Brain natriuretic peptide 32

Last updated
NPPB
Available structures
PDB Human UniProt search: PDBe RCSB
Identifiers
Aliases NPPB , natriuretic peptide B, BNP, Iso-ANP
External IDs OMIM: 600295 HomoloGene: 81698 GeneCards: NPPB
Orthologs
SpeciesHumanMouse
Entrez

4879

n/a

Ensembl

ENSG00000120937

n/a

UniProt

P16860

n/a

RefSeq (mRNA)

NM_002521

n/a

RefSeq (protein)

NP_002512
NP_002512

n/a

Location (UCSC) Chr 1: 11.86 – 11.86 Mb n/a
PubMed search [2] n/a
Wikidata
View/Edit Human

Brain natriuretic peptide 32 (BNP), also known as B-type natriuretic peptide, is a hormone secreted by cardiomyocytes in the heart ventricles in response to stretching caused by increased ventricular blood volume. [3] BNP is one of the three natriuretic peptides, in addition to ANP and CNP. [4]

Contents

The 32-amino acid polypeptide BNP is secreted attached to a 76–amino acid N-terminal fragment in the prohormone called NT-proBNP (BNPT), which is biologically inactive. Once released, BNP binds to and activates the atrial natriuretic factor receptor NPRA, and to a lesser extent NPRB, in a fashion similar to atrial natriuretic peptide (ANP) but with 10-fold lower affinity. The biological half-life of BNP, however, is twice as long as that of ANP, and that of NT-proBNP is even longer, making these peptides better targets than ANP for diagnostic blood testing.

The physiologic actions of BNP are similar to those of ANP and include decrease in systemic vascular resistance and central venous pressure as well as an increase in natriuresis. The net effect of these peptides is a decrease in blood pressure due to the decrease in systemic vascular resistance and, thus, afterload. Additionally, the actions of both BNP and ANP result in a decrease in cardiac output due to an overall decrease in central venous pressure and preload as a result of the reduction in blood volume that follows natriuresis and diuresis. [5]

Biosynthesis

BNP is synthesized as a 134-amino acid preprohormone (preproBNP), encoded by the human gene NPPB. Removal of the 25-residue N-terminal signal peptide generates the prohormone, proBNP, which is stored intracellularly as an O-linked glycoprotein; proBNP is subsequently cleaved between arginine-102 and serine-103 by a specific convertase (probably furin or corin) into NT-proBNP and the biologically active 32-amino acid polypeptide BNP-32, which are secreted into the blood in equimolar amounts. [6] Cleavage at other sites produces shorter BNP peptides with unknown biological activity. [7] Processing of proBNP may be regulated by O-glycosylation of residues near the cleavage sites. [8] The synthesis of BNP in cardiomyocytes is stimulated by pro-inflammatory cell factors, such as interleukin-1β, interleukin-6 and tumor necrosis factor-α. [9]

Physiologic effects

Renal

Adrenal

Vascular

Relaxes vascular smooth muscle in arterioles and venules by:

Promotes uterine spiral artery remodeling, which is important for preventing pregnancy-induced hypertension. [12]

Cardiac

Adipose tissue

Measurement

BNP and NT-proBNP are measured by immunoassay. [14]

Interpretation of BNP

A preoperative BNP can be predictive of a risk of an acute cardiac event during vascular surgery. A cutoff of 100 pg/ml has a sensitivity of approximately 100%, a negative predictive value of approximately 100%, a specificity of 90%, and a positive predictive value of 78% according to data from the United Kingdom. [19]

BNP is cleared by binding to natriuretic peptide receptors (NPRs) and neutral endopeptidase (NEP). Less than 5% of BNP is cleared renally. NT-proBNP is the inactive molecule resulting from cleavage of the prohormone Pro-BNP and is reliant solely on the kidney for excretion. The achilles heel of the NT-proBNP molecule is the overlap in kidney disease in the heart failure patient population. [20] [21]

