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Paul Holvoet, PhD; Désiré Collen, MD, PhD; Frans Van de Werf, MD, PhD

JAMA. 1999;281:1718-1721.

Context  Release of circulating malondialdehyde (MDA)-modified low-density lipoprotein (LDL) may reflect endothelial injury or plaque instability.

Objective  To determine the usefulness of MDA-modified LDL for identifying patients with unstable angina and acute myocardial infarction (AMI).

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 ischemia.

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 (²=10.2; P=.001), but not troponin I or C-reactive protein, discriminated between stable CAD and unstable angina. Troponin I (²=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 (²=14.5; P<.001 and ²=5.3; P=.02, 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 alone.

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.

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