BNP (Brain Natriuretic Peptide)

Measurement of levels provide information about left ventricular function.

Ref2242ed to as B-Type Natriuretic Peptide, a neurohormone.

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).

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