Does the BNP Level Have Prognostic Value in Acute MI?
Abstract & Commentary
Source: Mega JL, et al. B-type natriuretic peptide at presentation and prognosis in patients with ST-segment elevation myocardial infarction: An ENTIRE-TIMI23 substudy. J Am Coll Cardiol 2004;44:335-339.
B-type natriuretic peptide (BNP) is released from cardiac tissue in response to increased wall stress, and measurement of its level recently has been shown to aid in the diagnosis of congestive heart failure (CHF) in the emergency department (ED). As a result, BNP has been proposed as an additional marker for cardiac injury in the settling of acute coronary syndromes. However, less is known about the utility of this biomarker in this setting, and particularly with ST-segment elevation myocardial infarction (STEMI).
In this substudy of the ENTIRE-TIMI 23 trial (enoxaparin tenecteplase-tPA with or without glycoprotein IIb/IIIa inhibitor as reperfusion strategy in ST-segment elevation MI), 483 patients with STEMI were randomized to receive various treatment arms of fibrinolysis, glycoprotein inhibitor, and heparins, followed by immediate angiography to assess reperfusion. As part of this study, patients also had BNP, troponin I, and C-reactive protein (CRP) levels measured on arrival. Outcome measures were 30-day mortality and evidence of reperfusion success angiographically or electrocardiographically.
The median concentration of BNP in 438 patients who had results available (91%) was 15.6 pg/mL. That level was significantly higher in the 15 patients who died within 30 days of STEMI compared with those who did not (89 vs 15 pg/mL, P<0.0001). Patients with B-type natriuretic peptide (BNP) levels in the highest quartile (>32 pg/mL) had an 11-fold higher risk of death compared with all others (P<0.001). Using a pre-specified cut-off value of BNP > 80 pg/mL, patients with an elevated BNP level had a significantly higher rate of mortality (17.4% vs 1.8%, P<0.0001).
When compared with troponin I and CRP, BNP was a substantially more robust marker of 30-day mortality. Statistically, CRP was not associated with mortality in this study, and troponin levels, in fact, did not offer prognostic information independent of BNP. BNP levels remained associated independently with mortality, even when adjusted for major clinical predictors of mortality such as age, anterior myocardial infarction location, time of onset, heart rate, blood pressure, and CHF at presentation.
As for reperfusion, BNP levels > 80 pg/mL were associated with increased rates of incomplete reperfusion of the infarct-related artery on angiography and incomplete resolution of ST-segment elevation electrocardiographically. The authors speculate that elevated BNP levels on presentation may be associated with left ventricular hypertrophy, unrecognized ventricular dysfunction, or a large territory of infarct and ischemia that may be associated with impaired reperfusion and increased mortality. They conclude that this study supports the approach of combining BNP, a marker of hemodynamic stress, with more traditional markers of myocardial necrosis, for risk assessment of STEMI patients at the time of presentation.
Commentary by Theodore C. Chan, MD, FACEP
BNP has emerged as an important diagnostic biomarker for acute CHF exacerbations in patients presenting to the ED.1 Increased levels of BNP also have been associated with acute myocardial infarction, but the time course and utility of this finding is unclear. This is one of the first studies to assess the prognostic value of BNP on arrival to the ED in patients with STEMI.
The authors report that an elevated BNP level was associated with decreaed rates of successful reperfusion after fibrinolysis and increased rates of mortality at 30 days. In fact, in this study, BNP was a more robust prognostic marker when compared with CRP or even troponin.
A few points, however, need to be kept in mind regarding this study. First, as a substudy of a larger, industry-sponsored trial looking at pharmacologic treatment of STEMI, patients received multiple different treatment regimens. It is unclear what, if any, effect those differing pharmacologic treatment arms may have had on the relationship between BNP levels and mortality rates. Second, the overall STEMI mortality rate was quite low in this study (3.5%), with only 15 patients dying within 30 days. A larger study is needed to fully assess the prognostic value of BNP. Third, the cut-off level for BNP of 80 pg/mL is remarkably lower than the standard cut-off level for the diagnosis of CHF. No data are provided regarding the actual range of BNP levels, although quartile levels are provided and the 75th percentile level was still quite low — 192 pg/mL—in those who died at 30 days. It is unclear if this level represents an acute rise in BNP due to the STEMI event or a chronic elevation in patients who are at risk for poor outcome from the event. Indeed, the authors did report that BNP levels greater than 80 pg/mL were associated with patients who were older, had a history of hypertension, angina, and CHF, or were already receiving beta-blockers or angiotensin-converting enzyme inhibitors.
Despite these limitations, the findings of this study are still provocative. They suggest that even modest elevations in BNP levels in patients with STEMI are a marker for increased mortality. Just as important, BNP levels may identify patients who are less likely to respond with complete reperfusion following pharmacologic fibrinolysis and who might benefit from more interventional approaches.
Dr. Chan, Associate Professor of Clinical Medicine, Emergency Medicine, University of California, San Diego, is on the Editorial Board of Emergency Medicine Alert.
Reference
1. Maisel AS, et al. Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure. N Engl J Med 2002;347:161-167.
In this substudy of the ENTIRE-TIMI 23 trial (enoxaparin tenecteplase-tPA with or without glycoprotein IIb/IIIa inhibitor as reperfusion strategy in ST-segment elevation MI), 483 patients with STEMI were randomized to receive various treatment arms of fibrinolysis, glycoprotein inhibitor, and heparins, followed by immediate angiography to assess reperfusion.
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