To evaluate the prognostic role of novel biomarkers for the risk stratification of
patients admitted with ischemic-type chest pain, a prospective study of 664 patients
presenting to 2 coronary care units with ischemic-type chest pain was conducted over
3 years beginning in 2003. Patients were assessed on admission for clinical characteristics,
electrocardiographic findings, renal function, cardiac troponin T (cTnT), markers
of myocyte injury (heart fatty acid–binding protein [H-FABP] and glycogen phosphorylase
BB), neurohormonal activation (N-terminal–pro-brain natriuretic peptide [NT–pro-BNP]),
hemostatic activity (fibrinogen and d-dimer), and vascular inflammation (high-sensitivity C-reactive protein, myeloperoxidase,
matrix metalloproteinase–9, pregnancy-associated plasma protein–A, and soluble CD40
ligand). A ≥12-hour cTnT sample was also obtained. Myocardial infarction (MI) was
defined as peak cTnT ≥0.03 μg/L. Patients were followed for 1 year from the time of
admission. The primary end point was death or MI. Elevated fibrinogen, d-dimer, H-FABP, NT–pro-BNP, and peak cTnT were predictive of death or MI within 1
year (unadjusted odds ratios 2.5, 3.1, 5.4, 5.4, and 6.9, respectively). On multivariate
analysis, H-FABP and NT–pro-BNP were selected, in addition to age, peak cTnT, and
left ventricular hypertrophy on initial electrocardiography, as significant independent
predictors of death or MI within 1 year. Patients without elevations of H-FABP, NT–pro-BNP,
or peak cTnT formed a very low risk group in terms of death or MI within 1 year. A
very high risk group had elevations of all 3 biomarkers. In conclusion, the measurement
of H-FABP and NT–pro-BNP at the time of hospital admission for patients with ischemic-type
chest pain adds useful prognostic information to that provided by the measurement
of baseline and 12-hour cTnT.
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Article Info
Publication History
Published online: October 20, 2008
Accepted:
August 22,
2008
Received in revised form:
August 22,
2008
Received:
July 26,
2008
Footnotes
This study was supported by a research fellowship from Royal Victoria Hospital, Belfast, United Kingdom; the Heart Trust Fund at Royal Victoria Hospital, Belfast, United Kingdom; grant 200312 from the Northern Ireland Chest, Heart, and Stroke Association, Belfast, United Kingdom; and Merck, Sharp & Doehme Ltd., Hoddesdon, United Kingdom.
Identification
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© 2009 Elsevier Inc. Published by Elsevier Inc. All rights reserved.