Some laboratories report in units ng per Litre (ng/L), which is equivalent to pg/mL

There is a diagnostic 'gray area', often defined as between 100 and 500 pg/mL, for which the test is considered inconclusive, but, in general, levels above 500 pg/ml are considered to be an indicator of heart failure. This so-called gray zone has been addressed in several studies, and using clinical history or other available simple tools can help make the diagnosis. [22] [23]

BNP has been suggested as a predictor for a variety of medical states, including cardiovascular mortality in diabetics [24] and cardiac impairment in cancer patients. [25] [26]

BNP was found to have an important role in prognostication of heart surgery patients [27] and in the emergency department. [28] Bhalla et al. showed that combining BNP with other tools like ICG can improve early diagnosis of heart failure and advance prevention strategies. [29] [30] Utility of BNP has also been explored in various settings like preeclampsia, ICU and shock and ESRD. [31] [32] [33]

The effect or race and gender on value of BNP and its utility in that context has been studied extensively. [34] [35]

NT-proBNP levels (in pg/mL) by NYHA functional class [36]
NYHA INYHA IINYHA IIINYHA IV
5th Percentile33103126148
Mean1015166630293465
95th Percentile3410656710,44912,188

The BNP test is used as an aid in the diagnosis and assessment of severity of heart failure. A recent meta-analysis concerning effects of BNP testing on clinical outcomes of patients presenting to the emergency department with acute dyspnea revealed that BNP testing led to a decrease in admission rates and decrease in mean length of stay, although neither was statistically significant. Effects on all cause hospital mortality was inconclusive. [37] The BNP test is also used for the risk stratification of patients with acute coronary syndromes. [38] [39]

When interpreting an elevated BNP level, values may be elevated due to factors other than heart failure. Lower levels are often seen in obese patients. [40] Higher levels are seen in those with renal disease, in the absence of heart failure.

Therapeutic application

Recombinant BNP, nesiritide, has been suggested as a treatment for decompensated heart failure. However, a clinical trial failed to show a benefit of nesiritide in patients with acute decompensated heart failure. [41] Blockade of neprilysin, a protease known to degrade members of the natriuretic peptide family, has also been suggested as a possible treatment for heart failure. Dual administration of neprilysin inhibitors and angiotensin receptor blockers has been shown to be advantageous to ACE inhibitors, the current first-line therapy, in multiple settings. [42] [43]

See also

Related Research Articles

<span class="mw-page-title-main">Aortic stenosis</span> Narrowing of the exit of the hearts left ventricle

Aortic stenosis is the narrowing of the exit of the left ventricle of the heart, such that problems result. It may occur at the aortic valve as well as above and below this level. It typically gets worse over time. Symptoms often come on gradually with a decreased ability to exercise often occurring first. If heart failure, loss of consciousness, or heart related chest pain occur due to AS the outcomes are worse. Loss of consciousness typically occurs with standing or exercising. Signs of heart failure include shortness of breath especially when lying down, at night, or with exercise, and swelling of the legs. Thickening of the valve without causing obstruction is known as aortic sclerosis.

<span class="mw-page-title-main">Heart failure</span> Failure of the heart to provide sufficient blood flow

Heart failure (HF), also known as congestive heart failure (CHF), is a syndrome, a group of signs and symptoms, caused by an impairment of the heart's blood pumping function. Symptoms typically include shortness of breath, excessive fatigue, and leg swelling. The shortness of breath may occur with exertion or while lying down, and may wake people up during the night. The severity of the heart failure is mainly decided based on ejection fraction and also measured by the severity of symptoms. Other conditions that may have symptoms similar to heart failure include obesity, kidney failure, liver disease, anemia, and thyroid disease.

