Oxidative modification of LDL may occur via mechanisms, which are either dependent or independent of lipid peroxidation. Peroxidation of lipids in LDL, either initiated by radicals or catalysed by myeloperoxidase, results in the generation of aldehydes which substitute lysine residues in the apolipoprotein B-100 moiety and thus in the generation of oxidised LDL. Phospholipase activity, prostaglandin synthesis and platelet adhesion/activation are associated with the release of aldehydes which induce oxidative modifications of LDL in the absence of lipid peroxidation and thus in the generation of malondialdehyde-modified LDL. Recently, we have demonstrated an association between coronary artery disease and increased plasma levels of oxidised LDL. The increase of circulating oxidised LDL is most probably due to backdiffusion of oxidised LDL from the atherosclerotic arterial wall in the blood and is independent of plaque instability. Indeed, plasma levels of oxidised LDL were very similar in patients with stable coronary artery disease and in patients with acute coronary syndromes. Acute coronary syndromes were, however, associated with increased release of malondialdehyde-modified LDL that was independent of necrosis of myocardial cells. Indeed, plasma levels of malondialdehyde-modified LDL were very similar in patients with unstable angina and patients with acute myocardial infarction, in contrast with levels of troponin I which were significantly higher in acute myocardial infarction patients. These data suggest that oxidised LDL is rather a marker of coronary atherosclerosis whereas malondialdehyde-modified LDL is rather a marker of plaque instability and atherothrombosis. At present, in the absence of prospective studies, the causative role of oxidatively modified LDL in atherothrombosis is, however, not established.