Cardiol. 1988;12:426-440.[Abstract]
49. Stoddard MF, Pearson AC, Kern MJ, Ratcliff J, Mrosek DG, Labovitz AJ. Left ventricular diastolic function: comparison of pulsed Doppler echocardiographic and hemodynamic indexes in subjects with and without coronary artery disease. J Am Coll Cardiol. 1989;13:327-336.[Abstract]
50.
Hirota Y. A clinical study of left ventricular relaxation. Circulation. 1980;62:756-763.
This article has been cited by other articles:
 |
|
 |
|
  S Kurl, M Ala-Kopsala, H Ruskoaho, T Makikallio, K Nyyssonen, O Vuolteenaho, J Sivenius, J T Salonen, and J A Laukkanen Plasma N-terminal fragments of natriuretic peptides predict the risk of stroke and atrial fibrillation in men Heart, July 1, 2009; 95(13): 1067 - 1071. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Y.-M. Wang, C. W.-K. Lam, M. Wang, I. H.-S. Chan, S.-F. Lui, Y. Zhang, and J. E. Sanderson Diagnostic potential of serum biomarkers for left ventricular abnormalities in chronic peritoneal dialysis patients Nephrol. Dial. Transplant., June 1, 2009; 24(6): 1962 - 1969. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. Moertl, R. Berger, J. Struck, A. Gleiss, A. Hammer, N. G. Morgenthaler, A. Bergmann, M. Huelsmann, and R. Pacher Comparison of midregional pro-atrial and B-type natriuretic peptides in chronic heart failure: influencing factors, detection of left ventricular systolic dysfunction, and prediction of death. J. Am. Coll. Cardiol., May 12, 2009; 53(19): 1783 - 1790. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. W. Troughton and A. M. Richards B-type natriuretic peptides and echocardiographic measures of cardiac structure and function. J. Am. Coll. Cardiol. Img., February 1, 2009; 2(2): 216 - 225. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. Johansson, A. Brostrom, U. Dahlstrom, and U. Alehagen Global perceived health and ten-year cardiovascular mortality in elderly primary care patients with possible heart failure Eur J Heart Fail, October 1, 2008; 10(10): 1040 - 1047. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. Greenberg, B. Czerska, R. M. Delgado, R. Bourge, M. R. Zile, M. Silver, M. Klapholz, E. Haeusslein, M. R. Mehra, P. Mather, et al. Effects of Continuous Aortic Flow Augmentation in Patients With Exacerbation of Heart Failure Inadequately Responsive to Medical Therapy: Results of the Multicenter Trial of the Orqis Medical Cancion System for the Enhanced Treatment of Heart Failure Unresponsive to Medical Therapy (MOMENTUM) Circulation, September 16, 2008; 118(12): 1241 - 1249. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Ichinose, H. Otani, M. Oikawa, K. Takase, H. Saito, H. Shimokawa, and S. Takahashi MRI of Cardiac Sarcoidosis: Basal and Subepicardial Localization of Myocardial Lesions and Their Effect on Left Ventricular Function Am. J. Roentgenol., September 1, 2008; 191(3): 862 - 869. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Y.-M. Wang and K.-N. Lai Use of Cardiac Biomarkers in End-Stage Renal Disease J. Am. Soc. Nephrol., September 1, 2008; 19(9): 1643 - 1652. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. S. Kallistratos, A. Dritsas, I. D. Laoutaris, and D. V. Cokkinos N-terminal Prohormone Brain Natriuretic Peptide Plasma Levels in Heart Failure Are Affected Both Directly and Indirectly by Carvedilol Angiology, July 1, 2008; 59(3): 323 - 328. [Abstract] [PDF]
|
|
|
|
 |
|