<span class="mw-page-title-main">Atrial natriuretic peptide</span> Cardiac hormone which increases renal sodium excretion

Atrial natriuretic peptide (ANP) or atrial natriuretic factor (ANF) is a natriuretic peptide hormone secreted from the cardiac atria that in humans is encoded by the NPPA gene. Natriuretic peptides are a family of hormone/paracrine factors that are structurally related. The main function of ANP is causing a reduction in expanded extracellular fluid (ECF) volume by increasing renal sodium excretion. ANP is synthesized and secreted by cardiac muscle cells in the walls of the atria in the heart. These cells contain volume receptors which respond to increased stretching of the atrial wall due to increased atrial blood volume.

Hypertrophic cardiomyopathy is a condition in which muscle tissues of the heart become thickened without an obvious cause. The parts of the heart most commonly affected are the interventricular septum and the ventricles. This results in the heart being less able to pump blood effectively and also may cause electrical conduction problems. Specifically, within the bundle branches that conduct impulses through the interventricular septum and into the Purkinje fibers, as these are responsible for the depolarization of contractile cells of both ventricles.

<span class="mw-page-title-main">Cardiac marker</span>

Cardiac markers are biomarkers measured to evaluate heart function. They can be useful in the early prediction or diagnosis of disease. Although they are often discussed in the context of myocardial infarction, other conditions can lead to an elevation in cardiac marker level.

<span class="mw-page-title-main">Acute coronary syndrome</span> Medical condition

Acute coronary syndrome (ACS) is a syndrome due to decreased blood flow in the coronary arteries such that part of the heart muscle is unable to function properly or dies. The most common symptom is centrally located pressure-like chest pain, often radiating to the left shoulder or angle of the jaw, and associated with nausea and sweating. Many people with acute coronary syndromes present with symptoms other than chest pain, particularly women, older people, and people with diabetes mellitus.

Tachycardia-induced cardiomyopathy (TIC) is a disease where prolonged tachycardia or arrhythmia causes an impairment of the myocardium, which can result in heart failure. People with TIC may have symptoms associated with heart failure and/or symptoms related to the tachycardia or arrhythmia. Though atrial fibrillation is the most common cause of TIC, several tachycardias and arrhythmias have been associated with the disease.

Adenosine A<sub>1</sub> receptor Cell surface receptor found in humans

The adenosine A1 receptor (A1AR) is one member of the adenosine receptor group of G protein-coupled receptors with adenosine as endogenous ligand.

<span class="mw-page-title-main">Natriuretic peptide</span>

A natriuretic peptide is a hormone molecule that plays a crucial role in the regulation of the cardiovascular system. These hormones were first discovered in the 1980s and were found to have very strong diuretic, natriuretic, and vasodilatory effects. There are three main types of natriuretic peptides: atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP). Two minor hormones include Urodilatin (URO) which is processed in the kidney and encoded by the same gene as ANP, and Dendroaspis NP (DNP) that was discovered through isolation of the venom from the green mamba snake. Since they are activated during heart failure, they are important for the protection of the heart and its tissues.

<span class="mw-page-title-main">Natriuretic peptide precursor C</span> Protein-coding gene in the species Homo sapiens

Natriuretic peptide precursor C, also known as NPPC, is a protein that in humans is encoded by the NPPC gene. The precursor NPPC protein is cleaved to the 22 amino acid peptide C-type natriuretic peptide (CNP).

<span class="mw-page-title-main">NPR2</span> Protein-coding gene in Homo sapiens

Natriuretic peptide receptor B/guanylate cyclase B , also known as NPR2, is an atrial natriuretic peptide receptor. In humans it is encoded by the NPR2 gene.

The ST2 cardiac biomarker is a protein biomarker of cardiac stress encoded by the IL1RL1 gene. ST2 signals the presence and severity of adverse cardiac remodeling and tissue fibrosis, which occurs in response to myocardial infarction, acute coronary syndrome, or worsening heart failure.

