(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.
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
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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]
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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]
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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]
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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]
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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]
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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]
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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]
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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]
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