Brain natriuretic peptide (BNP)

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.

B-type natriuretic peptide.

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.

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