<span class="mw-page-title-main">CORIN</span> Mammalian protein found in Homo sapiens

Corin, also called atrial natriuretic peptide-converting enzyme, is a protein that in humans is encoded by the CORIN gene.

Management of heart failure requires a multimodal approach. It involves a combination of lifestyle modifications, medications, and possibly the use of devices or surgery.

Cardiorenal syndrome (CRS) is an umbrella term used in the medical field that defines disorders of the heart and kidneys whereby "acute or chronic dysfunction in one organ may induce acute or chronic dysfunction of the other". When one of these organs fails, the other may subsequently fail. The heart and the kidneys are involved in maintaining hemodynamic stability and organ perfusion through an intricate network. Patients who have renal failure first may be hard to determine if heart failure is concurrent. These two organs communicate with one another through a variety of pathways in an interdependent relationship. In a 2004 report from the National Heart, Lung and Blood Institute, CRS was defined as a condition where treatment of congestive heart failure is limited by decline in kidney function. This definition has since been challenged repeatedly but there still remains little consensus over a universally accepted definition for CRS. At a consensus conference of the Acute Dialysis Quality Initiative (ADQI), the CRS was classified into five subtypes primarily based upon the organ that initiated the insult as well as the acuity of disease.

The N-terminal prohormone of brain natriuretic peptide is a prohormone with a 76 amino acid N-terminal inactive protein that is cleaved from the molecule to release brain natriuretic peptide 32.

Cenderitide is a natriuretic peptide developed by the Mayo Clinic as a potential treatment for heart failure. Cenderitide is created by the fusion of the 15 amino acid C-terminus of the snake venom dendroaspis natriuretic peptide (DNP) with the full C-type natriuretic peptide (CNP) structure. This peptide chimera is a dual activator of the natriuretic peptide receptors NPR-A and NPR-B and therefore exhibits the natriuretic and diuretic properties of DNP, as well as the antiproliferative and antifibrotic properties of CNP.

Copeptin is a 39-amino acid-long peptide derived from the C-terminus of pre-pro-hormone of arginine vasopressin, neurophysin II and copeptin. Arginine vasopressin (AVP), also known as the antidiuretic hormone (ADH), is encoded by the AVP gene and is involved in multiple cardiovascular and renal pathways and abnormal level of AVP are associated with various diseases. Hence measurement of AVP would be useful, but is not commonly carried out in clinical practice because of its very short half-life making it difficult to quantify. In contrast, copeptin can be immunologically tested with ease and therefore can be used as a vasopressin surrogate marker.

The Q-Symbio study was an international multi-center clinical trial that was reported in the Journal of the American College of Cardiology: Heart Failure in September 2014.

Arthur Mark Richards is a New Zealand physician, academic and medical researcher. He is a professor of cardiology and director of the Cardiovascular Research Institute at the National University of Singapore, and a professor of medicine and founder of the Christchurch Heart Institute at the University of Otago, Christchurch, New Zealand, where he holds the National Heart Foundation (NZ) Chair of Cardiovascular Studies.

