Brain natriuretic peptide, a hormone released by the left and right cardiac ventricles, was originally identified in pig brain. It is now called B-type natriuretic peptide (BNP).
Levels can fluctuate rapidly, because it is released immediately from storage granules within the cardiac myocytes, and its half-life is less than 30 minutes. A normal heart secretes small amounts of BNP within a fairly narrow range, but an acutely strained heart can secrete very high levels.
BNP in primary care
These facts underpin the characteristics of BNP as a clinical test (see box). Elevated BNP always means trouble with the heart, but does not equate exactly to anything we label heart failure.
|BNP as a clinical test|
- Levels of BNP are always high in situations of acute, uncompressed heart strain
- Elevation is seen in a range of conditions with cardiac overload
- BNP cannot distinguish between right and left ventricular dysfunction, or between systolic and diastolic dysfunction
- Levels of BNP fall with successful treatment of cardiac overload or impairment, whatever the cause6
- As patients enter the end-stage of heart failure, levels remain high and no longer respond to treatment
- BNP is a good marker for prognosis
In primary care, it might be useful to know if the heart is in trouble when we suspect a cardiac cause for breathlessness, when screening for cardiac strain in high-risk groups, when guiding the management of established heart failure, or when giving a prognosis in advanced heart failure. There is no clear evidence from primary care to guide us in any of these situations except the first, and even this presents major problems (see below).
Heart failure presents overwhelmingly (>90 per cent) in patients with the risk factors listed above,1 so it is tempting to think BNP might be a good screening test in such patients. But this concept has yet to be fully tested.
Similar problems apply to the use of BNP in primary care to monitor treatment of heart failure. Although we know most heart failure drugs lower levels of BNP over time, this may not apply to all beta-blockers licensed for systolic dysfunction.2
We know BNP is a good indicator of prognosis, but this has not yet been put to use in primary or palliative care. Measuring BNP may help in deciding when it is appropriate to discuss palliative care with a patient with advanced heart failure.
BNP and heart failure
Several studies looked at the use of BNP in selecting patients with suspected heart failure for echocardiography. In new patients who are not on treatment for suspected heart failure, normal BNP makes it unlikely the echocardiogram will show systolic impairment.3 In such patients, it may be more useful than normal ECG as a rule-out test. In more heterogeneous groups, as in my own early study,4 it may show no advantage.
This brings us to the vexed question of what heart failure is.5 Almost all we know about treating it comes from studies that recruited mostly male patients under the age of 70 years, without co-morbidities but with lowered systolic ejection fractions.
In successive studies, more and more drugs were used with such patients, until no incremental benefit was detectable. So the standard management has been to measure the systolic ejection fraction and if this is reduced, to use as many drugs as possible at the highest tolerated dose. Most of the heart failure we see in general practice is not like this. The ejection fraction, measured at rest, is a poor guide here. By contrast, BNP tells us the degree of cardiac impairment at a particular point in time.
In the acute situation, we can use BNP to determine the degree of cardiac contribution to breathlessness in individual patients. Breathless elderly patients often present a mixed picture, because what affects the lungs affects the heart and vice versa. BNP gives us a ‘point-in-time’ measurement of heart strain and how it may be contributing to breathlessness. It varies, like blood sugar levels, and is not a measure of overall control, like HbA1c. When we have a better evidence base, we should be able to use BNP to fine-tune management of all cardiac impairment, not just patients with left systolic dysfunction. Now, managing heart failure is like trying to manage diabetes without being able to measure blood sugar levels. BNP’s potential is enormous.
- Dr Richard Lehman is a GP in Banbury, Oxfordshire, and senior research fellow at the department of public health and primary care, University of Oxford
1. Davies MK, Hobbs FDR, Davis R et al. Prevalence of left ventricular dysfunction and heart failure in the Echographic Heart of England Screening Study: a population based study. Lancet 2001; 358; 439-45.
2. Davis ME, Richards AM, Nicholls MG et al. Introduction of metoprolol increases plasma B-type cardiac natriuretic peptides in mild, stable heart failure. Circulation 2006; 113: 977-85.
3. Fuat A, Murphy JJ, Curry J et al. The diagnostic accuracy and utility of a B-type natriuretic peptide test in a community population of patients with suspected heart failure. Br J Gen Pract 2006; 56: 327-33.
4. Landray MJ, Lehman R, Arnold I. Measuring brain natriuretic peptide in suspected left ventricular dysfunction in general practice: cross-sectional study. BMJ 2000; 320: 985-6.
5. Lehman R, Doust J, Glasziou P. Cardiac impairment or heart failure? (editorial) BMJ 2005; 331: 415-6.
6. Troughton RW, Frampton CM, Yandle TG et al. Treatment of heart failure guided by plasma amino-terminal brain natriuretic peptide (N-BNP) concentrations. Lancet 2000; 355: 1126-30.