Platelet-Activating Factor Acetylhydrolase is Not Associated with Carotid Intima-Media Thickness in Hypercholesterolemic Sicilian Individuals (Lipids, Lipoproteins, And Cardiovascular Risk Factors‪)‬

Atherosclerosis is a chronic inflammatory disease characterized by endothelial dysfunction and lipid and macrophage accumulation in the arterial wall. In hypercholesterolemia, the atherosclerosic process is triggered by increased concentrations of LDL-cholesterol (LDL-C) [3] that lead to the retention and accumulation of oxidized bioactive lipids in the subendothelial space, inducing a proinflammatory reaction by vascular cells (1, 2). Thus, LDL oxidation is considered one of the first steps in the early stages of atherosclerosis (3). Platelet-activating factor acetylhydrolase (PAF-AH) is a hydrophobic enzyme associated with LDL and HDL that inactivates PAF and also plays an important role in preventing LDL oxidation by hydrolyzing oxidized phospholipids (4,5). PAF has already been described as a potent proinflammatory substance suggested to be a mediator involved in several diseases as well as allergy and atherosclerosis.