Letter Regarding Article by Winkler et al, “Platelet-Activating Factor Acetylhydrolase Activity Indicates Angiographic Coronary Artery Disease Independently of Systemic Inflammation and Other Risk Factors: The Ludwigshafen Risk and Cardiovascular Health Study”

Abstract

To the Editor: Winkler and colleagues1 have published an epidemiological study on the platelet-activating factor acetylhydrolase (PAF-AH) and coronary artery disease. The authors stated erroneously in the Introduction that PAF-AH releases arachidonic acid, a precursor of eicosanoid production including prostaglandins and leukotrienes. On the basis of this assumption, the authors suggest in the Discussion that PAF-AH possesses proinflammatory functions within the atherosclerotic plaque because it is preferentially associated with small dense LDL2; the latter may thus contribute to atherogenesis by functioning as a reservoir of the essential substrate (ie, the arachidonate-containing phosphatidylcholine), and the source of crucial enzyme activity necessary for prostaglandin synthesis. In addition, the authors emphasize that this concept would confer an …