 J. P. Dal-Bianco, A. S. Jaffe, M. R. Bell, and J. K. Oh Cardiac Function and Brain-Type Natriuretic Peptide in First-Time Flash Pulmonary Edema Mayo Clin. Proc., March 1, 2008; 83(3): 289 - 296. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Choudhary, A. Palm-Leis, R. C. Scott III, R. S. Guleria, E. Rachut, K. M. Baker, and J. Pan All-trans retinoic acid prevents development of cardiac remodeling in aortic banded rats by inhibiting the renin-angiotensin system Am J Physiol Heart Circ Physiol, February 1, 2008; 294(2): H633 - H644. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. M. Westerhout, M. S. Lauer, S. James, Y. Fu, L. Wallentin, P. W. Armstrong, and for the GUSTO IV ACS Investigators Electrocardiographic left ventricular hypertrophy in GUSTO IV ACS: an important risk marker of mortality in women Eur. Heart J., September 1, 2007; 28(17): 2064 - 2069. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. Mercuro, C. Cadeddu, A. Piras, M. Dessi, C. Madeddu, M. Deidda, R. Serpe, E. Massa, and G. Mantovani Early Epirubicin-Induced Myocardial Dysfunction Revealed by Serial Tissue Doppler Echocardiography: Correlation with Inflammatory and Oxidative Stress Markers Oncologist, September 1, 2007; 12(9): 1124 - 1133. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. J. McClure, S. Gall, C. B. Schechter, M. Kearney, and A. G. Zaman Percutaneous Coronary Revascularization Reduces Plasma N-Terminal Pro-B-Type Natriuretic Peptide Concentration in Stable Coronary Artery Disease J. Am. Coll. Cardiol., June 26, 2007; 49(25): 2394 - 2397. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. H. Olsen, T. W. Hansen, M. K. Christensen, F. Gustafsson, S. Rasmussen, K. Wachtell, H. Ibsen, C. Torp-Pedersen, and P. R. Hildebrandt N-terminal pro-brain natriuretic peptide, but not high sensitivity C-reactive protein, improves cardiovascular risk prediction in the general population Eur. Heart J., June 1, 2007; 28(11): 1374 - 1381. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Y.-M. Wang, C. W.-K. Lam, C.-M. Yu, M. Wang, I. H.-S. Chan, Y. Zhang, S.-F. Lui, and J. E. Sanderson N-Terminal Pro-Brain Natriuretic Peptide: An Independent Risk Predictor of Cardiovascular Congestion, Mortality, and Adverse Cardiovascular Outcomes in Chronic Peritoneal Dialysis Patients J. Am. Soc. Nephrol., January 1, 2007; 18(1): 321 - 330. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Cortes, M. Portoles, A. Salvador, V. Bertomeu, F. G. de Burgos, L. Martinez-Dolz, E. R. Lleti, V. Climent, A. Jordan, R. Paya, et al. Diagnostic and prognostic value of urine NT-proBNP levels in heart failure patients Eur J Heart Fail, October 1, 2006; 8(6): 621 - 627. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Belluardo, A. Cataliotti, L. Bonaiuto, E. Giuffre, E. Maugeri, P. Noto, G. Orlando, G. Raspa, B. Piazza, L. Babuin, et al. Lack of activation of molecular forms of the BNP system in human grade 1 hypertension and relationship to cardiac hypertrophy Am J Physiol Heart Circ Physiol, October 1, 2006; 291(4): H1529 - H1535. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. H. Chen and J. C. Burnett Jr Clinical application of the natriuretic peptides in heart failure Eur. Heart J. Suppl., September 1, 2006; 8(suppl_E): E18 - E25. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N Ambrosino and M Serradori Determining the cause of dyspnoea: linguistic and biological descriptors Chronic Respiratory Disease, July 1, 2006; 3(3): 117 - 122. [PDF]
|
|
|
|
|
|
J. Latour-Perez, F. J. Coves-Orts, C. Abad-Terrado, V. Abraira, and J. Zamora Accuracy of B-type natriuretic peptide levels in the diagnosis of left ventricular dysfunction and heart failure: A systematic review Eur J Heart Fail, June 1, 2006; 8(4): 390 - 399. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. E. Malavazos, L. Morricone, A. Marocchi, F. Ermetici, B. Ambrosi, and M. M. Corsi N-terminal pro-B-type natriuretic Peptide and echocardiographic abnormalities in severely obese patients: correlation with visceral fat. Clin. Chem., June 1, 2006; 52(6): 1211 - 1213. [Full Text] [PDF]