References

  1. 1 2 3 GRCh38: Ensembl release 89: ENSG00000120937 - Ensembl, May 2017
  2. ↑ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  3. ↑ Potter LR, Yoder AR, Flora DR, Antos LK, Dickey DM (2009). Natriuretic peptides: their structures, receptors, physiologic functions and therapeutic applications. Handbook of Experimental Pharmacology. Vol. 191. pp. 341–66. doi:10.1007/978-3-540-68964-5_15. ISBN   978-3-540-68960-7. PMC   4855512 . PMID   19089336.
  4. ↑ Potter LR, Yoder AR, Flora DR, Antos LK, Dickey DM (2009). "Natriuretic Peptides: Their Structures, Receptors, Physiologic Functions and Therapeutic Applications". CGMP: Generators, Effectors and Therapeutic Implications. Handbook of Experimental Pharmacology. Vol. 191. pp. 341–366. doi:10.1007/978-3-540-68964-5_15. ISBN   978-3-540-68960-7. ISSN   0171-2004. PMC   4855512 . PMID   19089336.
  5. ↑ "CV Pharmacology - Natriuretic Peptides". cvpharmacology.com. Archived from the original on 21 October 2017. Retrieved 29 April 2018.
  6. ↑ Schellenberger U, O'Rear J, Guzzetta A, Jue RA, Protter AA, Pollitt NS (July 2006). "The precursor to B-type natriuretic peptide is an O-linked glycoprotein". Archives of Biochemistry and Biophysics. 451 (2): 160–6. doi:10.1016/j.abb.2006.03.028. PMID   16750161.
  7. ↑ Niederkofler EE, Kiernan UA, O'Rear J, Menon S, Saghir S, Protter AA, et al. (November 2008). "Detection of endogenous B-type natriuretic peptide at very low concentrations in patients with heart failure". Circulation: Heart Failure. 1 (4): 258–64. doi: 10.1161/CIRCHEARTFAILURE.108.790774 . PMID   19808300.
  8. ↑ Semenov AG, Postnikov AB, Tamm NN, Seferian KR, Karpova NS, Bloshchitsyna MN, et al. (March 2009). "Processing of pro-brain natriuretic peptide is suppressed by O-glycosylation in the region close to the cleavage site". Clinical Chemistry. 55 (3): 489–98. doi: 10.1373/clinchem.2008.113373 . PMID   19168558.
  9. ↑ Fu S, Ping P, Wang F, Luo L (December 2018). "Synthesis, secretion, function, metabolism and application of natriuretic peptides in heart failure". Journal of Biological Engineering. 12 (1): 2. doi: 10.1186/s13036-017-0093-0 . PMC   5766980 . PMID   29344085.
  10. ↑ Kiberd BA, Larson TS, Robertson CR, Jamison RL (June 1987). "Effect of atrial natriuretic peptide on vasa recta blood flow in the rat". The American Journal of Physiology. 252 (6 Pt 2): F1112-7. doi:10.1152/ajprenal.1987.252.6.F1112. PMID   2954471.
  11. ↑ Reeves WB, Andreoli TE (2008). "Chapter 31 – Sodium Chloride Transport in the Loop of Henle, Distal Convoluted Tubule, and Collecting Duct". In Giebisch GH, Alpern RA, Herbert SC, Seldin DW (eds.). Seldin and Giebisch's the kidney: physiology and pathophysiology . Amsterdam: Elsevier/Academic Press. pp.  849–887. doi:10.1016/B978-012088488-9.50034-6. ISBN   978-0-12-088488-9.
  12. ↑ Cui Y, Wang W, Dong N, Lou J, Srinivasan DK, Cheng W, et al. (March 2012). "Role of corin in trophoblast invasion and uterine spiral artery remodelling in pregnancy". Nature. 484 (7393): 246–50. Bibcode:2012Natur.484..246C. doi:10.1038/nature10897. PMC   3578422 . PMID   22437503.
  13. ↑ Tamura N, Ogawa Y, Chusho H, Nakamura K, Nakao K, Suda M, et al. (April 2000). "Cardiac fibrosis in mice lacking brain natriuretic peptide". Proceedings of the National Academy of Sciences of the United States of America. 97 (8): 4239–44. Bibcode:2000PNAS...97.4239T. doi: 10.1073/pnas.070371497 . PMC   18212 . PMID   10737768.
