Abstract
Oxidative stress (OS), derived from an imbalance between reactive oxygen species (ROS) accumulation and impaired antioxidant defense, is a recognized cause of atherothrombosis, through a complex interaction between low-grade inflammation and platelet activation. Lipid peroxidation, as reflected by the urinary excretion of 8-iso-Prostaglandin F2α (8-iso-PGF(2α)), is central in the pathogenesis of atherosclerosis. This biochemical abnormality has been observed in patients with cardiovascular risk factors, including diabetes mellitus, obesity, cigarette smoking, hypercholesterolemia, hypertension, atrial fibrillation, and in clinical settings associated with aging, such as acute and chronic cardiovascular diseases and chronic kidney disease. Despite the treatment with acetylsalicylic acid or with any other antithrombotic drugs, patients may undergo recurrent events due to the complex nature of atherothrombosis. A large body of evidence supports the relationship between OS and less-than-expected response to aspirin. Several disease-modifying agents and antioxidant supplementation, as well as modulation of the primary metabolic abnormalities driving lipid peroxidation, have been shown to reduce urinary 8-iso-PGF(2α) excretion. Overall, these observations pave the way for potential therapeutic approaches able to target these mechanisms, resulting in the reduction of atherothrombosis progression. This will be an overview of the significance of 8-iso-PGF(2α) in the pathogenesis of atherothrombosis and as a potential mechanism-based biomarker of cardiovascular events.