|
|
|
|
 |
|
 M. F. Elnoamany and A. K. Abdelhameed Mitral annular motion as a surrogate for left ventricular function: Correlation with brain natriuretic peptide levels Eur J Echocardiogr, June 1, 2006; 7(3): 187 - 198. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. A. Laukkanen, S. Kurl, M. Ala-Kopsala, O. Vuolteenaho, H. Ruskoaho, K. Nyyssonen, and J. T. Salonen Plasma N-terminal fragments of natriuretic propeptides predict the risk of cardiovascular events and mortality in middle-aged men Eur. Heart J., May 2, 2006; 27(10): 1230 - 1237. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Koch, S. Zink, and H. Singer B-type natriuretic peptide in paediatric patients with congenital heart disease Eur. Heart J., April 1, 2006; 27(7): 861 - 866. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. E. H. Christoffersen, M. Aplin, C. C. Strom, S. P. Sheikh, O. Skott, P. K. Busk, S. Haunso, and L. B. Nielsen Increased natriuretic peptide receptor A and C gene expression in rats with pressure-overload cardiac hypertrophy Am J Physiol Heart Circ Physiol, April 1, 2006; 290(4): H1635 - H1641. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Iwanaga, I. Nishi, S. Furuichi, T. Noguchi, K. Sase, Y. Kihara, Y. Goto, and H. Nonogi B-Type Natriuretic Peptide Strongly Reflects Diastolic Wall Stress in Patients With Chronic Heart Failure: Comparison Between Systolic and Diastolic Heart Failure J. Am. Coll. Cardiol., February 21, 2006; 47(4): 742 - 748. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Talens-Visconti, M. Rivera Otero, M. J. Sancho-Tello, F. G. de Burgos, L. Martinez-Dolz, B. Sevilla, V. Climent, R. Cortes, A. Salvador, F. Sogorb, et al. Left ventricular cavity area reflects N-terminal pro-brain natriuretic peptide plasma levels in heart failure Eur J Echocardiogr, January 1, 2006; 7(1): 45 - 52. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. De Sutter, D. De Bacquer, S. Cuypers, J. Delanghe, M. De Buyzere, M. Kornitzer, and G. De Backer Plasma N-terminal pro-brain natriuretic peptide concentration predicts coronary events in men at work: a report from the BELSTRESS study Eur. Heart J., December 2, 2005; 26(24): 2644 - 2649. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. M. Hawkridge, D. M. Heublein, H. R. Bergen III, A. Cataliotti, J. C. Burnett Jr., and D. C. Muddiman Quantitative mass spectral evidence for the absence of circulating brain natriuretic peptide (BNP-32) in severe human heart failure PNAS, November 29, 2005; 102(48): 17442 - 17447. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. W. Knudsen, T. Omland, P. Clopton, A. Westheim, A. H.B. Wu, P. Duc, J. McCord, R. M. Nowak, J. E. Hollander, A. B. Storrow, et al. Impact of Atrial Fibrillation on the Diagnostic Performance of B-Type Natriuretic Peptide Concentration in Dyspneic Patients: An Analysis From the Breathing Not Properly Multinational Study J. Am. Coll. Cardiol., September 6, 2005; 46(5): 838 - 844. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Isobe, H. Izawa, M. Iwase, M. Nanasato, M. Nonokawa, A. Ando, S. Ohshima, K. Nagata, K. Kato, T. Nishizawa, et al. Cardiac 123I-MIBG Reflects Left Ventricular Functional Reserve in Patients with Nonobstructive Hypertrophic Cardiomyopathy J. Nucl. Med., June 1, 2005; 46(6): 909 - 916. