Basics of proBNP in Heart Failure
Introduction
The cardiac marker known as proBNP is useful in the assessment and diagnosis of cardiac failure. In this short article, we will expand on some of its usefulness. One need to remember that the GOLD standard for diagnosis of cardiac failure is the cardiac ultrasound. This is because the cardiac ultrasound will assist with the measurement of the EJECTION FRACTION.
However, cardiac ultrasound is not an investigation that is always readily available. In low-resource settings, you may not have an echocardiogram or the preferred trained staff to perform such an investigation. The “turn-around time” for the echocardiogram is also usually slow as well. However, with proBNP, all these issues are resolved. ProBNP also has a turn-around of approximately 1-2 hours.
ProBNP forms part of a family of peptides known as “Natriuretic peptides”, some common ones include Atrial Natriuretic Peptide, Brain Natriuretic Peptide, and a few others. They all cause sodium and water excretion in order to lower blood pressure. The heart is able to secret two of these peptides: Atrial Natriuretic Peptide (ANP) and Brain Natriuretic Peptide (BNP). ANP is secreted from the atria of the heart while BNP is secreted by the ventricles of the heart (including the brain).
In comparison with all the Natriuretic Peptides, BNP is the better one for assessing ventricular function and a good marker as a prognostic indicator.
Basics
When there is a large intravascular volume/fluid overload, the cardiac walls become stretched and this stimulates the cardiac myocyte to produce BNP. This is done as: pre-proBNP -> proBNP, then proBNP is cleaved/split into BNP (half life of 20 mins, which is active) and NT-proBNP (half life of 60 – 120mins, which is inactive) which is then released into the blood.
Why use proBNP?
When you request proBNP or BNP in the NHLS request form, the laboratory will usually give you results for NT-proBNP. Although it is “inactive”, it is the preferred cardiac marker because of the longer half life. There is also a good correlation in the raise of NT-proBNP and its synthesis from a failing heart. It is also correlates directly with the severity of the heart failure.
Causes of raised proBNP
- Systolic and diastolic left ventricular dysfunction
- Stable coronary heart disease
- Valvular heart disease
- Acute right ventricular failure
- Left and right ventricular hypertrophy secondary to arterial or pulmonary hypertension
- sepsis
It is very important to understand that when measuring the proBNP, the reference range is less valuable than the “Baseline level of the patient” and the “cut-off value” for what is normal in this patient. The proBNP levels should be correlated with the age-stratified cut points. Therefore, do NOT look at the reference ranges, but look at the (1)age of the patient(2) cut-off points (3) trends (4) clinical picture.
| If NT-proBNP: 300 – 1800 ng/L, then consider age-stratified cutpoints | ||
|---|---|---|
| Age (years) | NT-proBNP (ng/L) | |
| <50 | 300-450 | >450 |
| 50-75 | 300-900 | >900 |
| >75 | 300-1800 | >1800 |
| Interpretation | Acute heart failure less likely, alternative causes must be considered | Acute heart failure likely, consider confounding factors |
However, NHLS currently advices that for patients presenting with symptoms consistent with a possible diagnosis of acute heart failure, the cut-off points should be: Age < 75 (>125ng/L) and Age >75 (>450ng/L).
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