  14. ↑ Clerico A, Zaninotto M, Prontera C, Giovannini S, Ndreu R, Franzini M, et al. (December 2012). "State of the art of BNP and NT-proBNP immunoassays: the CardioOrmoCheck study". Clinica Chimica Acta; International Journal of Clinical Chemistry. 414: 112–9. doi:10.1016/j.cca.2012.07.017. hdl: 11382/365432 . PMID   22910582.
  15. ↑ Maisel AS, Krishnaswamy P, Nowak RM, McCord J, Hollander JE, Duc P, et al. (July 2002). "Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure". The New England Journal of Medicine. 347 (3): 161–7. doi: 10.1056/NEJMoa020233 . PMID   12124404.
  16. ↑ Bhalla V, Willis S, Maisel AS (2004). "B-type natriuretic peptide: the level and the drug--partners in the diagnosis of congestive heart failure". Congestive Heart Failure. 10 (1 Suppl 1): 3–27. doi: 10.1111/j.1527-5299.2004.03310.x . PMID   14872150.
  17. ↑ Hadziselimovic E, Greve AM, Sajadieh A, Olsen MH, Kesäniemi YA, Nienaber CA, et al. (2022-04-01). "Association of Annual N-Terminal Pro-Brain Natriuretic Peptide Measurements With Clinical Events in Patients With Asymptomatic Nonsevere Aortic Stenosis: A Post Hoc Substudy of the SEAS Trial". JAMA Cardiology. 7 (4): 435–444. doi:10.1001/jamacardio.2021.5916. ISSN   2380-6583. PMC   8851368 . PMID   35171199.
  18. ↑ Atisha D, Bhalla MA, Morrison LK, Felicio L, Clopton P, Gardetto N, et al. (September 2004). "A prospective study in search of an optimal B-natriuretic peptide level to screen patients for cardiac dysfunction". American Heart Journal. 148 (3): 518–23. doi:10.1016/j.ahj.2004.03.014. PMID   15389242.
  19. ↑ Berry C, Kingsmore D, Gibson S, Hole D, Morton JJ, Byrne D, et al. (March 2006). "Predictive value of plasma brain natriuretic peptide for cardiac outcome after vascular surgery". Heart. 92 (3): 401–2. doi:10.1136/hrt.2005.060988. PMC   1860808 . PMID   16501204.
  20. ↑ Austin WJ, Bhalla V, Hernandez-Arce I, Isakson SR, Beede J, Clopton P, et al. (October 2006). "Correlation and prognostic utility of B-type natriuretic peptide and its amino-terminal fragment in patients with chronic kidney disease". American Journal of Clinical Pathology. 126 (4): 506–12. doi: 10.1309/M7AAXA0J1THMNCDF . PMID   16938661.
  21. ↑ Daniels LB, Clopton P, Bhalla V, Krishnaswamy P, Nowak RM, McCord J, et al. (May 2006). "How obesity affects the cut-points for B-type natriuretic peptide in the diagnosis of acute heart failure. Results from the Breathing Not Properly Multinational Study". American Heart Journal. 151 (5): 999–1005. doi:10.1016/j.ahj.2005.10.011. PMID   16644321.
  22. ↑ Strunk A, Bhalla V, Clopton P, Nowak RM, McCord J, Hollander JE, et al. (January 2006). "Impact of the history of congestive heart failure on the utility of B-type natriuretic peptide in the emergency diagnosis of heart failure: results from the Breathing Not Properly Multinational Study". The American Journal of Medicine. 119 (1): 69.e1–11. doi: 10.1016/j.amjmed.2005.04.029 . PMID   16431187.
  23. ↑ Brenden CK, Hollander JE, Guss D, McCullough PA, Nowak R, Green G, et al. (May 2006). "Gray zone BNP levels in heart failure patients in the emergency department: results from the Rapid Emergency Department Heart Failure Outpatient Trial (REDHOT) multicenter study". American Heart Journal. 151 (5): 1006–11. doi:10.1016/j.ahj.2005.10.017. PMID   16644322.