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T.v. Lukowicz, M. Fischer, H.W. Hense, A. Doring, J. Stritzke, G. Riegger, H. Schunkert, and A. Luchner BNP as a marker of diastolic dysfunction in the general population: Importance of left ventricular hypertrophy Eur J Heart Fail, June 1, 2005; 7(4): 525 - 531. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Detaint, D. Messika-Zeitoun, J.-F. Avierinos, C. Scott, H. Chen, J. C. Burnett Jr, and M. Enriquez-Sarano B-Type Natriuretic Peptide in Organic Mitral Regurgitation: Determinants and Impact on Outcome Circulation, May 10, 2005; 111(18): 2391 - 2397. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Ala-Kopsala, H. Ruskoaho, J. Leppaluoto, L. Seres, R. Skoumal, M. Toth, F. Horkay, and O. Vuolteenaho Single Assay for Amino-Terminal Fragments of Cardiac A- and B-Type Natriuretic Peptides Clin. Chem., April 1, 2005; 51(4): 708 - 718. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Souza, H. B. Bogossian, M. Humbert, C. Jardim, R. Rabelo, M. B. P. Amato, and C. R. R. Carvalho N-terminal-pro-brain natriuretic peptide as a haemodynamic marker in idiopathic pulmonary arterial hypertension Eur. Respir. J., March 1, 2005; 25(3): 509 - 513. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. Anderson Candidate-based proteomics in the search for biomarkers of cardiovascular disease J. Physiol., February 15, 2005; 563(1): 23 - 60. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Wei, C. Zeng, L. Chen, Q. Chen, R. Zhao, G. Lu, C. Lu, and L. Wang Bedside tests of B-type natriuretic peptide in the diagnosis of left ventricular diastolic dysfunction in hypertensive patients Eur J Heart Fail, January 1, 2005; 7(1): 75 - 79. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Vanderheyden, M. Goethals, S. Verstreken, B. De Bruyne, K. Muller, E. Van Schuerbeeck, and J. Bartunek Wall stress modulates brain natriuretic peptide production in pressure overload cardiomyopathy J. Am. Coll. Cardiol., December 21, 2004; 44(12): 2349 - 2354. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Kawakami, Y. Saito, I. Kishimoto, M. Harada, K. Kuwahara, N. Takahashi, Y. Nakagawa, M. Nakanishi, K. Tanimoto, S. Usami, et al. Overexpression of Brain Natriuretic Peptide Facilitates Neutrophil Infiltration and Cardiac Matrix Metalloproteinase-9 Expression After Acute Myocardial Infarction Circulation, November 23, 2004; 110(21): 3306 - 3312. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Connell Review: Aldosterone -- the future challenge in cardiovascular disease? The British Journal of Diabetes & Vascular Disease, November 1, 2004; 4(6): 370 - 376. [Abstract] [PDF]
|
|
|
|
 |
|
 J. A. Doust, P. P. Glasziou, E. Pietrzak, and A. J. Dobson A Systematic Review of the Diagnostic Accuracy of Natriuretic Peptides for Heart Failure Arch Intern Med, October 11, 2004; 164(18): 1978 - 1984. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. B. Yap, D. Mukerjee, P. M. Timms, H. Ashrafian, and J. G. Coghlan Natriuretic Peptides, Respiratory Disease, and the Right Heart Chest, October 1, 2004; 126(4): 1330 - 1336. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. S. Villars, S. K. Hamlin, A. D. Shaw, and J. T. Kanusky Role of Diastole in Left Ventricular Function, I: Biochemical and Biomechanical Events Am. J. Crit. Care., September 1, 2004; 13(5): 394 - 403. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y.J. Akashi, H. Musha, K. Nakazawa, and F. Miyake Plasma brain natriuretic peptide in takotsubo cardiomyopathy QJM, September 1, 2004; 97(9): 599 - 607. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. J. Rodeheffer Measuring plasma B-type natriuretic peptide in heart failure: Good to go in 2004? J. Am. Coll. Cardiol., August 18, 2004; 44(4): 740 - 749. