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Volume 158, Issue 5, Pages 777-783 (November 2009)


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Prognostic value of B-type natriuretic peptide for cardiovascular events independent of left ventricular end-diastolic pressure

Robert Kevin Rogers, MD, MSCIaCorresponding Author Informationemail address, Heidi T. May, PhD, MSPHb, Jeffrey L. Anderson, MDab, J. Brent Muhlestein, MDab

Received 20 May 2009; accepted 3 September 2009.

Background

B-type natriuretic peptide (BNP) correlates with left ventricular (LV) end-diastolic pressure (LVEDP) and predicts cardiovascular events. We sought to determine whether BNP has prognostic value independent of LVEDP.

Methods

Eligible patients were referred for coronary angiography between March 15, 2002, and April 30, 2008, at a single institution. Inclusion criteria were having BNP, LV ejection fraction (EF), and LVEDP measured within 24 hours of the angiogram. The predictive value of BNP for events independent of LVEDP, EF, and other confounders was determined.

Results

The study population (n = 1,059) was followed for a mean of 1.8 ± 1.7 years. The mean age was 63 ± 13 years. The median BNP value was 182 pg/mL; 59% of patients had LVEDP ≥16 mm Hg. B-type natriuretic peptide and LVEDP had a modest but statistically significant correlation (r = 0.24, P < .0001). After adjustment for LVEDP and EF, the hazard ratio for the composite outcome of heart failure admissions and death was 1.37 (1.21-1.55, P < .0001) per unit increase in log BNP. After adjustment for BNP and EF, LVEDP did not predict heart failure admissions and death (hazard ratio 1.05 [0.95-1.10], per 5-mm Hg increase, P = .30). Those with BNP value below the median had longer event-free survival as compared to those with BNP value above the median, regardless of the LVEDP strata (log-rank P < .0001 for LVEDP ≥16 and <16 mm Hg).

Conclusion

B-type natriuretic peptide has prognostic value independent of LVEDP in this cohort with suspected coronary artery disease, suggesting this biomarker is not just a prognostic surrogate for elevated LV filling pressure.

a University of Utah, Division of Cardiology, Salt Lake City, UT

b Intermountain Health Care, Division of Cardiology, Murray, UT

Corresponding Author InformationReprint requests: Robert Kevin Rogers, MD, Division of Cardiology, University of Utah Health Sciences, 30 North 1900 East, Rm 4A100, Salt Lake City, UT 84132-2401.

PII: S0002-8703(09)00719-4

doi:10.1016/j.ahj.2009.09.002


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