  24. ↑ Bhalla MA, Chiang A, Epshteyn VA, Kazanegra R, Bhalla V, Clopton P, et al. (September 2004). "Prognostic role of B-type natriuretic peptide levels in patients with type 2 diabetes mellitus". Journal of the American College of Cardiology. 44 (5): 1047–52. doi: 10.1016/j.jacc.2004.05.071 . PMID   15337217.
  25. ↑ Palumbo I, Palumbo B, Fravolino M, et al. (2016). "Brain natriuretic peptide as a cardiac marker of transient radiotherapy-related damage in left-sided breast cancer patients: A prospective study". The Breast. 25: 45–50. doi:10.1016/j.breast.2015.10.004. PMID   26547836.
  26. ↑ Bando S, Soeki T, Matsuura T, et al. (2017). "Plasma brain natriuretic peptide levels are elevated in patients with cancer". PLOS ONE. 12 (6): e0178607. Bibcode:2017PLoSO..1278607B. doi: 10.1371/journal.pone.0178607 . PMC   5453551 . PMID   28570595.
  27. ↑ Hutfless R, Kazanegra R, Madani M, Bhalla MA, Tulua-Tata A, Chen A, et al. (May 2004). "Utility of B-type natriuretic peptide in predicting postoperative complications and outcomes in patients undergoing heart surgery". Journal of the American College of Cardiology. 43 (10): 1873–9. doi: 10.1016/j.jacc.2003.12.048 . PMID   15145114.
  28. ↑ Maisel A, Hollander JE, Guss D, McCullough P, Nowak R, Green G, et al. (September 2004). "Primary results of the Rapid Emergency Department Heart Failure Outpatient Trial (REDHOT). A multicenter study of B-type natriuretic peptide levels, emergency department decision making, and outcomes in patients presenting with shortness of breath". Journal of the American College of Cardiology. 44 (6): 1328–33. doi: 10.1016/j.jacc.2004.06.015 . PMID   15364340.
  29. ↑ Bhalla V, Isakson S, Bhalla MA, Lin JP, Clopton P, Gardetto N, et al. (February 2005). "Diagnostic ability of B-type natriuretic peptide and impedance cardiography: testing to identify left ventricular dysfunction in hypertensive patients". American Journal of Hypertension. 18 (2 Pt 2): 73S–81S. doi: 10.1016/j.amjhyper.2004.11.044 . PMID   15752936.
  30. ↑ Castellanos LR, Bhalla V, Isakson S, Daniels LB, Bhalla MA, Lin JP, et al. (February 2009). "B-type natriuretic peptide and impedance cardiography at the time of routine echocardiography predict subsequent heart failure events". Journal of Cardiac Failure. 15 (1): 41–7. doi:10.1016/j.cardfail.2008.09.003. PMID   19181293.
  31. ↑ Resnik JL, Hong C, Resnik R, Kazanegra R, Beede J, Bhalla V, et al. (August 2005). "Evaluation of B-type natriuretic peptide (BNP) levels in normal and preeclamptic women". American Journal of Obstetrics and Gynecology. 193 (2): 450–4. doi:10.1016/j.ajog.2004.12.006. PMID   16098869.
  32. ↑ Bhalla V, Bhalla MA, Maisel AS (August 2004). "Evolution of B-type natriuretic peptide in evaluation of intensive care unit shock". Critical Care Medicine. 32 (8): 1787–9. doi:10.1097/01.CCM.0000135748.75590.54. PMID   15286561.
  33. ↑ Sheen V, Bhalla V, Tulua-Tata A, Bhalla MA, Weiss D, Chiu A, et al. (February 2007). "The use of B-type natriuretic peptide to assess volume status in patients with end-stage renal disease". American Heart Journal. 153 (2): 244.e1–5. doi:10.1016/j.ahj.2006.10.041. PMID   17239684.
