N-terminal prohormone of brain natriuretic peptide

Last updated

natriuretic peptide B
Identifiers
Symbol NPPB
NCBI gene 4879
HGNC 7940
OMIM 600295
RefSeq NM_002521
UniProt P16860
Other data
Locus Chr. 1 p36.2
Search for
Structures Swiss-model
Domains InterPro

N-terminal prohormone of brain natriuretic peptide (NT-proBNP or BNPT) is a 76 amino acid long protein that is cleaved from the N-terminal end of the 108 amino acid long prohormone proBNP to release brain natriuretic peptide 32 (BNP, also known as B-type natriuretic peptide). [1] [2] [3] [4]

Contents

Both BNP and NT-proBNP levels in the blood are used for screening, diagnosis of acute congestive heart failure (CHF) and may be useful to establish prognosis in heart failure, as both markers are typically higher in patients with worse outcome. [5] The plasma concentrations of both BNP and NT-proBNP are also typically increased in patients with asymptomatic or symptomatic left ventricular dysfunction and is associated with coronary artery disease, myocardial ischemia, and severity of aortic valve stenosis. [6] [7] [8] [9] [10] [11]

Blood levels

Upper limit (95th percentile) of blood ranges
for NT-proBNP in healthy people [12]
SexAgeLimit
in pg/mL
Male19-44 yrs93
45-54 yrs138
55-64 yrs177
65-74 yrs229
> 75 yrs852
Females19-44 yrs178
45-54 yrs192
55-64 yrs226
65-74 yrs353
> 75 yrs624
InterpretationAgeRange
Congestive heart failure likely <75 years > 125 pg/mL [13]
>75 years>450pg/mL [13]

There is no level of BNP that perfectly separates patients with and without heart failure. [14]

In screening for congenital heart disease in pediatric patients, an NT-proBNP cut-off value of 91 pg/mL could differentiate an acyanotic heart disease (ACNHD) patient from a healthy patient with a sensitivity of 84% and specificity of 42%. [15] On the other hand, an NT-proBNP cut-off value of 318 pg/mL is more appropriate in differing patients with congenital nonspherocytic hemolytic disease (CNHD) from healthy patients, with 94% sensitivity and 97% specificity. [15] An NT-proBNP value of 408 pg/mL has been estimated to be 83% sensitive and 57% specific in differentiating patients with ACNHD from patients with CNHD. [15] In patients with non-severe asymptomatic aortic valve stenosis, increased age- and sex adjusted NT-proBNP levels alone and combined with a 50% or greater increase from baseline had been found associated with increased event rates of aortic valve stenosis related events (cardiovascular death, hospitalization with heart failure due to progression of aortic valve stenosis, or aortic valve replacement surgery). [16] In severe aortic valve stenosis, NT-proBNP provide important prognostic information beyond clinical and echocardiographic evaluation. [17]

Test usage in a clinical setting

Canada

While discussed in Canadian medical journals in the mid to late 2000s, [18] the test is not widely used. It was only approved for use in Alberta in February 2012. [19]

Test usage in the life insurance industry

The test has been widely used in the life insurance industry to screen applicants as part of the routine requirements when applying for a life insurance policy. It is also inexpensive and can be measured from blood samples routinely drawn as part of the application process. The test can be used to evaluate for a number of health conditions. [11] [20] [21]

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 caused by an impairment in the heart's ability to fill with and pump blood.

<span class="mw-page-title-main">Echocardiography</span> Medical imaging technique of the heart

Echocardiography, also known as cardiac ultrasound, is the use of ultrasound to examine the heart. It is a type of medical imaging, using standard ultrasound or Doppler ultrasound. The visual image formed using this technique is called an echocardiogram, a cardiac echo, or simply an echo.

<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">Diastole</span> Part of the cardiac cycle

Diastole is the relaxed phase of the cardiac cycle when the chambers of the heart are refilling with blood. The contrasting phase is systole when the heart chambers are contracting. Atrial diastole is the relaxing of the atria, and ventricular diastole the relaxing of the ventricles.

<span class="mw-page-title-main">Aortic regurgitation</span> Medical condition

Aortic regurgitation (AR), also known as aortic insufficiency (AI), is the leaking of the aortic valve of the heart that causes blood to flow in the reverse direction during ventricular diastole, from the aorta into the left ventricle. As a consequence, the cardiac muscle is forced to work harder than normal.

