What is the role of BNP measurements in medical decision making in the diagnosis and treatment of acute heart failure?

Updated: Jul 30, 2021
  • Author: Kamal (Komo) Gursahani, MD, MBA; Chief Editor: Barry E Brenner, MD, PhD, FACEP  more...
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Based on level A evidence from guidelines for the management of heart failure by the American College of Cardiology, American Heart Association, and the Heart Failure Society of America (ACC/AHA/HFSA), early measurement of BNP levels is recommended to support medical decision making in the diagnosis of acute heart failure, especially if there is clinical uncertainty, and to assess disease severity in chronic heart failure. [71, 72] Although the authors noted that serial BNP or NT-proBNP measurements have not been shown to improve meaningful outcomes (eg, reduction in hospitalizations, mortality from heart failure), a growing body of evidence supports the use of a single NP measurement on admission and a predischarge measure to guide prognosis. Several studies have revealed that when levels of NPs are higher prior to discharge than they were at admission for heart failure, patients are at risk of worse outcomes such as readmission and death. [71, 72]

Additionally, a growing body of literature suggests the use of BNP and/or NT-proBNP as a screening diagnostic tool for asymptomatic patients at risk of developing heart failure may be useful; however, more information is needed to determine the value proposition of this intervention. [72, 73]

Multiple studies have demonstrated that BNP may also be a useful prognostic indicator in acute coronary syndrome (ACS). Several investigations by the Thrombolysis in Myocardial Infarction (TIMI) Study Group showed that the BNP level predicted cardiac mortality and other adverse cardiac events across the entire spectrum of ACS. The mortality rate nearly doubled when both troponin I (TnI) and BNP levels were elevated.

In the Treat Angina with Aggrastat and Determine Cost of Therapy with an Invasive or Conservative Strategy (TACTICS)-TIMI 18 trial, an elevated BNP level was associated with tighter culprit stenosis, higher corrected TIMI frame count, and left anterior descending artery involvement. [61] These data suggest that increased BNP levels may correlate with greater severity of myocardial ischemia and could partially explain the association between increased BNP levels and adverse outcomes.

Data from the Oral Glycoprotein IIb/IIIa Inhibition with Orbofiban in Patients with Unstable Coronary Syndromes (OPUS)-TIMI 16 and TACTICS-TIMI 18 demonstrated that baseline elevations of TnI, C-reactive protein (CRP), and BNP levels in patients with non-ST-elevated MI (NSTEMI) were independent predictors of the composite endpoint of death, MI, or heart failure. [74] The Proteomic Testing (PROMPT)-TIMI 35 trial demonstrated that transient myocardial ischemia during exercise testing was associated with an immediate rise in BNP levels. [75] In addition, the severity of ischemia was directly proportional to the elevation in BNP.

Heart failure

The presence of acute heart failure in patients with ACS is a well-known predictor of adverse cardiac events and higher risk. Therefore, it is not surprising that an elevated BNP level, as a marker of heart failure, is also predictive of adverse cardiac events in patients with ACS. Furthermore, the use of BNP and cardiac troponins on admission to the hospital is recommended by the ACC to help with prognosis in acutely decompensated heart failure. [72] Both natriuretic peptides and cardiac troponins, therefore, are clinically useful for the management of both ACS and heart failure in hospitalized patients.


There are limitations to the use of NPs, mostly related to their lack of specificity. Elevated baseline serum levels have been found due to noncardiac patient factors, such as increasing age, female sex, pulmonary disease, sepsis, renal dysfunction, and the use of a relatively newer class of pharmacotherapy for heart failure known as angiotensin receptor-neprilysin inhibitors (ARNIs). Neprilysin is an enzyme involved in the degradation of NPs in the circulation. ARNIs inhibit neprilysin, resulting in elevated levels of NPs, which then may interfere with the prognostic utility of BNP. [76]

However, note that obese patients may have lower circulating BNP, not NT-proBNP. And NP levels may not be elevated in those patients who develop flash pulmonary edema, as the symptoms and signs may develop before the rise in levels occurs.

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