Referred to as B-Type Natriuretic Peptide, a neurohormone.
Originally described in porcine brain extracts but is found to be highly expressed in ventricular myocardium, and stress of the ventricular wall due to volume or pressure overload is the primary inducer of its synthesis.
Can help identify those patients at highest risk of cardiovascular events and more specifically of newly diagnosed heart failure.
Is a response to established cardiovascular damage.
Elevated levels reflect stretching of ventricular myocytes.
Is a risk identifier for heart failure and cardiovascular events and provides information that can potentially benefit the use of this peptide as a guide for care.
Commonly used to predict systolic dysfunction in CHF.
Secreted by cardiomyocytes in response to intravascular volume increases.
Release from cardiomyocytes in response to increase cardiac chamber wall stress and filling pressures.
A peptide with diuretic and vasodilatorty effects.
A neurohormone synthesized and released primarily from the ventricles of the heart.
Initially synthesized as pre–proBNP, cleaved to proBNP, and subsequently to the biologically active 32 amino acid BNP and the inactive 76 amino acid N-terminal fragment (NT proBNP).
Synthesized as the 134 amino acid pre-pro hormone, which is then split into signal peptide and a108 amino acid pro peptide (pro BNP).
Following secretion from the cardiomyocyte, pro-BNP is split into equimolar amounts to the physiologically active BNP with 32 amino acids in a biologically inactive 76 amino acid fragment NT pro-BNP.
Structurally similar to ANP (biologically active C-terminal hormone), with 17 of the 32 is the new asses sharing a common amino acid sequence.
BNP is synthesized and released in response to pressure and volume overload and results in vasodilation, natriuresis, and diuresis.
Half-life is approximately 20 minutes.
It is cleared primarily by neutral endopeptidase and natriuretic peptide receptors with some clearance by renal filtration.
NTproBNP as a half life of one-two hours and is dependent on renal filtration for elimination .
Both BNP and NTpro BNP are helpful in the prognosis, diagnosis and management of heart failure.
May be used to estimate LV end diastolic volume when pulmonary artery catherization and echocardiography are not available.
In patients with systolic failure levels greater than 100 pg/mL correlate with capillary wedge pressure greater than 15 mm Hg with a sensitivity of 57% to 74%.
BNP does not correlate with pulmonary capillary wedge pressure in patients with normal systolic function with pulmonary embolism, ARDS, septic shock or acute renal insufficiency.
Can predict cardiac morbidity after major vascular surgery.
When less than 100 pg/mL hypervolemia is unlikely.
Both atrial fibrillation and CHF increase BNP and NT-proBnp levels.
If BNP is less than 100 pg/mL heart failure is unlikely and alternative causes of dyspnea are pursued.
If BNP is between 100 and 500 pg/mL, clinical judgement is used to decide if congestive heart failure is the cause of dyspnea, and if BNP was greater than 500 PG /milliliter, heart failure is considered likely and rapid heart failure therapy is recommended.
Obese patients with heart failure have levels of BNP there are disproportionately lower then might be predicted from the elevation of left ventricular filling pressures.
A moderate increase in natriuretic peptide in an obese patient suggests a meaningful increase in left ventricular filling pressures.
Measurement of levels provide information about left ventricular function.
Functions as a counter-regulatory hormone to angiotensin II, norepinephrine and endothelin.
Synthesized in the normal heart by atrial myocardium secretory granules.
Synthesized as a prohormone in ventricular cardiocytes as a response to pressure overload and cardiac wall stress.
Pro-BNP is the precursor of BNP and is stored in secretory granules in myocytes.
Released from cardiac myocytes in response to cardiac wall stress, myocardial ischemia, during exercise testing induced ischemia, and after myocardial infarction.
Pro-BNP is cleaved into active BNP and inactive NT-proBNP by protease enzymes.
The family of natriuretic peptides made up of at least four entities.
N-terminal pro-BNP has 76 amino acids, BNP has 32 amino acids are the are the result of cleavage of prohormone BNP.
N-terminal pro-BNP has a longer half life than BNP 60-120 minutes versus 15-20 minutes.
Transient myocardial ischemia results in immediate increase of BNP and NT-proBNP with degree of elevation related to the severity of ischemia.
Has low specificity for heart failure but has prognostic implications for sepsis, pulmonary embolism, pulmonary hypertension, and stable coronary artery disease.
Causes decreases in blood pressure via vasodilatation, promotes diuresis and natriuresis and decreases sympathetic nervous system activity as well as the activities of the renin angiotensin system.
Chronic atrial fibrillation associated with marked increased in BNP levels even without CHF.
Can be elevated in other processes beside fluid overload and include renal failure, myocardial infarction, and lung disease associated with right sided heart failure.
Elevated with pulmonary embolism, pulmonary hypertension, and in older individuals.
BNP (brain natriuretic peptide)-cleared by the kidney, so elevated levels may be seen in patients with renal insufficiency.
When measured upon presentation and up to 7 days after the onset of an acute coronary syndrome BNP levels associated with short and long term risk os death and new congestive heart failure.
Obesity alters BNP levels with an inverse correlation between body mass index and plasma levels.
BNP and NT-pro-BNP plasma concentrations useful in diagnosis of acute decompensated heart failure.
BNP and NT-pro-BNP peptides can be used as prognostic indicators help predict mortality and clinical outcome in patients with chronic heart failure.
Lower BNP levels are predictive of lower number of major cardiovascular events.
With constrictive pericarditis the myocardium being encased in a constrictive pericardial sac, prevents lack of cardiac stretch and therefore BNP levels are normal or only slightly elevated.
Hormone replacement treatment increases BNP levels significantly suggesting estrogens influence natriuretic peptide regulation.
Aging affects the degradation, clearance and production of BNP so that levels increase with increasing age.
Metabolized by a specific neutral endpeptidase in the renal proximal tubular brush border membrane after glomerular filtration.
Use of angiotensin II receptor blockers, beta-blockers and aldosterone antagonists lower levels of natriuretic peptides in patients with CHF.
Long-term treatment with Beta-adrenergic blockers can reduce BNP levels, although levels may increase in the short-term (Kawai K).
Levels increase 1.5 fold in patients who develop transfusion overload but do not change in a control group of transfusion recipients.
Meta-analysis of 8 studies revealed that BNP guided treatment for CHF can decrease all cause mortality compared to patients treated by usual clinical care, especially in patients younger than 75 years (Porapakkham, P).
BNP guided treatment of CHF does not reduce all cause hospitalization or increase survival free of hospitalization (Porapakkham, P).