<span class="mw-page-title-main">Bicuspid aortic valve</span> Medical condition

Bicuspid aortic valve (BAV) is a form of heart disease in which two of the leaflets of the aortic valve fuse during development in the womb resulting in a two-leaflet (bicuspid) valve instead of the normal three-leaflet (tricuspid) valve. BAV is the most common cause of heart disease present at birth and affects approximately 1.3% of adults. Normally, the mitral valve is the only bicuspid valve and this is situated between the heart's left atrium and left ventricle. Heart valves play a crucial role in ensuring the unidirectional flow of blood from the atria to the ventricles, or from the ventricle to the aorta or pulmonary trunk. BAV is normally inherited.

Aortic valve replacement is a cardiac surgery procedure whereby a failing aortic valve is replaced with an artificial heart valve. The aortic valve may need to be replaced because of aortic regurgitation, or if the valve is narrowed by stenosis.

<span class="mw-page-title-main">Cardiac marker</span> Biomarkers relevant to heart function

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">Valvular heart disease</span> Disease in the valves of the heart

Valvular heart disease is any cardiovascular disease process involving one or more of the four valves of the heart. These conditions occur largely as a consequence of aging, but may also be the result of congenital (inborn) abnormalities or specific disease or physiologic processes including rheumatic heart disease and pregnancy.

<span class="mw-page-title-main">Aortic valvuloplasty</span>

Aortic valvuloplasty, also known as balloon aortic valvuloplasty (BAV), is a procedure used to improve blood flow through the aortic valve in conditions that cause aortic stenosis, or narrowing of the aortic valve. It can be performed in various patient populations including fetuses, newborns, children, adults, and pregnant women. The procedure involves using a balloon catheter to dilate the narrowed aortic valve by inflating the balloon.

<span class="mw-page-title-main">Transcatheter aortic valve replacement</span> Aortic valve implantation technique

Transcatheter aortic valve replacement (TAVR) is the implantation of the aortic valve of the heart through the blood vessels without actual removal of the native valve. The first TAVI was performed on 16 April 2002 by Alain Cribier, which became a new alternative in the management of high-risk patients with severe aortic stenosis. The implantated valve is delivered via one of several access methods: transfemoral, transapical, subclavian, direct aortic, and transcaval, among others.

<span class="mw-page-title-main">Troponin T</span> Protein family

Troponin T is a part of the troponin complex, which are proteins integral to the contraction of skeletal and heart muscles. They are expressed in skeletal and cardiac myocytes. Troponin T binds to tropomyosin and helps position it on actin, and together with the rest of the troponin complex, modulates contraction of striated muscle. The cardiac subtype of troponin T is especially useful in the laboratory diagnosis of heart attack because it is released into the blood-stream when damage to heart muscle occurs. It was discovered by the German physician Hugo A. Katus at the University of Heidelberg, who also developed the troponin T assay.

<span class="mw-page-title-main">Natriuretic peptide</span> Hormone used in regulating the cardiovascular system

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.

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.

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.

<span class="mw-page-title-main">Brain natriuretic peptide 32</span> Hormone secreted in the heart

Brain natriuretic peptide (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. BNP is one of the three natriuretic peptides, in addition to atrial natriuretic peptide (ANP) and C-type natriuretic peptide ( CNP). BNP was first discovered in porcine brain tissue in 1988, which led to its initial naming as "brain natriuretic peptide", although subsequent research revealed that BNP is primarily produced and secreted by the ventricular myocardium in response to increased ventricular blood volume and stretching. To reflect its true source, BNP is now often referred to as "B-type natriuretic peptide" while retaining the same acronym.

<span class="mw-page-title-main">Richard Gorlin</span> American cardiologist

Richard Gorlin was an American cardiologist known for his contributions to the fields of valvular heart disease, coronary artery disease and cardiac catheterization, digitalis and vasodilators in congestive heart failure, and thrombolysis in myocardial infarctions. Along with his father, developed the Gorlin formula used to calculate valve areas in aortic valve stenosis and mitral valve stenosis.