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Hammerer-Lercher, W. Ludwig, G. Falkensammer, S. Muller, E. Neubauer, B. Puschendorf, O. Pachinger, and J. Mair Natriuretic Peptides as Markers of Mild Forms of Left Ventricular Dysfunction: Effects of Assays on Diagnostic Performance of Markers Clin. Chem., July 1, 2004; 50(7): 1174 - 1183. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B A Groenning, I Raymond, P R Hildebrandt, J C Nilsson, M Baumann, and F Pedersen Diagnostic and prognostic evaluation of left ventricular systolic heart failure by plasma N-terminal pro-brain natriuretic peptide concentrations in a large sample of the general population Heart, March 1, 2004; 90(3): 297 - 303. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. J. Wang, M. G. Larson, D. Levy, E. J. Benjamin, E. P. Leip, T. Omland, P. A. Wolf, and R. S. Vasan Plasma Natriuretic Peptide Levels and the Risk of Cardiovascular Events and Death N. Engl. J. Med., February 12, 2004; 350(7): 655 - 663. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. de Denus, C. Pharand, and D. R. Williamson Brain Natriuretic Peptide in the Management of Heart Failure: The Versatile Neurohormone Chest, February 1, 2004; 125(2): 652 - 668. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. Yamaguchi, J. Yoshida, K. Yamamoto, Y. Sakata, T. Mano, N. Akehi, M. Hori, Y.-J. Lim, M. Mishima, and T. Masuyama Elevation of plasma brain natriuretic peptide is a hallmark of diastolic heart failure independent of ventricular hypertrophy J. Am. Coll. Cardiol., January 7, 2004; 43(1): 55 - 60. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Prahash and T. Lynch B-Type Natriuretic Peptide: A Diagnostic, Prognostic, and Therapeutic Tool in Heart Failure Am. J. Crit. Care., January 1, 2004; 13(1): 46 - 53. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Bibbins-Domingo, M. Ansari, N. B. Schiller, B. Massie, and M. A. Whooley B-Type Natriuretic Peptide and Ischemia in Patients With Stable Coronary Disease: Data From the Heart and Soul Study Circulation, December 16, 2003; 108(24): 2987 - 2992. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Mirotsou, C. M.H. Watanabe, P. G. Schultz, R. E. Pratt, and V. J. Dzau Elucidating the molecular mechanism of cardiac remodeling using a comparative genomic approach Physiol Genomics, October 17, 2003; 15(2): 115 - 126. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 V. Sim, D. Hampton, C. Phillips, S.-N. Lo, S. Vasishta, J. Davies, and M. Penney The use of brain natriuretic peptide as a screening test for left ventricular systolic dysfunction-- cost-effectiveness in relation to open access echocardiography Fam. Pract., October 1, 2003; 20(5): 570 - 574. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y.J. Akashi, K. Nakazawa, M. Sakakibara, F. Miyake, H. Koike, and K. Sasaka The clinical features of takotsubo cardiomyopathy QJM, August 1, 2003; 96(8): 563 - 573. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Mariano-Goulart, M.-C. Eberle, V. Boudousq, A. Hejazi-Moughari, C. Piot, C. C. de Kerleau, R. Verdier, M.-L. Barge, F. Comte, N. Bressot, et al. Major increase in brain natriuretic peptide indicates right ventricular systolic dysfunction in patients with heart failure Eur J Heart Fail, August 1, 2003; 5(4): 481 - 488. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. J. O'Brien, I. B. Squire, B. Demme, J. E. Davies, and L. L. Ng Pre-discharge, but not admission, levels of NT-proBNP predict adverse prognosis following acute LVF Eur J Heart Fail, August 1, 2003; 5(4): 499 - 506. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Cardarelli and T. G. Lumicao Jr B-type Natriuretic Peptide: A Review of Its Diagnostic, Prognostic, and Therapeutic Monitoring Value in Heart Failure for Primary Care Physicians J Am Board Fam Med, July 1, 2003; 16(4): 327 - 333. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
