Differential platelet oxidation-inflammatory phenotype in coronary artery disease versus peripheral artery disease supports diverse pathophysiological processes

Platelets are major contributors to atherothrombosis. There is emerging evidence that atherothrombosis pathogenesis may be different between vascular beds. In a prospective case-control study, we compared platelet oxidation-inflammatory status from patients with coronary artery disease CAD, peripheral artery disease (PAD) and a young healthy cohort. All patients had stable disease with no recent acute CAD or PAD events. Assessment of 75 eligible patients revealed a typical outpatient cardiology cohort. A significant increase in platelet activation (soluble P-selectin and CD40L) was seen in CAD. Consistent with this platelet activation, the CAD group had the highest levels of oxidants (reactive oxygen species, lipid peroxidation and protein carbonylation) and the lowest levels of antioxidants (catalase and superoxide dismutase enzyme activity). IL1bwas significantly increased in the PAD group. The significant differences in the oxidation-inflammatory parameters, between patients with CAD versus PAD, may explain different atherothrombosis pathology, as well differential response to therapies, such as aspirin and P2Y12 inhibitors. Whether these are the cause or consequence of disease or both, requires further extensive exploration. Such mechanistic understanding is important in developing disease targeted therapies.