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. ↑ McKie PM, Burnett JC (2016-12-06). "NT-proBNP". Journal of the American College of Cardiology. 68 (22): 2437–2439. doi:10.1016/j.jacc.2016.10.001.
  2. ↑ Hall C (2004). "Essential biochemistry and physiology of (NT-pro)BNP". European Journal of Heart Failure. 6 (3): 257–260. doi:10.1016/j.ejheart.2003.12.015. ISSN   1879-0844.
  3. ↑ Hall C (2004). "Essential biochemistry and physiology of (NT-pro)BNP". European Journal of Heart Failure. 6 (3): 257–260. doi:10.1016/j.ejheart.2003.12.015. ISSN   1879-0844.
  4. ↑ "UpToDate". www.uptodate.com. Retrieved 2024-12-21.
  5. ↑ 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.
  6. ↑ 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): 518–523. doi:10.1016/j.ahj.2004.03.014. PMID   15389242.
  7. ↑ Nakamura T, Sakamoto K, Yamano T, Kikkawa M, Zen K, Hikosaka T, et al. (May 2002). "Increased plasma brain natriuretic peptide level as a guide for silent myocardial ischemia in patients with non-obstructive hypertrophic cardiomyopathy". Journal of the American College of Cardiology. 39 (10): 1657–1663. doi: 10.1016/s0735-1097(02)01813-2 . PMID   12020494.
  8. ↑ Talwar S, Squire IB, Downie PF, Davies JE, Ng LL (October 2000). "Plasma N terminal pro-brain natriuretic peptide and cardiotrophin 1 are raised in unstable angina". Heart. 84 (4): 421–424. doi:10.1136/heart.84.4.421. PMC   1729429 . PMID   10995414.
  9. ↑ Kim H, Yang DH, Park Y, Han J, Lee H, Kang H, et al. (November 2006). "Incremental prognostic value of C-reactive protein and N-terminal proB-type natriuretic peptide in acute coronary syndrome". Circulation Journal. 70 (11): 1379–1384. doi: 10.1253/circj.70.1379 . PMID   17062957.
  10. ↑ Ruwald MH, Goetze JP, Bech J, Nielsen OW, Madsen BK, Nielsen LB, et al. (January 2014). "NT-ProBNP independently predicts long-term mortality in patients admitted for coronary angiography". Angiology. 65 (1): 31–36. doi:10.1177/0003319712462758. PMID   23070682. S2CID   33475819.
  11. 1 2 Hadziselimovic E, Greve AM, Sajadieh A, Olsen MH, Kesäniemi YA, Nienaber CA, et al. (April 2022). "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. PMC   8851368 . PMID   35171199.
  12. ↑ "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.
  13. 1 2 Lee MA (2009). Basic Skills in Interpreting Laboratory Data. Amer Soc of Health System. p. 220. ISBN   978-1-58528-180-0.
  14. ↑ 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): 161–167. doi: 10.1056/NEJMoa020233 . PMID   12124404.
  15. 1 2 3 Moses EJ, Mokhtar SA, Hamzah A, Abdullah BS, Yusoff NM (2011). "Usefulness of N-Terminal-Pro-B-Type Natriuretic Peptide as a Screening Tool for Identifying Pediatric Patients With Congenital Heart Disease". Laboratory Medicine. 42 (2): 75–80. doi: 10.1309/LMW0U87COTHXGELF .
  16. ↑ Hadziselimovic E, Greve AM, Sajadieh A, Olsen MH, Kesäniemi YA, Nienaber CA, et al. (April 2022). "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. PMC   8851368 . PMID   35171199.
  17. ↑ Bergler-Klein J, Klaar U, Heger M, Rosenhek R, Mundigler G, Gabriel H, Binder T, Pacher R, Maurer G, Baumgartner H (2004-05-18). "Natriuretic Peptides Predict Symptom-Free Survival and Postoperative Outcome in Severe Aortic Stenosis". Circulation. 109 (19): 2302–2308. doi:10.1161/01.CIR.0000126825.50903.18. ISSN   0009-7322. PMID   15117847.
  18. ↑ Murray H, Cload B, Collier CP, Sivilotti ML (July 2006). "Potential impact of N-terminal pro-BNP testing on the emergency department evaluation of acute dyspnea". CJEM. 8 (4): 251–258. doi: 10.1017/s1481803500013798 . PMID   17324304.
  19. ↑ "B-type Natriuretic Peptide (BNP) & NT-proBNP Test Implementation". Alberta Health Services. Archived from the original on 22 April 2015. Retrieved 3 January 2013.
  20. ↑ George H (2010). "NT-proBNP The Finest Cardiovascular Screening and Reflexive Test In the History of Life Underwriting" (PDF). Insureintell. Retrieved 11 July 2016.
  21. ↑ Clark M, Kaufman V, Fulks M, Dolan VF, Stout RL (2014). "NT-proBNP as a predictor of all-cause mortality in a population of insurance applicants". Journal of Insurance Medicine. 44 (1): 7–16. PMID   25004594.
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.