I Raymond, B A Groenning, P R Hildebrandt, J C Nilsson, M Baumann, J Trawinski, and F Pedersen The influence of age, sex and other variables on the plasma level of N-terminal pro brain natriuretic peptide in a large sample of the general population Heart, July 1, 2003; 89(7): 745 - 751. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. M. Richards, M. G. Nicholls, E. A. Espiner, J. G. Lainchbury, R. W. Troughton, J. Elliott, C. Frampton, J. Turner, I. G. Crozier, and T. G. Yandle B-Type Natriuretic Peptides and Ejection Fraction for Prognosis After Myocardial Infarction Circulation, June 10, 2003; 107(22): 2786 - 2792. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. J. Wang, D. Levy, E. J. Benjamin, and R. S. Vasan The Epidemiology of "Asymptomatic" Left Ventricular Systolic Dysfunction: Implications for Screening Ann Intern Med, June 3, 2003; 138(11): 907 - 916. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Ruskoaho Cardiac Hormones as Diagnostic Tools in Heart Failure Endocr. Rev., June 1, 2003; 24(3): 341 - 356. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M Bay, V Kirk, J Parner, C Hassager, H Nielsen, K Krogsgaard, J Trawinski, S Boesgaard, and J Aldershvile NT-proBNP: a new diagnostic screening tool to differentiate between patients with normal and reduced left ventricular systolic function Heart, February 1, 2003; 89(2): 150 - 154. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. M. Redfield, S. J. Jacobsen, J. C. Burnett Jr, D. W. Mahoney, K. R. Bailey, and R. J. Rodeheffer Burden of Systolic and Diastolic Ventricular Dysfunction in the Community: Appreciating the Scope of the Heart Failure Epidemic JAMA, January 8, 2003; 289(2): 194 - 202. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
O. W. Nielsen, T. A. McDonagh, S. D. Robb, and H. J. Dargie Retrospective analysis of thecost-effectiveness of using plasmabrain natriuretic peptide inscreening for left ventricularsystolic dysfunction in the general population J. Am. Coll. Cardiol., January 1, 2003; 41(1): 113 - 120. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Ambrosi, C. Oddoze, and G. Habib Utility of B-Natriuretic Peptide in Detecting Diastolic Dysfunction: Comparison With Doppler Velocity Recordings Circulation, October 8, 2002; 106 (15): e70 - e70. [Full Text] [PDF]
|
|
|
|
|
|
R. S. Vasan, E. J. Benjamin, M. G. Larson, E. P. Leip, T. J. Wang, P. W. F. Wilson, and D. Levy Plasma Natriuretic Peptides for Community Screening for Left Ventricular Hypertrophy and Systolic Dysfunction: The Framingham Heart Study JAMA, September 11, 2002; 288(10): 1252 - 1259. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. M. Richards, M. G. Nicholls, R. W. Troughton, J. G. Lainchbury, J. Elliott, C. Frampton, E. A. Espiner, I. G. Crozier, T. G. Yandle, and J. Turner Antecedent hypertension and heart failure after myocardial infarction J. Am. Coll. Cardiol., April 3, 2002; 39(7): 1182 - 1188. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. Ogawa, Y. Saito, K. Kuwahara, M. Harada, Y. Miyamoto, I. Hamanaka, N. Kajiyama, N. Takahashi, T. Izumi, R. Kawakami, et al. Fibronectin signaling stimulates BNP gene transcription by inhibiting neuron-restrictive silencer element-dependent repression Cardiovasc Res, February 1, 2002; 53(2): 451 - 459. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Luchner, C. Hengstenberg, H. Lowel, J. Trawinski, M. Baumann, G. A.J. Riegger, H. Schunkert, and S. Holmer N-Terminal Pro-Brain Natriuretic Peptide After Myocardial Infarction: A Marker Of Cardio-Renal Function Hypertension, January 1, 2002; 39(1): 99 - 104. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J.o. Koglin, S. Pehlivanli, M. Schwaiblmair, M. Vogeser, P. Cremer, and W. vonScheidt Role of brain natriuretic peptide in risk stratification of patients with congestive heart failure J. Am. Coll. Cardiol., December 1, 2001; 38(7): 1934 - 1941. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. A. Groenning, J. C. Nilsson, L. Sondergaard, A. Kjaer, H. B.W. Larsson, and P. R. Hildebrandt Evaluation of impaired left ventricular ejection fraction and increased dimensions by multiple neurohumoral plasma concentrations Eur J Heart Fail, December 1, 2001; 3(6): 699 - 708. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Nishina, K. Nishimura, S. Yuasa, S. Miwa, T. Nomoto, Y. Sakakibara, N. Handa, I. Hamanaka, Y. Saito, and M. Komeda Initial Effects of the Left Ventricular Repair by Plication May Not Last Long in a Rat Ischemic Cardiomyopathy Model Circulation, September 18, 2001; 104 (2009): I-241 - I-245. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. C Kone Molecular biology of natriuretic peptides and nitric oxide synthases Cardiovasc Res, August 15, 2001; 51(3): 429 - 441. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. Boomsma and A. H. van den Meiracker Plasma A- and B-type natriuretic peptides: physiology, methodology and clinical use Cardiovasc Res, August 15, 2001; 51(3): 442 - 449. [Full Text] [PDF]
|
|
|
|
|
|
T. Suzuki, T. Yamazaki, and Y. Yazaki The role of the natriuretic peptides in the cardiovascular system Cardiovasc Res, August 15, 2001; 51(3): 489 - 494. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Hirata, A. Matsumoto, T. Aoyagi, K. Yamaoki, I. Komuro, T. Suzuki, T. Ashida, T. Sugiyama, Y. Hada, I. Kuwajima, et al. Measurement of plasma brain natriuretic peptide level as a guide for cardiac overload Cardiovasc Res, August 15, 2001; 51(3): 585 - 591. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C Briguori, S Betocchi, F Manganelli, B Gigante, M.A Losi, Q Ciampi, R Gottilla, A Violante, C.G Tocchetti, M Volpe, et al. Determinants and clinical significance of natriuretic peptides and hypertrophic cardiomyopathy Eur. Heart J., August 1, 2001; 22(15): 1328 - 1336. [Abstract] [PDF]
|
|
|
|
|
|
C. ZOCCALI, F. MALLAMACI, F. A. BENEDETTO, G. TRIPEPI, S. PARLONGO, A. CATALIOTTI, S. CUTRUPI, G. GIACONE, I. BELLANUOVA, E. COTTINI, et al. Cardiac Natriuretic Peptides Are Related to Left Ventricular Mass and Function and Predict Mortality in Dialysis Patients J. Am. Soc. Nephrol., July 1, 2001; 12(7): 1508 - 1515. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. M. Richards, R. Doughty, M. G. Nicholls, S. MacMahon, N. Sharpe, J. Murphy, E. A. Espiner, C. Frampton, T. G. Yandle, and for the Australia-New Zealand Heart Failure Group Plasma N-terminal pro-brain natriuretic peptide and adrenomedullin: Prognostic utility and prediction of benefit from carvedilol in chronic ischemic left ventricular dysfunction J. Am. Coll. Cardiol., June 1, 2001; 37(7): 1781 - 1787. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Klemola, I. Tikkanen, O. Vuolteenaho, L. Toivonen, and M. Laine Plasma and pericardial fluid natriuretic peptide levels in postinfarction ventricular dysfunction Eur J Heart Fail, January 1, 2001; 3(1): 21 - 26. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. H. Chen, J. A. Grantham, J. A. Schirger, M. Jougasaki, M. M. Redfield, and J. C. Burnett Jr. Subcutaneous administration of brain natriuretic peptide in experimental heart failure J. Am. Coll. Cardiol., November 1, 2000; 36(5): 1706 - 1712. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G.Y.H Lip, D.C Felmeden, F.L Li-Saw-Hee, and D.G Beevers Hypertensive heart disease. A complex syndrome or a hypertensive 'cardiomyopathy'? Eur. Heart J., October 2, 2000; 21(20): 1653 - 1665. [PDF]