  34. ↑ Maisel AS, Clopton P, Krishnaswamy P, Nowak RM, McCord J, Hollander JE, et al. (June 2004). "Impact of age, race, and sex on the ability of B-type natriuretic peptide to aid in the emergency diagnosis of heart failure: results from the Breathing Not Properly (BNP) multinational study". American Heart Journal. 147 (6): 1078–84. doi:10.1016/j.ahj.2004.01.013. PMID   15199359.
  35. ↑ Daniels LB, Bhalla V, Clopton P, Hollander JE, Guss D, McCullough PA, et al. (May 2006). "B-type natriuretic peptide (BNP) levels and ethnic disparities in perceived severity of heart failure: results from the Rapid Emergency Department Heart Failure Outpatient Trial (REDHOT) multicenter study of BNP levels and emergency department decision making in patients presenting with shortness of breath". Journal of Cardiac Failure. 12 (4): 281–5. doi:10.1016/j.cardfail.2006.01.008. PMID   16679261.
  36. ↑ "N-terminal-pro-BNP". LABORATORY SERVICES HANDBOOK. The University of Iowa (UIHC), Department of Pathology. 28 May 2020. Archived from the original on 2008-10-11. Showing 95th percentiles. Epic Lab Code: LAB649.
  37. ↑ Lam LL, Cameron PA, Schneider HG, Abramson MJ, Müller C, Krum H (December 2010). "Meta-analysis: effect of B-type natriuretic peptide testing on clinical outcomes in patients with acute dyspnea in the emergency setting". Annals of Internal Medicine. 153 (11): 728–35. doi:10.7326/0003-4819-153-11-201012070-00006. PMID   21135296. S2CID   27272593.
  38. ↑ Bibbins-Domingo K, Gupta R, Na B, Wu AH, Schiller NB, Whooley MA (January 2007). "N-terminal fragment of the prohormone brain-type natriuretic peptide (NT-proBNP), cardiovascular events, and mortality in patients with stable coronary heart disease". JAMA. 297 (2): 169–76. doi:10.1001/jama.297.2.169. PMC   2848442 . PMID   17213400.
  39. ↑ Fitzgerald RL, Cremo R, Gardetto N, Chiu A, Clopton P, Bhalla V, et al. (September 2005). "Effect of nesiritide in combination with standard therapy on serum concentrations of natriuretic peptides in patients admitted for decompensated congestive heart failure". American Heart Journal. 150 (3): 471–7. doi:10.1016/j.ahj.2004.11.021. PMID   16169326.
  40. ↑ Wang TJ, Larson MG, Levy D, Benjamin EJ, Leip EP, Wilson PW, et al. (February 2004). "Impact of obesity on plasma natriuretic peptide levels". Circulation. 109 (5): 594–600. CiteSeerX   10.1.1.541.9955 . doi:10.1161/01.CIR.0000112582.16683.EA. PMID   14769680. S2CID   13454777.
  41. ↑ O'Connor CM, Starling RC, Hernandez AF, Armstrong PW, Dickstein K, Hasselblad V, et al. (July 2011). "Effect of nesiritide in patients with acute decompensated heart failure" (PDF). The New England Journal of Medicine. 365 (1): 32–43. doi:10.1056/NEJMoa1100171. hdl: 11379/60663 . PMID   21732835.
  42. ↑ McMurray JJ, Packer M, Desai AS, Gong J, Lefkowitz MP, Rizkala AR, et al. (September 2014). "Angiotensin-neprilysin inhibition versus enalapril in heart failure". The New England Journal of Medicine. 371 (11): 993–1004. doi:10.1056/NEJMoa1409077. hdl: 10993/27659 . PMID   25176015. S2CID   11383.
  43. ↑ Velazquez EJ, Morrow DA, DeVore AD, Duffy CI, Ambrosy AP, McCague K, et al. (February 2019). "Angiotensin-Neprilysin Inhibition in Acute Decompensated Heart Failure". The New England Journal of Medicine. 380 (6): 539–548. doi: 10.1056/NEJMoa1812851 . PMID   30415601.

Further reading

attribution: copied from Brain natriuretic peptide version as of 13:57, 4 December 2019

This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.