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Holvoet P, Collen D, Van de Werf F. Malondialdehyde-Modified LDL as a Marker of Acute Coronary Syndromes. JAMA. 1999;281(18):1718–1721. doi:10.1001/jama.281.18.1718
Author Affiliations: Center for Molecular and Vascular Biology (Drs Holvoet and Collen) and the Department of Cardiology (Dr Van de Werf), University of Leuven, Leuven, Belgium.
Context Release of circulating malondialdehyde (MDA)-modified
low-density lipoprotein (LDL) may reflect endothelial injury or plaque
Objective To determine the usefulness of MDA-modified LDL for
identifying patients with unstable angina and acute myocardial
Design Blinded comparison of MDA-modified LDL, C-reactive protein,
and troponin I followed by multiple receiver operating curve analysis.
Setting University hospital.
Participants A total of 104 consecutive patients with acute
coronary syndromes (42 with unstable angina and 62 with AMI), and 64
patients with stable coronary artery disease (CAD) without evidence of
Main Outcome Measures Ability of MDA-modified LDL, C-reactive
protein, and troponin I to discriminate patients with stable CAD,
unstable angina, or AMI.
Results Malondialdehyde-modified LDL
P=.001), but not troponin I or C-reactive
protein, discriminated between stable CAD and unstable angina. Troponin
I (χ2=14.5; P<.001), but not
MDA-modified LDL or C-reactive protein, discriminated between unstable
angina and AMI. Both MDA-modified LDL and troponin I
(χ2=14.5; P<.001 and
respectively) but not C-reactive protein discriminated between stable
CAD and AMI. The sensitivity of MDA-modified LDL was 95% for unstable
angina and 95% for AMI, with a specificity of 95%. Values for
troponin I were 38% and 90%, respectively, with a specificity of
95%. The combination of MDA-modified LDL and troponin I had a
sensitivity of 98% for unstable angina and 100% for AMI, with a
specificity of 99%.
Conclusion The combination of MDA-modified LDL, which
may reflect endothelial injury or plaque instability, and troponin I,
which reflects myocardial cell injury, allows better discrimination
between stable CAD and acute coronary syndromes than troponin I
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