|
|
|
|
|
|
B. Frey, R. Pacher, G. Locker, A. Bojic, E. Hartter, W. Woloszczuk, and B. Stanek Prognostic Value of Hemodynamic vs Big Endothelin Measurements During Long-term IV Therapy in Advanced Heart Failure Patients Chest, June 1, 2000; 117(6): 1713 - 1719. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Langenickel, I. Pagel, K. Hohnel, R. Dietz, and R. Willenbrock Differential regulation of cardiac ANP and BNP mRNA in different stages of experimental heart failure Am J Physiol Heart Circ Physiol, May 1, 2000; 278(5): H1500 - H1506. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Nakayama, M. Soma, Y. Takahashi, D. Rehemudula, K. Kanmatsuse, and K. Furuya Functional Deletion Mutation of the 5'-Flanking Region of Type A Human Natriuretic Peptide Receptor Gene and Its Association With Essential Hypertension and Left Ventricular Hypertrophy in the Japanese Circ. Res., April 28, 2000; 86(8): 841 - 845. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Chen, M. Garami, and D. G. Gardner Doxorubicin Selectively Inhibits Brain Versus Atrial Natriuretic Peptide Gene Expression in Cultured Neonatal Rat Myocytes Hypertension, December 1, 1999; 34(6): 1223 - 1231. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Silberbach, T. Gorenc, R. E. Hershberger, P. J. S. Stork, P. S. Steyger, and C. T. Roberts Jr. Extracellular Signal-regulated Protein Kinase Activation Is Required for the Anti-hypertrophic Effect of Atrial Natriuretic Factor in Neonatal Rat Ventricular Myocytes J. Biol. Chem., August 27, 1999; 274(35): 24858 - 24864. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. M. Mills, T. H. LeJemtel, D. P. Horton, C.-s. Liang, R. Lang, M. A. Silver, C. Lui, K. Chatterjee, and on Behalf of the Natrecor Study Group Sustained hemodynamic effects of an infusion of nesiritide (human b-type natriuretic peptide) in heart failure: A randomized, double-blind, placebo-controlled clinical trial J. Am. Coll. Cardiol., July 1, 1999; 34(1): 155 - 162. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Kelly and A.D. Struthers Screening for left ventricular systolic dysfunction in patients with stroke, transient ischaemic attacks, and peripheral vascular disease QJM, June 1, 1999; 92(6): 295 - 297. [Full Text] [PDF]
|
|
|
|
|
|
A M Richards, M G Nicholls, T G Yandle, H Ikram, E A Espiner, J G Turner, R C Buttimore, J G Lainchbury, J M Elliott, C Frampton, et al. Neuroendocrine prediction of left ventricular function and heart failure after acute myocardial infarction Heart, February 1, 1999; 81(2): 114 - 120. [Abstract] [Full Text]
|
|
|
|
|
|
B. M. Y. Cheung and C. R. Kumana Natriuretic Peptides--Relevance in Cardiovascular Disease JAMA, December 16, 1998; 280(23): 1983 - 1984. [Full Text] [PDF]
|
|
|
|
|
|
C. J. Pemberton, T. G. Yandle, M. T. Rademaker, C. J. Charles, G. D. Aitken, and E. A. Espiner Amino-terminal proBNP in ovine plasma: evidence for enhanced secretion in response to cardiac overload Am J Physiol Heart Circ Physiol, October 1, 1998; 275(4): H1200 - H1208. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||